Frontal, Emocion y Psicopatologia PDF

Biological Psychology 67 (2004) 1–5
Editorial
Frontal EEG asymmetry, emotion, and
psychopathology: the first, and the next 25 years
Over 25 years ago, at the annual meeting of the Society for Psychophysiological Research
in Madison, Wisconsin, in September of 1978, Richie Davidson presented a paper suggesting
that the experiences of positive and negative effect were associated with differential patterns
asymmetrical frontal brain electrical activity. The abstract of this presentation represented
the first published account of the use of frontal electroencephalographic (EEG) asymmetry
in emotional experience (Davidson et al., 1979), and there was a dearth of work on this topic
in the ensuing decade. How things have changed! Research on frontal EEG asymmetry and
emotion has enjoyed considerable popularity in recent years. The tabular review of this
literature in Coan and Allen (2004) reveals that after this initial paper in 1979, there were
five empirical papers from 1980–1985, 10 more papers by 1990, another 19 by 1995, an
additional 40 by 2000, and now 29 papers published or in press since 2000. Frontal EEG
asymmetries have been examined as a trait individual difference that has been found to
be related to other trait individual differences, that has been found to identify those with
depressive and anxious psychopathology and possibly those at risk for psychopathology,
and that has been found to predict subsequent emotional responses. Additionally, alterations
of frontal EEG asymmetry have been found in response to tasks or emotion manipulations.
In an era where functional neuroimaging methodologies, such as positron emission to-
mography (PET) and functional magnetic resonance imaging (fMRI), have seen an expo-
nential increase in the study of emotion and psychopathology, one might question whether
there remains a role for frontal EEG asymmetry in the study of emotion, motivation, and
psychopathology. Aside from the obvious advantages of EEG as a measure that is less
invasive, less expensive, and more widely available than many neuroimaging modalities,
frontal EEG asymmetry has established—by virtue of the nearly 100 studies using this
measure—a sizable literature that embeds the measure in a network of psychological and
behavioral constructs, thus bestowing frontal EEG asymmetry with sizable construct va-
lidity as a measure of an underlying approach-related or withdrawal-related motivational
style (e.g. Davidson et al., 2000; Harmon-Jones, 2004), or as an index of potential risk
for emotion-related psychopathology (Coan and Allen, 2004). As such, frontal EEG asym-
metry has greater construct validity as a measure of this motivational style than does any
neuroimaging measure to date.
On the other hand, the evidence linking frontal EEG asymmetry to the activity of under-
lying neural systems involved in the experience, expression, and regulation of emotion is
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2 Editorial / Biological Psychology 67 (2004) 1–5
considerably lacking. When one reads the frontal EEG asymmetry literature, one might be
struck by the irony that this psychophysiological measure seems much more psychological
than physiological in terms of the inferences that can be drawn from the findings to date. As
one reads the papers in this special issue, it is apparent (Cacioppo, 2004) that they in large
part continue in this tradition of linking frontal EEG asymmetry to important psychological
constructs, including depression and related constructs (Jones et al., 2004; Minnix et al.,
2004; Nitschke et al., 2004; Tomarken et al., 2004) as well as states of anger or cogni-
tive dissonance (Harmon-Jones, 2004). As such, the psychological construct validity (see
Cacioppo, 2004; Hagemann, 2004) of frontal EEG asymmetry is bolstered, suggesting it
may have considerable utility in studies of motivation, emotion, and psychopathology, even
in the absence of strong links to activity in underlying neural structures.
If one wishes, however, to develop a theory of how neural systems give rise to emotional
experience, expression, and regulation, then studies that solely link EEG asymmetry to
psychological or behavioral measures will ultimately prove insufficient (Davidson, 2004).
A complete account of the constructs assessed by frontal EEG asymmetry must link frontal
EEG asymmetry to both psychological/behavioral constructs and also to neurophysiological
constructs. Hagemann (2004) argues EEG asymmetry can be better linked to underlying
neural activity using specific reference montages that highlight local activity, and Davidson
(2004) suggests the merit of measuring EEG in the context of functional neuroimaging
studies. Heeding such advice will bolster the neurophysiological construct validity of EEG
asymmetry (Cacioppo, 2004; Hagemann, 2004), and, moreover, identify neural systems
involved in emotion and psychopathology that may not generate electrical signatures which
would be detectable using a rather global and spatially imprecise measure like frontal EEG
asymmetry.
Optimally, such work will inform and help refine the psychological theories of the con-
structs assessed by frontal EEG asymmetry. By identifying brain structures and systems
involved in aspects of emotional experience, expression, or regulation, or those that may be
related to individual differences or psychopathology, research can shape the psychological
theory by drawing on what is known about such structures and systems (cf. Willingham
and Dunn, 2003). But one must also be cautious in this approach, as localization per se
is not necessarily informative, unless such localization efforts employ careful behavioral
designs, and take advantage of extant knowledge of the functional significance of neural
systems involved in emotion. Stated more provocatively, although brain activation is indeed
potentially highly informative, as an independent or—especially—mediating or interven-
ing variable brain activation is not often informative when treated as a criterion variable
(Coan, personal communication). Brain activations that differ between conditions, tasks, or
individuals constitute weak evidence for a neural substrate (Cacioppo et al., 2003). Sim-
ilarly, EEG asymmetry should not be mistaken for a substrate, a claim that has appeared
occasionally in this literature (Sutton and Davidson, 1997; Wiedemann et al., 1999).
Particularly challenging for EEG asymmetry research is the fact that a vast majority of
the studies involve assessing individual differences in resting activity across a relatively
long interval of several minutes, rather than tightly controlled experimental paradigms.
Under such conditions, it may be especially challenging to use PET or fMRI to find neu-
ral activity that is well localized in a consistent fashion across subjects, and inferring the
meaning of such activity may be additionally vexing. It is possible that EEG asymmetry
Editorial / Biological Psychology 67 (2004) 1–5 3
may serve as a useful summary index of individual differences in the recruitment of un-
derlying neuronal systems by virtue of it being a measure with such coarse spatial and
temporal resolution, as it integrates information across systems and across time to provide
a summary index of an underlying propensity or affective style. It may therefore be the
case that establishing links between frontal EEG asymmetry and underlying neural systems
may not easily be accomplished using data obtained under relatively uncontrolled resting
conditions. The identification of such relationships may be enhanced, instead, by examin-
ing surface-recorded EEG and underlying neural activity in well-controlled state and task
manipulations.
As researchers continue to use measures of frontal EEG asymmetry, and as new re-
searchers come to use these measures, several important methodological issues are high-
lighted in this special issue (Allen et al., 2004; Hagemann, 2004) that may help provide some
greater standardization for this field, thus reducing the variation across studies in terms of
analysis and recording methods and procedures, which hopefully will promote a more sys-
tematic approach for the investigation of emotion, motivation, and psychopathology using
measures of frontal EEG asymmetry.
In this special issue readers will find integrative reviews of the work in this area. In
the first paper, Coan and Allen (2004) selectively review the nearly 100 studies in this
area, challenging researchers to think about the way in which frontal EEG asymmetry
may index factors that moderate, or mediate relationships with emotion, motivation, and
psychopathology. Harmon-Jones (2004) then addresses theoretical models of frontal EEG
asymmetry, and with an extensive series of clever studies from his laboratory, provides
evidence that favors a model that frontal EEG asymmetry taps motivational propensities
along a motivational dimension of approach and withdrawal.
Following these reviews are four empirical studies reporting new original research on de-
pression. In common among these papers is the finding that the relationship between frontal
EEG asymmetry and depression or risk for depression is not independent of the influence
of other important factors. Tomarken et al. (2004), with a highly valuable dataset comprised
of adolescents of depressed mothers, examine whether resting frontal EEG asymmetry may
serve as a marker of vulnerability for depression among adolescents, identifying also the
important role of socioeconomic status as a relevant factor in this relationship. Jones et al.
(2004) report that although infants of depressed mothers generally show relatively less left
frontal activity and more reactive temperaments, these relationships are not apparent if the
depressed mothers demonstrate a stable pattern of breastfeeding. Nitschke et al. (2004)
identified that features of frontal EEG activity preceding and during encoding of sad ma-
terial predict subsequent memory performance, but differently for subjects high or low in
depression. Whereas overall frontal power prior to encoding predicted memory performance
in low depressed controls, relatively greater right frontal activity during encoding of a sad
narrative predicted better memory performance among those with higher depression scores.
Finally, Minnix et al. (2004) report that the expected relationship between relatively less
left frontal activity depression was moderated by the extent to which subjects report they
engage in reassurance-seeking.
As research in this field moves from the first to the next 25 years, attention to method-
ological and interpretive details will be paramount. Research in this field had the luxury
in the early years of using limited montages, employing single (and possibly non-optimal)
4 Editorial / Biological Psychology 67 (2004) 1–5
reference schemes, and analyzing data using rather simple univariate statistical models.
Three papers in this special issue (Allen et al., 2004; Coan and Allen, 2004; Hagemann,
2004) challenge us to be more demanding researchers and discerning consumers of the lit-
erature on frontal EEG asymmetry, emotion, and psychopathology. The promise of frontal
EEG asymmetry for informing the study of emotion and psychopathology is apparent as
one reads this special issue. Yet the future of frontal EEG asymmetry research will bene-
fit from deliberately strategic use; such strategic use should further our understanding of
psychological phenomena—including emotional experience, expression, and regulation as
well as risk for psychopathology—or should serve as a bridge that can help identify the
links between social, behavioral, experiential, psychological, neuroanatomical, and cellular
levels of analysis (Anderson and Scott, 1999). There is sufficient work to be done using
measures of frontal EEG asymmetry to occupy scientists for at least another 25 years.
We wish to thank the authors whose work is featured in this issue, and also Bob Simons
for providing the idea for this special issue and entrusting us with its construction. We are
also indebted to the reviewers for their thoughtful critiques, especially to John Cacioppo and
Richie Davidson, who provided highly thoughtful commentaries at miserably short notice.
John J.B. Allen
(Guest Editor)
Department of Psychology
University of Arizona, P.O. Box 210068
Tucson, AZ 85721-0068, USA
E-mail address: jallen@u.arizona.edu (J.J.B. Allen)
John P. Kline
Department of Psychology
University of South Alabama, USA
References
Allen, J.J.B., Coan, J.A., Nazarian, M., 2004. Issues and assumptions on the road from raw signals to metrics of
frontal EEG asymmetry in emotion. Biological Psychology 67, 183–218.
Anderson, N.B., Scott, P.A., 1999. Making the case for psychophysiology during the era of molecular biology.
Psychophysiology 36, 1–13.
Cacioppo, J.T., Berntson, G.G., Lorig, T.S., Norris, C.J., Rickett, E., Nusbaum, H., 2003. Just because you’re
imaging the brain doesn’t mean you can stop using your head: A primer and set of first principles. Journal of
Personality and Social Psychology 85, 650–661.
Cacioppo, J.T., 2004. Feelings and emotions: Roles for electrophysiological markers. Biological Psychology 67,
235–243.
Coan, J.A. Allen, J.J.B., 2004. EEG Asymmetry as a moderator and mediator of emotion. Biological Psychology
67, 7–49.
Davidson, R.J., Schwartz, G.E., Saron, C., Bennett, J., Goleman, D.J., 1979. Frontal versus parietal EEG asymmetry
during positive and negative affect. Psychophysiology 16, 202–203.
Davidson, R.J., Jackson, D.C., Kalin, N.H., 2000. Emotion, plasticity, context, and regulation: perspectives from
affective neuroscience. Psychological Bulletin 126 (6), 890–909.
Davidson, R.J., 2004. What does the prefrontal cortex “do” in affect: Perspectives on frontal EEG asymmetry
research. Biological Psychology 67, 219–233.
Editorial / Biological Psychology 67 (2004) 1–5 5
Hagemann, D., 2004. Individual differences in anterior EEG-asymmetry: Methodological problems and solutions.
Biological Psychology 67, 157–182.
Harmon-Jones, E., 2004. Contributions from research on anger and cognitive dissonance to understanding the
motivational functions of asymmetrical frontal brain activity. Biological Psychology 67, 51–76.
Jones, N.A., McFall, B.A., Diego, M.A., 2004. Patterns of brain electrical activity in infants of depressed mothers
who breastfeed and bottle feed: The mediating role of infant temperament. Biological Psychology 67, 103–124.
Minnix, J.A., Kline, J.P., Blackhart, G.C., Pettit, J.W., Perez, M., Joiner, T.E., 2004. Relative left frontal activity
is associated with increased depression in high reassurance-seekers. Biological Psychology 67, 145–155.
Nitschke, J.B., Heller, W., Etienne, M.A., Miller, G.A., 2004. Prefrontal cortex activity differentiates processes
affecting memory in depression. Biological Psychology 67, 125–143.
Sutton, S.K., Davidson, R.J., 1997. Prefrontal brain asymmetry: A biological substrate of the behavioral approach
and inhibition systems. Psychological Science 8, 204–210.
Tomarken, A.J., Dichter, G.S., Garber, J., Simien, C., 2004. Resting frontal brain activity: Linkages to maternal
depression and socioeconomic status among adolescents. Biological Psychology 67, 77–102.
Wiedemann, G., Pauli, P., Dengier, W., Lutzenberger, W., Birbaumer, N., Buchkremer, G., 1999. Frontal brain
asymmetry as a biological substrate of emotions in patients with panic disorders. Archives of General Psychiatry
56, 78–84.
Willingham, D.T., Dunn, E.W., 2003. What neuroimaging and brain localization can do, cannot do, and should
not do for social psychology. Journal of Personality and Social Psychology 85, 662–671.
Review
Frontal EEG asymmetry as a moderator and
mediator of emotion
James A. Coan∗ , John J.B. Allen
University of Arizona, Tucson, AZ 85721-0068, USA
Abstract
Frontal EEG asymmetry appears to serve as (1) an individual difference variable related to emotional
responding and emotional disorders, and (2) a state-dependent concomitant of emotional responding.
Such findings, highlighted in this review, suggest that frontal EEG asymmetry may serve as both
a moderator and a mediator of emotion- and motivation-related constructs. Unequivocal evidence
supporting frontal EEG asymmetry as a moderator and/or mediator of emotion is lacking, as insuf-
ficient attention has been given to analyzing the frontal EEG asymmetries in terms of moderators
and mediators. The present report reviews the frontal EEG asymmetry literature from the framework
of moderators and mediators, and overviews data analytic strategies that would support claims of
moderation and mediation.
© 2004 Elsevier B.V. All rights reserved.
Keywords: Frontal EEG Asymmetry; Emotion; Mediators; Moderators
1. Introduction
Over 70 published studies have now examined the relationship between emotion or
emotion-related constructs and asymmetries in electroencephalographic (EEG) activity
over the frontal cortex. A review of these studies suggests asymmetries in frontal EEG
activity—including resting levels of activity as well as state-related activation—are ubiqui-
tous and involved in both trait predispositions to respond to emotional stimuli and changes
in emotional state (Coan and Allen, 2003a).
∗ Corresponding author. Present address: W.M. Keck Laboratory for Functional Brain Imaging and Behavior,
Waisman Center, University of Wisconsin–Madison, Madison, WI 53705, USA. Corresponding author.

Tel.: +1-608-265-6602.
E-mail address: jacoan@wisc.edu (J.A. Coan).
doi:10.1016/j.biopsycho.2004.03.002
8 J.A. Coan, J.J.B. Allen / Biological Psychology 67 (2004) 7–49
Studies of asymmetry can be classified as one of four types: (1) studies examining frontal
EEG asymmetry as an individual difference that is related to other traits or trait-like mea-
sures; (2) Studies examining frontal EEG asymmetry as an individual difference that can
predict state-related emotional changes and responses; (3) Studies examining frontal EEG
asymmetry as an individual difference that is related to psychopathology or risk for psy-
chopathology, especially depression and anxiety; and (4) Studies examining state-related
change in asymmetry as a function of state changes in emotion. The first three types of
studies explicitly assume that frontal EEG asymmetry has trait-like properties, whereas the
fourth type of study assumes that state-related changes in EEG asymmetry can be elicited
and observed.
Such findings suggest the possibility that the brain systems tapped by frontal EEG
asymmetries may moderate, in the case of activity, and mediate, in the case of activa-
tion, emotional responding. In particular, Davidson (e.g., Davidson, 1993) has proposed
that frontal EEG asymmetries reflect the activity of brain systems that moderate trait
tendencies to approach, and withdraw from, novel stimuli, and mediate approach and
withdrawal-motivational tendencies that underlie state emotional responding. Nevertheless,
definitive analyses of frontal EEG asymmetry as a moderator and mediator of emotion1 are
rare, possibly due to insufficient attention paid to the precise differences between moderators
and mediators, as well as to the data analytic demands that the differentiation of moderators
and mediators entail. This article reviews the large and growing literature on frontal EEG
asymmetry, emphasizing its potential as an important moderator and mediator of emotional
responding. Additionally, conceptual and statistical considerations in assessing the extent
to which frontal EEG asymmetry functions as both a moderator and mediator of emotional
responding are reviewed, and recommendations are made for future investigations.
2. Moderators, mediators and frontal EEG asymmetry
Conceptually, moderators and mediators have been confused in the literature at large
(Baron and Kenny, 1986). This may be particularly true of the literature on frontal EEG
asymmetry, which frequently implicates moderators and mediators—sometimes both—
conceptually, but making use of neither term, nor the special statistical considerations that
optimize the specification of moderators and mediators. Though important statistical con-
siderations will be discussed in detail later, it will be useful to review moderators and
mediators conceptually before continuing.
Moderators: Moderators are essentially third variables that represent conditions under
which some independent variable becomes maximally potent or effective. For example,
in many people, images of poisonous snakes (indeed, any snakes) elicit fear responses,
while, by contrast, more neutral images (such as, for example, images of elephants), do
1 To be precise, we would seldom be interested in whether frontal asymmetries in electrical activity per se
represent moderators or mediators of emotional responding, but rather would like to know whether activity in
the system(s) tapped by frontal EEG asymmetries serve as a moderators or mediators of emotional responding
(see Kline et al., 2003). For brevity and ease of reading, in the present discussion, we will talk about frontal EEG
asymmetry as a moderator and/or a mediator.
J.A. Coan, J.J.B. Allen / Biological Psychology 67 (2004) 7–49 9
not. If one were to argue that resting frontal EEG activity functions as a moderator of
such responses, one might draw from the literature to formulate the following argument:
Since resting asymmetries characterized by greater right-than-left frontal activity seem to
be associated with traits and behaviors indicative of withdrawal behaviors (e.g., Wheeler
et al., 1993), and since the emotion of fear is considered by many to be an emotion with
withdrawal-related motivational properties (e.g., Coan et al., 2001), one might predict that
individuals who possess a greater trait tendency toward relatively greater right frontal resting
EEG activity would be more sensitive to fear cues, or, at the very least, would react more
strongly to fear-related cues. Using the emerging example of snakes versus elephants, such
a prediction would be borne out by evidence that (1) individuals normatively respond with
more fear to images of snakes than to images of elephants and (2) that individuals possessing
relatively greater right frontal activity at rest would respond to images of snakes with still
more fear than is otherwise normative. This type of sensible prediction has indeed been
made by Davidson (1998a,b), who has referred to trait capacities to respond affectively in
characteristic ways as affective style. Davidson (1998a,b) has argued that an individual’s
affective style is in part moderated by asymmetries in frontal cortical activity, and his model
enjoys substantial, though not unequivocal, empirical support.2
Mediators: Mediators, by contrast, are third variables that represent the mechanism
through which (or partially through which) the effect of a given independent variable is
made manifest. For example, if one of the components of an ordinary fear experience is
a motivational tendency to withdraw, then eliciting that component of fear might require
activity in the brain systems tapped by frontal EEG asymmetries. This needn’t necessarily
mean that cortical activation asymmetries are always involved as a third variable mediator of
fear. It might mean, however, that whenever fear is characterized by a withdrawal-oriented
motivational component (and some would no doubt argue that this is always the case), that
component is dependent upon systems that are tapped by frontal EEG asymmetries. To
the extent that this is true, frontal EEG asymmetry would then function as a mediator of
emotional responses.
3. The measurement of frontal EEG asymmetry
Various issues surrounding the measurement and analysis of cortical EEG asymmetries
can make apprehending results in this area challenging. Thus, some discussion of mea-
surement and data analytic issues is warranted up front, though many of these issues are
addressed in greater detail elsewhere in this volume (see Allen et al., this volume). First,
evidence suggests that activity within the alpha range (typically 8–13 Hz) may be inversely
related to underlying cortical processing, since decreases in alpha tend to be observed when
underlying cortical systems engage in active processing. With this in mind, all results re-
viewed here will be reported in terms of theoretically assumed cortical activity rather than
alpha power per se.
2 An equally plausible prediction, though one not as frequently or explicitly encountered in the research
literature, is that the effects of frontal EEG asymmetry on, for example, depression, are themselves moderated by
other psychological traits (for a discussion of this possibility, see Minnix et al., this volume).
Second, in reviewing the literature, one will variously encounter references to frontal
EEG activity and frontal EEG activation. At first blush, insistence upon this distinction may
appear pedantic, but in fact, strict attention here can significantly enhance understanding of
research in this area, and is relevant to making inferences concerning the distinction between
frontal EEG asymmetry as a moderator or a mediator. For the purposes of this article, and
as a general recommendation, activity will refer to a tonic recording of cortical processes as
measured by EEG, while activation will refer to the change in EEG activity in response to
a provocation, such as the presentation of an emotional stimulus. For example, one may be
interested in measuring an individual’s asymmetry in frontal EEG activity at rest as well as
that same individual’s asymmetrical frontal EEG activation in response to an experimental
manipulation, such as the presentation of an image of a venomous snake. While this implies
that activity refers only to resting or baseline measures, this is not necessarily the case.
Indeed, one could measure an individual’s resting activity both at baseline and following
a stimulus presentation. The difference between those post-stimulus and baseline activity
measures, however, would represent that individual’s inferred activation in response to the
stimulus. This distinction is important for maintaining conceptual clarity when reviewing the
literature on frontal EEG asymmetry. Thus, in reviewing the literature, one of the functions
of this article will be to make clear this distinction in past literature as well as in the
arguments and data presented here.
Finally, an occasional difficulty in reviewing the literature on frontal EEG asymmetry
involves discerning precisely what specific hemispheric effects are responsible for observed
asymmetries. This difficulty frequently results from the widespread practice of computing
and analyzing an asymmetry index, typically a difference score, rather than analyzing hemi-
sphere as a two-level factor. The most commonly reported of these indexes is computed
by subtracting the natural log of left hemisphere alpha power from the natural log of right
hemisphere alpha power (ln[right alpha] − ln[left alpha]). This approach results in a unidi-
mensional scale representing the relative activity of the right and left hemispheres, with the
middle point of the scale equaling zero or symmetrical activity. In interpreting this scale,
higher scores indicate relatively greater left frontal activity whereas lower scores indicate
relatively greater right frontal activity (again keeping in mind that higher scores result from
relatively greater right frontal alpha power—the putative inverse of activity). A limitation of
this particular metric—and other similar metrics—is that the metric provides no information
regarding the extent to which each hemisphere is contributing to the observed difference
score (e.g., Jones et al., 1998).
It is not necessarily the case, however, that the use of asymmetry metrics is either un-
warranted or particularly problematic. Asymmetry scores have some distinct advantages,
not least of which is their capacity for controlling individual differences in skull thickness
that might produce artifactual and non-neurogenic individual differences in recorded power
values. Asymmetry metrics can also make statistical tests more sensitive by reducing the
number of contrasts in a particular model and increasing statistical power. When such dif-
ference score based asymmetry effects are followed up by specific hemisphere analyses,
such an approach is not only warranted but may be the most efficient data analytic approach
to these kinds of data (cf. Coan and Allen, 2003b). Asymmetry scores also conceptually
simplify certain analyses, such as those involving correlations between frontal asymmetries
(as a difference score) and other individual difference measures (e.g., behavioral activation;
Coan and Allen, 2003b; Harmon-Jones and Allen, 1997; Sutton and Davidson, 1997). Ad-
ditionally, difference scores based on alpha power asymmetries tend to show high internal
consistency and acceptable test-retest reliability, dispelling fears about reduced reliability
attributable to difference scores per se (Allen et al., this issue; Jones et al., 1997; Tomarken
et al., 1992b). Nevertheless, reports of specific hemispheric effects will be important for the
ultimate understanding of the precise nature of cortical asymmetries in emotional respond-
ing. Thus, tables presented in this article include a column labeled “Hem” that specifies
whether a given report investigated specific hemispheric effects (“yes”) or used an asym-
metry metric only (“no”).
4. What frontal EEG asymmetry measures: evidence from its associations with
other traits
Resting measures of asymmetrical frontal EEG activity have been associated with other
trait measures. Such relationships suggest the functional properties of the underlying cortical
systems that give rise to frontal EEG asymmetry. Findings from numerous studies reflect
an emerging consensus that relatively greater trait left frontal activity is associated with
trait tendencies toward a general appetitive, approach, or behavioral activation motivational
system, and that relatively greater trait right frontal activity is associated with trait tendencies
toward a general avoidance or withdrawal system (Coan and Allen, 2003a; Davidson, 1993).
This has resulted in Davidson’s highly influential approach/withdrawal motivational model
of emotion (Davidson, 1993; Davidson, 1998a,b). According to this model, left frontal
activity, either as a state or a trait, indicates a propensity to approach or engage a stimulus,
while relatively greater right frontal activity indicates a propensity to withdraw or disengage
from a stimulus. A comprehensive tabular summary of the literature associating trait frontal
EEG asymmetry with other trait measures can be found in Table 1. Though no attempt to
review every report in this literature will be made within the body of this article, a number
of particularly noteworthy studies will be highlighted in the remainder of this section.
An obvious paper and pencil measure for assessing Davidson’s approach-withdrawal
model of frontal EEG asymmetry in emotion might be Carver and White’s (1994) BIS/BAS
scales, which purport to measure Gray’s (1972, 1987) behavioral inhibition and activation
systems (BIS and BAS, respectively) as human traits. According to Gray, the BIS initially
inhibits action, increases arousal and attention and subsequently guides behavior toward re-
moving or avoiding an undesirable stimulus. The BAS essentially functions in the opposite
manner, responding to incentives, and guiding organisms toward attaining a desirable stimu-
lus, including negative reinforcers. Researchers have identified relationships between these
systems and frontal EEG asymmetry (Coan and Allen, 2003b; Harmon-Jones and Allen,
1997; Sutton and Davidson, 1997). In particular, Sutton and Davidson (1997) proposed that
the BIS and BAS should map closely onto withdrawal and approach tendencies, respec-
tively, arguing that these constructs are functionally identical. They found that relatively
greater left frontal activity was associated with both higher BAS scores and greater BAS-BIS
difference scores. Further, they found that relatively greater right frontal activity was as-
sociated with higher BIS scores (Sutton and Davidson, 1997). Work by Harmon-Jones
and Allen (1997) and Coan and Allen (2003b), however, suggest that the relationship is
Table 1
12
Trait frontal EEG asymmetry and other trait-like measures
Citation N Age Handedness Reference Independent variable Dependent Hem Results summary
scheme variable
Buss et al., 2003 From 85 infants 6 months NA AR, Cz Extreme right (ER), Cortisol level Yes ER, ↑ C
samples sizes for intermediate (I) and extreme (C), fear (F) and ER and Str., ↑ F
specific analyses Left (EL) groups from EEG sadness (S) ER and Str., ↑ S
vary (5–9 Hz) at FP1/2, F3/4, F7/8; ratings
J.A. Coan, J.J.B. Allen / Biological Psychology 67 (2004) 7–49

baseline (B) vs. stranger (Str.)
groups
Coan, 2003 250 (132 female) Mean = 19 No Cz, LM Sex (M vs. F); positive EEG at F3/4; No In M, no significant
years information emotionality (PEM) and findings
negative emotionality (NEM) In F, ↑ RFA, ↑ PEM
and others from the In F, ↑ RFA, ↑ NEM
multidimensional personality In F, h2 of F3/4 ≈
questionnaire (MPQ); 0.22
monozygotic twins (MT) and In F, h2 of bivariate
dizygotic twins (DT); twins phenotypic
used to assess heritability (h2 ) correlation between
F3/4 and NEM ≈
0.42
Coan and Allen, 32 (26 female) 17–24 years R AR, LM EEG at FP1/2, F3/4, F7/8, BIS/BAS Yes ↑ LFA, ↑ BAS
2003 FTC1/2, C3/4, T3/4, TCP1/2,
T5/6, P3/4, O12
Davidson et al., 24 (9 female) 17–21 years R LM EEG at F3/4, F7/8 and T3/4 Natural killer No ↓ RFA, ↓ NK (rest)
1999 (NK) cell ↓ RFA, ↓ NK (exam)
activity at rest, ↑ LFA, ↑ NK (pos
before exam, film clip)
and following
pos and neg film
clips
Ehlers et al., 2001 134 (68 female) 7–13 years Both No Handedness (L vs. R); EEG at F3/4, No SNA, ↓ LFA
information strongly native American C3/4, P3/4, O1/2
(SNA) vs. native American
(NA); sex (M vs. F); positive
family history of alcohol
abuse (FHP) vs. no such
history (FHN)
Field et al., 2002 48 infants (29 newborn NA Cz Infant EEG at F3/4, P3/4 Maternal No ↑ infant RFA, ↓ MS
female) serotonin (MS), ↑ infant RFA, ↓
maternal MPC
postnatal cortisol ↑ infant RFA, ↑
(MPC), maternal maternal RFA
EEG at F3/4, ↑ infant RFA, ↓
P3/4, maternal maternal VT
↑ infant RFA, ↑ IC

vagal tone (VT),
infant cortisol ↑ infant RFA, ↓ BA
(IC), infant sleep
state changes
(SS), infant
Brazelton
assessment (BA)
Fox et al., 1995 48 (28 female) 49–62 No Cz EEG at F3/4, P3/4 and O1/2 Social Yes ↑ RFA, ↓ SC
months information competence ↑ LFA, ↑ SC
(SC)
Hagemann et al., 36 (24 female) Mean R Cz Positive affectivity (PA), EEG at F3/4, Yes ↑ NA, ↑ LATA
1999 = 24.7 negative affectivity (NA), T3/4, C3/4, P3/4
extroversion (E), and A1/2
neuroticism (N)
Harmon-Jones and 37 females No R Cz EEG at F3/4 and P3/4 BIS/BAS No ↑ LFA, ↑ BAS
Allen, 1997 information
Harmon-Jones and 26 (11 female) Mean = 13 R Cz EEG at FP1/2, F3/4, C3/4, Dispositional No ↑ LFA, ↑ A
Allen, 1998 years P3/4, T5/6, T3/4, O1/2 anger (A)
Jacobs and Snyder, 40 males 18–53 years R LM EEG at F3/4, P3/4 PANAS (PA and No ↑ LFA, ↓ NA score
1996 NA); BDI ↑ LFA, ↓ BDI score
Jackson et al., 2003 47 (30 female) 57–60 years R LE Unpleasant (U), pleasant (P) EEG at FPF1/2, No ↑ RFA, ↑ C
and neutral (N) pictures; FP1/2, F3/4, negativity
startle probe during early F7/8, FC3/4,
viewing (A), later during FC/8, C3/4,
viewing (B), and after CP3/4, CP5/6,
viewing (C) T3/4, T5/6, P3/4,
PO3/4
13
14
Table 1 (Continued )
Citation N Age Handedness Reference Independent variable Dependent Hem Results summary
scheme variable
Jones et al., 1997 87 (infants) No No Cz Baby groups: overstimulating EEG at F3/4 and Yes O babies, ↑ LFA
information information (O) vs. understimulating (U) P3/4, various U babies, ↑ RFA
mothers physio and beh. (Mothers showed the
measures same pattern as
infants)

Kang et al., 1991 20 females 17–20 years R Cz, LM Extreme LFA and RFA Natural killer No RFA group, ↓ NK
groups (NK) cell, activity
lymphocyte and
T-cell activity
Kalin et al., 2000 49 (23 female; Longitudinal No No Extreme LFA and RFA Cerebrospinal No ↑ RFA, ↑ CRH
rhesus monkeys) data at 4, 8, information information groups in monkeys fluid CRH
14, 40 and
52 months
Kline et al., 1998 85 (60 females) 17–33 years R Linked ears Defensive coping (EPQ-L EEG at F3/4, Yes For women, ↑ LFA ↑
(LE) scale) FP1/2, F7/8, defensiveness
C3/4, T3/4, For men, ↑ LFA ↓
T5/6, P3/4, O1/2 defensiveness
Kline et al., in 72 (42 female) Mean = R No Defensiveness (D), parental EEG at FP1/2, Yes ↑ defensiveness, ↑
press-a, in 20.4 information caring (PC) T3/4, F7/8, and LFA
press-b F3/4
Kline et al., in 235 (141 Mean = R No High (HD) vs. low (LD) EEG at F3/4, Yes HD, ↑ LFA in
press-a, in females) 20.4 information defensiveness groups; FP1/2, F7/8, presence of opposite
press-b experimenter gender: same C3/4, T3/4, sex.
vs. opposite T5/6, P3/4, O1/2
McManis et al., 166 children 10–12 years R LM Low fear (LF), moderate fear EEG at F3/4, No HF and HR, ↑ RFA
2002 (MF) and high fear (HF) at 2 P3/4, A1/2
years old; low reactivity (LR)
vs. high reactivity (HR) at 2
years old
Moss et al., 1985 12 (Japanese), J, mean = R Cz Cultural group (J vs. W) EEG at T3/4 and Yes W = ↑ LPA
12 (Western), all 32.6 years; P3/4
Female W, mean =
29.1 years
Merckelbach et al., 29 females 22–38 years No A1 L vs. R hemisphere EEG at F3/4 and No ↑ LHP, ↑LFA
1996 information preference (questionnaire) P3/4
Schmidt, 1999 40 females M = 20.97 R Cz Low shy vs. high shy; low soc EEG at F3/4, Yes ↑ shyness, ↑RFA
(extreme scorers years vs. high soc P3/4 and O1/2 ↑ soc, ↑ LFA
selected from High shy, high soc
among 271) had ↑ LFA than high
shy, low soc
Schmidt and Fox, 40 females No R Cz Low shy vs. high shy; low soc EEG at F3/4, Yes ↓ soc, ↑ RFA
1994 (extreme scorers information vs. high soc P3/4, A1/2 and Low shy, high soc

selected from O1/2 = ↑ RPA
among 282) Low shy, low soc
= ↑ LPA
Stough et al., 2001 16 (11 females) 20–30 years No No Measures of openness (O), EEG at FP1/2, Yes No effects in alpha
information information agreeableness (A) and F3/4, F7/8, T3/4, band.
conscientiousness (C) T5/6, C3/4,
O1/2.
Sutton and 46 (23 female) 18–22 years R LM EEG at F3/4 7 and P3/4 BIS/BAS, No ↑ LFA, ↑ BAS
Davidson, 1997 BAS–BIS diff ↑ RFA, ↑ BIS
score ↑ LFA, ↑ BAS-BIS
diff
Tomarken and 90 females No R Cz High defensive (HD) vs. low EEG at F3/4, Yes HD = ↑ LFA in F3/4
Davidson, 1994 information defensive (LD) F7/8, T3/4, C3/4 and F7/8
and P3/4
Tomarken et al., 90 females 17–21 years R Cz, LM EEG at F3/4, F7/8, T3/4, General positive No ↑ LFA, ↑ PA
1992a P3/4, C3/4 and negative ↑ LFA, ↓ NA
affect (PA and
NA)
Urry et al., in press 84 57–60 years R AR, LM EEG at 29 sites, including Eudaimonic ↑ LFA in FC3/4, ↑
FPF1/2, FC3/4, FP1/2, F7/8, well-being EWB
F3/4, and FC7/8 (EWB), hedonic ↑ LFA in FC3/4, ↑
well-being HWB
(HWB)
RFA: right frontal activity, LFA: left frontal activity; RATA: right anterior temporal activity, LATA: left anterior temporal activity; RPA: right parietal activity, LPA: left parietal activity.
15
robust for BAS, but not so robust for BIS. While both Harmon-Jones and Allen and Coan
and Allen found associations between relative left frontal activity and higher BAS scores,
neither study detected a strong association between relative right frontal activity and BIS
scores (though Coan and Allen did detect a statistical trend suggestive of this relationship).
In both reports, it was suggested that the theoretical association between withdrawal mo-
tivations and the BIS is more complex than that between approach motivations and the
BAS (Coan and Allen, 2003b; Harmon-Jones and Allen, 1997). Theoretically, Davidson’s
(1998a) withdrawal construct may be more general than that of the BIS. For example, the
hypothetical systems underlying Davidson’s withdrawal construct are thought to motivate
or predispose organisms to withdraw from sources of aversive stimulation, whereas the
BIS has been described as a system that, among other things, interrupts behavior, increases
arousal and increases attention (Gray, 1994), none of which are necessarily involved in
withdrawal behaviors or predispositions. Indeed, Davidson’s withdrawal construct could
overlap with functions included in any of the motivational systems described by Gray (for
a more detailed discussion, see Coan and Allen, 2003b). By contrast, Davidson’s approach
and Gray’s BAS constructs (as well as the similar construct of the behavioral facilitation
system; Depue and Collins, 1999; Depue and Iacono, 1989) may share substantial overlap.
The rather robust relationship between frontal EEG asymmetry and the BAS is further bol-
stered from findings designed to test the primarily motivational approach-withdrawal model
of frontal asymmetry against a valence model (cf. Heller and Nitschke, 1997). For example,
Harmon-Jones and Allen (1998), and more recently Harmon-Jones (2000), found that left
frontal activity was associated with trait anger, a negatively-valenced but approach-related
emotion conceivably related to BAS functions. Indeed, in at least one study, BAS sensi-
tivity as measured by Carver and White’s (1994) BAS scale was associated with a greater
likelihood of aggressive behavior (Wingrove and Bond, 1998).
While the relationship between the self-reported BIS scores and trait withdrawal propen-
sities remains uncertain, other evidence that trait frontal EEG asymmetries are related to
both behavioral propensities to approach and withdraw is available. One source of this
evidence derives from measures of social behavior. For example, Fox et al. (1995) found
evidence that children with greater relative right frontal activity at rest were generally more
inhibited socially, and scored lower on measures of social competency (Fox et al., 1995).
Moreover, children were more sociable and more socially competent to the extent they had
relatively greater left frontal activity. Schmidt and colleagues (Schmidt, 1999; Schmidt and
Fox, 1994) investigated the relationship between frontal EEG asymmetry and measures
of sociability in adults and found that individuals scoring low on measures of sociabil-
ity showed relatively greater right frontal activity at rest (Schmidt and Fox, 1994). Further,
Schmidt (1999) found that shyness was associated with relatively greater right frontal activ-
ity, while sociability was associated with relatively greater left frontal activity. Interestingly,
Schmidt (1999) also found that shy individuals who nevertheless scored high on measures
of sociability possessed greater left frontal activity than other shy individuals with low
sociability scores. More recently, Kalin et al. (2000) have investigated the relationship be-
tween frontal EEG asymmetry and other physiological traits that may underlie processes
related to those reviewed above. For example, they have reported a positive relationship
between extreme right frontal EEG activity and high cerebrospinal fluid concentrations of
corticotrophin-releasing hormone (CRH) in rhesus monkeys (Kalin et al., 2000). CRH is
itself thought to mediate stress responses, as well as fear, anxiety and depression. Accord-
ing to this work, higher CRH levels are associated with higher levels of stress (De Souza,
1995; Kalin et al., 2000). Further, Kalin and colleagues have supplied evidence that rhesus
monkeys showing extreme relative right frontal EEG activity have both elevated cortisol
levels and exaggerated defensive behaviors (Kline et al., 1998).
5. Frontal EEG asymmetry as a possible moderator of emotional responding
When considering how resting frontal EEG asymmetry may serve as a predictor of sub-
sequent emotional responses, two non-mutually exclusive relationships are possible.
1. Resting frontal EEG asymmetry taps an individual difference that may facilitate or
diminish an emotional response (e.g., happiness) across many classes of stimuli (e.g.,
happy, sad, angry, fearful, and disgusting stimuli). For example, greater relative left
frontal activity might be expected to be associated with greater self-reported happiness,
for positively- as well as negatively-valenced stimuli.
2. Resting frontal EEG asymmetry taps an individual difference that may facilitate or
diminish emotional responses preferentially for some but not other classes of stimuli.
For example, greater relative right frontal activity might be expected to potentiate startle
in response to negatively-valenced stimuli, but not to positively-valenced or neutral
stimuli.
Strictly speaking, it is only the second case that qualifies as a moderator variable (cf.
Baron and Kenny, 1986), as will be detailed below. The first instance is nonetheless a
theoretically useful and interesting finding that frontal EEG asymmetry may serve as an
individual difference variable that predicts emotional responses.
Davidson (1998a) has proposed that trait EEG asymmetries index propensities for react-
ing in predictable ways to emotionally evocative stimuli. Davidson (1998a) has called this
propensity “affective style,” and he proposes that frontal EEG asymmetry indexes a system
that may have emotion-specific or valence-specific (p. 309) moderating influences, with
implications for risk for psychopathology. The intent of the following section is therefore
to review the literature suggestive of frontal EEG asymmetry as a possible moderator of
emotional responding. The question of whether and to what extent this evidence unequiv-
ocally implicates frontal EEG asymmetry as such a moderator, however, depends upon a
deeper consideration of what is meant, not only conceptually but also statistically, by the
term moderator.
5.1. Modeling frontal EEG asymmetry as a moderator
Before describing the data analytic identification of a moderator variable, it is important

to understand precisely what a moderator variable should look like in terms of statistical
effects. Fig. 1 depicts a general moderator model that will serve as a useful guide to such
a discussion. For the purposes of the illustration, assume that frontal EEG asymmetry may
moderate the intensity rating of a fear experience following the stimulus presentation of an
image of a poisonous snake versus some more affectively neutral image, such as that of an
Stimulus Type
(snake vs. elephant)
a
b
Moderator Emotional
(EEG Asymmetry) Response
Stimulus Type
X
Moderator (EEG Asymmetry)
Fig. 1. Frontal EEG asymmetry as a moderator. Model adapted from Baron and Kenney (1986).
elephant. In this example, we might expect fear ratings in response to images of a poisonous
snake to be relatively high and those to images of an elephant to be relatively low, with
ratings in response to one, the other, or both images varying as a function of frontal EEG
asymmetry.
According to this model, there are three causal paths to the emotional response—the
rating of fear intensity according to our example. The first of these paths, path a, represents
the causal influence of the independent variable, in this case, image type (poisonous snake
verses an elephant). Path b would represent the unique contribution of trait frontal EEG
activity. Path c represents the causal influence of the interaction between the type of image
presented and an individual’s trait pattern of resting frontal EEG asymmetry.
At its simplest, the moderator hypothesis states that path c is significant. Baron and Kenny
(1986) note, however, that a significant contribution of this path alone does not necessarily
present a strong case for a moderator effect. While a main effect of the independent variable
is possible in this model, and in the case of this example even likely, it is preferred that
the moderator variable be uncorrelated with both the stimulus and emotional response
variables, if the moderator is specifically to be identified as a moderator only (i.e. not
simultaneously a moderator and mediator). It is easy to see that a correlation would not
exist between frontal EEG asymmetry and the likelihood of encountering an image of a
poisonous snake versus an elephant (at least in the experimental context). Less certain,
however, is that frontal EEG asymmetry is unrelated to continuous measures of affective
intensity, regardless of the particular stimulus being rated. If frontal EEG activity predicted
fear intensity ratings independent of the eliciting stimulus, it could be somewhat difficult to
disambiguate the moderating influence (path c) of frontal EEG asymmetry on our specific
construct of interest—emotion responsivity—from its main effect (path b) of predicting
intensity. Such a condition would not preclude the identification of a moderator, however.
A statistical method for dealing with this problem is outlined below.
Moderator models of frontal EEG asymmetry assume that frontal EEG asymmetry itself
is most likely a continuous variable. This is true, even if hemispheres act independently of
each other to achieve their moderating effects. Raw EEG is always measured as a continuous
variable, and while frontal EEG asymmetry can be artificially dichotomized into categorical
variable, such an approach is not recommended, in part because doing so reduces statistical
power and may result in artificially obtained “groups” that distort the underlying continuous
relationships. Following from Davidson’s diathesis/stress theory of psychopathology and
affective style, it makes the most sense to analyze frontal EEG asymmetry as a continuous
moderator, and the following examples adhere to this. This data analytic approach is perhaps
best illustrated with the snake/fear example, because the diathesis/stress theory models
“stress” as an environmental event beyond an individual’s direct control. Recall that this
example assumes that any given individual’s trait pattern of frontal EEG asymmetry will
serve to either attenuate or amplify a fear response to the visual stimuli.
Baron and Kenney (1986) present three possible models representing the interaction
between an independent variable (e.g., snake versus elephant) and a continuous moderator
variable (e.g., resting frontal EEG asymmetry). These are (1) the linear model, (2) the
non-linear model, and (3) the step–function model. In the linear model, one would expect
to find a gradual, linear change in the effect of the independent variable on the outcome
criterion as a function of the moderator. In terms of the example, the relationship between
the interaction term (the snake/elephant by EEG asymmetry interaction) and fear ratings
would be gradual and steady. That is, frontal EEG asymmetry should both attenuate and
amplify the effect of the fear-relevant (but not fear-irrelevant) stimulus, depending on the
relative difference between the left and right hemispheres. This model would then predict
that individuals with relatively greater right frontal EEG asymmetry would be expected to
show an amplified fear response, and individuals with relatively greater left frontal activity
should show an equal and opposite attenuation in their fear response, with these effects
specific to the snake stimulus.
In the non-linear model, a quadratic equation would best exemplify the relationship
between the interaction term and the outcome criterion. Following from the example, it
might be expected that relative right frontal activity would correspond with a more intense
fear rating in response to the snake image presentation, while finding that relative left frontal
activity was not different from symmetrical activity in terms of influencing fear ratings,3
with effects again specific to the snake and not the elephant stimulus.
In the step–function model, some critical level of the moderator variable is assumed. In
terms of the example, this model would state that fear responses are at a clearly defined
normative level until a particular threshold in relative right frontal EEG asymmetry is
crossed, the result of which would be a large jump in the intensity ratings of fear in response
to the snake but not elephant image presentation. There is no evidence to suggest such a
model is likely.
In data analytic terms, each of these models can be tested with simple regression equations
per the recommendations of Cohen and Cohen (1983) and Aiken and West (1986). This
recommendation holds if the independent variable is continuous as well. Further, standard
3 The potentially independent contributions of the left and right frontal regions to the observed interaction
would be important to examine in subsequent analyses. Although parsimonious to assume relatively comparable
magnitude of effects from the left and right hemisphere in the linear model, this need not be the case, as a single
hemisphere could be responsible for a majority of the effect, with the other hemisphere contributing little. In the
case of the nonlinear model, it obviously cannot be assumed that both hemispheres contribute equally across the
whole range of asymmetry scores, and underscores the desirability of follow-up analyses involving hemisphere
(cf. Allen et al., this issue).
general linear model (GLM) approaches are essentially equivalent to regression approaches,
and their flexibility makes them in many cases more desirable, especially with regard to cer-
tain common statistical packages, such as SPSS, etc. In cases where the moderator variable
is independently correlated with the criterion variable, it may be desirable to calculate one’s
general linear model using a type 1 sum of squares in order to control for multicolinearity
with the moderator by independent variable interaction term. This is easily accomplished
in most popular statistical packages.
5.2. Empirical support for frontal EEG asymmetry as a moderator
Thumbnail reviews of a large number of studies relevant to this section can be found
in Table 2. Early studies suggest that frontal EEG asymmetry may serve as a moderator
involved in predictions of emotional reactions in infants. For example, Davidson and Fox
(1989) found that infants who cried in response to maternal separation had greater right
frontal activity at rest than those who did not. This result was replicated by Fox et al.
(1992), who also found that this effect was modestly stable over 5 months.
Similar findings have been obtained in adults. For example, when asked by Tomarken et al.
(1990) to report affective responses to emotional film clips, individuals with greater right
frontal activity at rest responded with more intense levels of negative affect to negatively-
valenced film clips, particularly those involving fear (Tomarken et al., 1990). In a similar
report, Wheeler et al. (1993) found that individuals with greater right frontal activity re-
sponded with more intense negative affect to negatively valenced films, and that individuals
with greater left frontal activity responded with more intense positive affect to positively
valenced films. These studies suggest that individual differences in emotional responding
are in part a function of individual differences in trait frontal EEG asymmetry. Indeed,
Davidson (1998a) has cited these findings to argue that one’s affective style—as indicated
by one’s trait frontal EEG asymmetry—may in part determine one’s risk for certain affec-
tive disorders such as depression and anxiety, a proposal that clearly identifies frontal EEG
asymmetry as a moderator of emotion and related affective processes. While neither of these
studies explicitly assessed the moderator hypothesis in terms of the recommendations of
Baron and Kenny (1986), each adopted a similar approach. Each study can be conceptual-
ized in terms of Fig. 1 as follows: (a) the stimulus type is the film type (positive or negative);
(b) resting frontal EEG asymmetry is the potential moderator; and (c) intensity rating would
be the emotional response. In the end, both Wheeler et al. (1993) and Tomarken et al. (1990)
provide compelling—though not definitive—evidence that resting frontal EEG asymmetry
is a genuine moderator of emotional responding.
Recently, Henderson et al. (2001) explicitly tested frontal EEG asymmetry recorded
at 9 months of age as a moderator of the relationship between negative affectivity, also
measured at 9 months, and social wariness at approximately 4 years of age. In this work,
9-month-old negative emotionality predicted social wariness at 4-year follow-up in infants
who’d shown relatively greater right frontal EEG activity at 9 months. No relationship was
found between social wariness behaviors at follow-up and infant frontal EEG asymmetries
favoring the left. It is noteworthy that these results are consistent with Baron and Kenny’s
(1989) non-linear moderator model. More recently, Coan and Allen (2003c) conducted a
moderator analysis of resting frontal EEG asymmetry and emotional experience using a
Table 2
Trait frontal asymmetry as a predictor of state dependent changes
Citation N Age Handedness Reference Independent variable Dependent variable Hem Results summary
scheme

Davidson and 13 infant females 10 months R (parents) Cz EEG at F3/4, P3/4 Infant response to Yes Criers, ↑ RFA non-criers, ↑ LFA
Fox, 1989 maternal separation
(crying vs. not-crying)
Fox et al., 1992 (1) 33 infants (17 (1) 14–24 months, R/L Cz EEG at F3/4, P3/4 Infant response to Yes Criers, ↑ RFA effects consistent over time
female), (2) 13 cross-sectional, (2) maternal separation
infants (7 7–12 months, (crying vs. not-crying)
females) longitud-inal
Hagemann et al., 37 (22 female) 19–44 years R Cz, LM EEG at F3/4, T3/4, Positive affect (PA), No Cz, 8 min resting: ↑ LFA, ↑ PA
1998 C3.4, P3/4, A1/2 negative affect (NA), Cz, 4 min eyes closed: ↑ LFA, ↑ PA
affective bias (AB), and LM reference: no effects ↑ R T3/4, ↑ NA
generalized reactivity Note: overall results equivocal with regard
(GR), all in response to to A/W model
affective slides
Henderson et al., 97 infants (51 Longitud-inal; time No information AR EEG at F3/4, C3/4, Sociability (S) and social No ↑ RFA and ↑ NR, ↑ SW
2001 females) 1, 9 months; time 2, P3/4 and O1/2; wariness (SW)
48 months negative reactivity
(NR)
Tomarken et al., 32 females 17–41 years R Cz EEG at F3/4, T3/4, Reported positive affect No ↑ RFA, ↑ NA
1990 P3/4, C3/4 (PA) and negative affect ↑ RFA, ↑ PA-NA difference
(NA) following film clips ↑ RFA, ↑ fear report
Wheeler et al., 26 females with 17–21 years R Cz EEG at F3/4, T3/4, Reported positive affect No ↑ LFA, ↑ PA
1993 stable asymmetry P3/4, C3/4 (PA) and negative affect ↑ RFA, ↑ NA
across sessions (NA) following film clips
21
general linear model approach similar to that used by Henderson et al. (2001). Using data
previously reported on in Coan et al. (2001); Coan and Allen (2003c) sought to assess the
extent to which trait frontal EEG asymmetries moderated self-reported emotional experi-
ence in response to posed emotional facial expressions that depicted anger, disgust, fear, joy
and sadness. To explicitly test a moderator hypothesis, Coan and Allen (2003c) constructed
a single general linear model where emotion type, trait frontal EEG asymmetry, and an
emotion by trait EEG asymmetry interaction were used to predict emotional experience.
This model was able to accommodate both the categorical (emotion) and continuous (trait
frontal EEG asymmetry) predictors, as well as their interaction, easily. Additionally, these
predictors were interacted with the other categorical factors of reference scheme (average
versus linked mastoid) and particular frontal region (F3/4, F7/8 and FTC1/2) to assess the
degree to which these additional factors influenced the effects of interest. If frontal EEG
asymmetry moderates emotional experience and intensity, then this model would result in a
significant emotion by frontal EEG asymmetry interaction. Coan and Allen (2003c) found
that relatively greater left frontal activity at rest predicted an increased likelihood of report-
ing an experience of anger, joy, disgust, but not sadness and fear (trait EEG asymmetry by
emotion interaction, F(4, 865) = 3.53, P < 0.01) independently of reference scheme (aver-
age and linked mastoid) or specific frontal region (F7/8, F3/4 and FTC1/2). This moderator
effect was, however, only partially consistent with predictions of the approach/withdrawal
model of frontal brain asymmetry. Positive correlations between frontal EEG asymmetry
and experience were found, as predicted, in the cases of joy and anger, but the predicted
negative relationships between trait frontal EEG asymmetry and disgust, in addition to fear
and sadness, were not. These findings may in part be due to methodological idiosyncrasies
such as the use of voluntary emotional facial expressions as emotional stimuli, but suggest
that the role of frontal EEG asymmetry as a moderator of emotional response may only
partially support of the approach/withdrawal model.
Other studies suggest the same. Using normed emotion eliciting images, Hagemann et al.
(1998) essentially failed to replicate earlier findings. In their study, Hagemann et al. (1998)
did indeed find that individuals with relatively greater left frontal activity at rest tended to
respond more positively to positively valenced images, but only when using a Cz reference
(arguably the most problematic of all reference montages; see Hagemann et al., 2001).
The effect did not generalize to frontal EEG recorded using a linked mastoids reference
montage. Other results reported by Hagemann et al. (1998) were generally inconsistent
with the approach/withdrawal model advocated by Davidson and colleagues. For example,
Hagemann et al. (1998) found that relatively greater left anterior temporal activity at rest was
associated with more intense experience reports associated with negative affect, whereas
the approach/withdrawal model would predict precisely the opposite. Such discrepant find-
ings have prompted Davidson (1998b) to suggest that that Hagemann et al.’s (1998) study
was methodologically inconsistent with earlier ones supportive of the approach-withdrawal
model, pointing out that in Wheeler et al.’s (1993) study, only data from individuals with
highly stable frontal EEG asymmetry patterns (across 3 weeks of measurement) were an-
alyzed. Both authors have noted the need to resolve these inconsistencies with further
research.
Inconsistencies aside, if the possibility of frontal EEG activity as a moderator of emo-
tional responses is ultimately borne out, there are likely to be consequences for affectively
based psychological disorders. Indeed, Davidson’s theory of frontal EEG asymmetry as a

partial determinant of affective style proposes explicitly that certain affective styles serve
as diatheses that, in response to the appropriate stimuli, can increase risk for certain forms
of psychopathology. Thus, evidence that frontal EEG asymmetry may moderate risk for
psychopathology merits consideration.
6. Frontal EEG asymmetry as a risk factor and possible moderator of

psychopathology
Resting frontal EEG asymmetry may serve as an index of risk for a variety of emotion-
related disorders, including depression and anxiety. Whether it indexes a general propensity
to respond in ways consistent with depression or anxiety, or a specific tendency to do so in
some emotionally evocative situations and not others, remains an empirical question. Yet
evidence of frontal EEG asymmetry’s role in moderating emotional responsivity suggests
a similar role in the development of various disorders involving affect.
Researchers have identified a link between relatively greater right frontal resting activity—
or relatively lower left frontal resting activity—and depression (e.g., Henriques and
Davidson, 1990, 1991; Schaffer et al., 1983) including seasonal depression (Allen et al.,
1993). In the first report of this type, Schaffer et al. (1983) found that higher scores on
the Beck Depression Inventory (BDI) were associated with relatively greater right frontal
resting activity in their sample of undergraduate research participants (see Table 3). Sub-
sequent studies have identified the same relationship in clinically diagnosed participants
(Allen et al., 1993; Gotlib et al., 1998; Henriques and Davidson, 1991). In some of these
studies, participant samples have included euthymic individuals who have suffered previ-
ous bouts of depression (e.g., Gotlib et al., 1998; Henriques and Davidson, 1990). Some
researchers, however, have failed to replicate the relationship between resting frontal EEG
asymmetry and depression (Reid et al., 1998). For example, despite the use of two separate
and large samples, Reid et al. (1998) were unable to detect such a relationship. In interpreting
the findings, Reid et al. (1998) suggested that given the heterogeneity of depression, frontal
EEG asymmetry might tap only one of several risk trajectories associated with depression.
Reid et al. also speculated that some unidentified qualities of their research environment
may have been to blame, noting that traits may interact in particular ways within particular
environments and that these interactions may have masked preexisting asymmetries in their
research participants.
Evidence that infants of depressed mothers show relatively greater right frontal resting ac-
tivity further suggests a link between frontal EEG asymmetry and depression (e.g., Dawson
et al., 1999a; Field et al., 1995). For example, Dawson et al. (1997) found that infants of
depressed mothers showed less left frontal activity than those of non-depressed mothers and
that such lower left frontal activity discriminated infants whose mothers were diagnosed
with major depression from those with mothers whose symptoms were sub-threshold. More
recently, Dawson and colleagues have found that infants of depressed mothers are less af-
fectionate and show evidence of relatively less left frontal activity not only at rest, but also
while interacting with their mothers and while interacting with familiar strangers (Dawson
et al., 1999b). In independent investigations, Field et al. (1995) have achieved similar ef-
24
Table 3
Trait frontal EEG asymmetry and measures of psychopathology
scheme
Allen et al., 8 females (4 with No information R Cz SAD (S) vs. control EEG at F3/4, P3/4 Yes S ↓ LFA Unchanged by
1993 seasonal affective (C) groups; pre–post treatment
disorder; SAD) bright light treatment

Allen et al., in 30 depressed females 18–45 R Cz, LM, AR Time of assessment to EEG at F3/4, F7/8, No Asymmetry stable
press examine stability of FTC1/2, others across 3–5 monthly
asymmetry over time assessments, median
in depression intraclass correlation =
0.61
Baehr et al., 24 (13 depressed; no sex 43–57 years No information Cz Depressed (D) and Percent time spent with No D, ↑ pct time with RFA
1998 information) non-depressed (ND) RFA vs. LFA in F3/4
groups (BDI median
split)
Bruder et al., 53 (28 females) 18–65 No information Nose Resting EEG at F3/4, Recovery vs. Yes In women:
2001 FP1/2, F7/8, FC5/6, non-recovery from non-responders, ↑ RFA
FT9/10, C3/4, T7/8, depression following
CP5/6, TP9/10, P3/4, SSRI (fluoxetine)
P7/8, P9/10, O1/2 treatment
Davidson 28 (no sex information) 19–68 years R LM Social phobics vs. EEG at AF1/2, F3/4, Yes Alpha 1: phobics, ↑
et al., 2000 controls—anticipating F7/8, T3/4, P3/4, C3/4, RFA/RATA
public speech Cz, and Fz in alpha 1
(8–10 Hz); and alpha 2
(10–13 Hz)
Davidson 20 (10 depressed; 7 18–23 years R Cz Happy, sad and neutral EEG at F3/4, P3/4 Yes Group differences in
et al., 1985 females in each group) face pictures, frontal asymmetry
depressed vs. between RVF and LVF
non-depressed, left presentations appears to
visual field (LVF) vs. account for group
right visual field (RVF) differences in self-report
ratings of happiness in
response to lateralized
picture presentations
Dawson et al., 117 infants (52 females) 13–15 months No information LM Depressed (D) vs. Infant EEG at F3/4 and Yes D, ↓ LFA
1997 non-depressed (ND) P3/4 MD, ↓ LFA compared to
mothers; major SD
depression (MD) vs.
sub-depression (SD)
Dawson et al., 99 infants (60 females) 13–15 months R/L LM Depressed (D) vs. Infant EEG at F3/4 and Yes D, ↓ LFA (across other
1999a,b non-depressed (ND) P3/4 conditions)
mothers; interaction
with mother vs.

familiar adult
Dawson et al., 117 infants (52 females) 13–15 months No information LM Depressed (D) vs. Infant EEG at F3/4 and Yes D, ↓ AB (D and ↓AB),
1999a,b non-depressed (ND) P3/4; affection behaviors ↓ LFA
mothers (AB)
Dawson et al., 30 infants (21 females) 11–17 months No information Cz Emotional faces Infant EEG at F3/4 and Yes Bilateral ↓ in activation
1997 during emotional P3/4 during negative faces in
stimuli; depressed (D) D group
vs. non-depressed
(ND) mothers
Dawson et al., 27 infants (no sex 11–17 months No information Cz Emotion conditions Infant EEG at F3/4 and Yes S: If D, ↓ LFA during P
1992 information) (play w/mother (P), P3/4 D, ↓ RFA
stranger approach
(SA), maternal
separation (MS);
depressed (D) vs.
non-depressed (ND)
mothers; secure (S) vs.
insecure (IS)
attachment
Debener et al., 37 (25 female) 23–64 years L/R (most R) Linked Depressed (D) vs. EEG at Fp1/2, F3/4, Yes D, ↓ LFA, but not stable
2000 earlobes non-depressed (ND) F7/8, C3/4, T3/4, T5/6, over time
groups P3/4, O1/2 C, ↑ temporal stability
in asymmetry
Earnest, 1999 1 female (case study) 14 years No information Cz Pre and post BDI score No ↓ BDI score post
biofeedback treatment treatment
to ↑ LFA
Field et al., 32 (16 female) 3–6 months R (mothers) Cz Depressed (D) vs. Infant and mother EEG at Yes D, ↑ RFA (mothers and
1995 non-depressed (ND) F3/4 and P3/4 infants)
25
mothers
26
scheme
Field et al., 160 depressed, 100 Mean = 17.8 No information Cz Depressed (D) vs. Infant and mother EEG at Yes D, ↑ RFA (mothers and
2000 non-depressed, all non-depressed (ND) F3/4 and P3/4 infants)
females mothers and their
respective infants

Fox et al., 96 (56 female) 46–62 months No information Cz EEG at F3/4, P3/4 and Sociability (S), Yes (↑ S and ↑RFA), ↑ E
1996 O1/2 externalizing (E) and (↓ S and ↑RFA), ↑ I
internalizing (I)
Gilbert et al., 50 male smokers Mean = 28.1 R Smoking (S) and EEG at F3/4 and P3/4 No ↑ NM, ↑RFA
1999 non-smoking (NS) NS, ↑RFA
conditions, NEO
personality inventory
(NEO-PI), fagerstrom
TOLERANCE
questionnaire (FTQ),
negative mood (NM)
Gotlib et al., Study 1: 77, study 2: 59 No information R Cz Previously depressed EEG at F3/4, Yes PD, D, ↓ LFA
1998 all female (PD), depressed (D) mood/cognitive measures No other effects,
and never depressed suggesting no cognitive
(Nev) groups mediation
Henriques and 14 (6 previously Dmean : 37.4 R Cz, LM Never depressed (Nev) EEG at F3/4, F7/8, T3/4, Yes D, ↓ LFA
Davidson, depressed) years, Cmean : and previously T5/6, P3/4, C3/4 D, ↑ RPA
1990 34.7 years depressed (PD) groups
Henriques and 28 (18 female) 31–57 years R Cz, LM, AR Depressed (D) vs. EEG at F3/4, F7/8, T3/4, Yes Cz: D, ↑ RFA
Davidson, non-depressed (ND) T5/6, P3/4, C3/4 AR: D, ↑ RFA
1991 groups LM: no effects
Heller et al., 40 (22 female) No information R LM Anxious (A) and EEG at F3/4, A1/2, P3/4 Yes A, ↑ LFA (A and Ar), ↑
1997 control (C) groups; RPA
anxious arousal (Ar)
vs. worry (W) tasks
Jones and 30 (no sex information) Mean = 18.8 No information Cz Music (Mu) vs. Depression measures and No ↑ LFA from pre to
Field, 1999 years massage (Ma) therapy; EEG at F3/4, P3/4 during, and from during
pre, during and post to post in both Mu and
tests Ma
Jones et al., 25 infants (25 female) 1 month No information Cz Pre, during and post Infant EEG at F3/4 and No ↓ RFA from pre to
1998 massage P3/4 during and from during
to post
Jones et al., 63 infants (no sex 1 week No information Cz Depressed (D) vs. Infant EEG at F3/4 and Yes D, ↓ LFA
1998 information) non-depressed (ND) P3/4, vagal tone D, ↓ vagal tone

mothers
Jones et al., 44 infants (no sex 1 month, 3 No information Cz Depressed (D) vs. Infant EEG at F3/4 and Yes D, ↑ RFA
1997 information) months non-depressed (ND) P3/4 ↑ RFA, ↑ Neg affect
(longitudinal) mothers pattern stable
Kentgen et al., 25 females 12.2–18.8 years R Nose Depressed (D) vs. EEG at F3/4, F7/8, C3/4, Yes No frontal relationships.
2000 non-depressed (ND) T7/8, P3/4, P7/8 D, ↓ RPA
adolescents, anxiety
comorbidity (A), no
anxiety
Miller et al., 110 (66 female) Mean = 26.6 R AR Males (M) vs. females EEG at F3/4, AF3/4, Yes D and M, ↑ LFA
2002 (F), history of F7/8, FC1/2, FC5/6,
childhood depression C3/4, T7/8, P3/4, P7/8, D and F, ↑ RFA
(D) vs. No depression O1/2
history (ND)
Minnix et al., 12 (6 females) 19–52 years R LE Reassurance seeking EEG at F3/4, FP1/2, No ↑ RS and ↑ BDI, ↑ LFA
this volume (RS); Beck Depression F7/8, C3/4, T3/4, T5/6, ↓ RS and ↑ BDI, ↑ RFA
Inventory (BDI) P3/4, O1/2
Nitschke et al., 67 (39 female) 17–20 years R LM Anxious apprehension EEG at F3/4, F7/8, T3/4, Yes AAr, ↓ LFA
1999 (AAp), anxious T5/6, P3/4
arousal (AAr), Aap no ↓ LFA
depressed (D),
co-morbid (CM) and
control groups (C)
Papousek and 50 (25 females) No information R Nose Resting EEG and EEG at FP1/2, F3/4, P3/4 No If ↑ RFA AND ↑
Schulter, electrodermal activity anxiety, ↑ EDA
2001 (EDA) at two time If ↑ LFA and ↑
points (T1 and T2); depression, ↑ EDA
depression (D) and
27
anxiety (A) measured
28
scheme
Papousek and Study 1: 56 (30 female), Study 1: 18–36 R Nose Study 1: anxious EEG atFP1/2, F3/4, T3/4, No In both studies, AT
Schulter, study 2: 128 (68 female) years, study 2: tension (AT); negative P3/4 for both Alpha 1 covaries with ␣2
2002 18–31 years mood (NM); Time 1 (␣1) and Alpha 2 (␣2) asymmetry in the
(T1) vs. Time 2 (T2), fronto-polar region

study 2: anxious
tension (AT);
depression (D);
anxiety; Time 1 (T1)
vs. Time 2 (T2)
Petruzzello 19 males Mean = 22.7 R LM Pre and post rigorous EEG at F3/4, T3/4; state Yes ↓ Anxiety post-exercise
and years exercise conditions measures of anxiety level
Landers,
1994 ↑ LFA post-exercise
Reid et al., Study1: 36 (17 Study 1: mean R Cz, LM, AR Study 1: depressed (D) EEG at Fp1/2, F3/4, No D and ND not different
1998 depressed), study 2: 27 = 18.53 years, vs. non-depressed F7/8, T3/4, T5/6, P3/4, (both studies)
(13 depressed), all female study 2: mean (ND) groups (BDI); C3/4, O1/2, A1/2, ↑ left anterior temporal
= 27.54 years study 2: depressed (D) FTC1/2, TCP1/2, PO1/2 activation in depressed
vs. non-depressed (study 2, in LM
(ND) groups (SCID) reference, trend in AR
reference)
Rosenfeld 5 (4 female) No information R Cz EEG at F3/4 Pre and post therapy No Subjects with ↑ LFA at
et al., 1996 session reports of affect; beginning of session
affect change (AC) score show ↑ change from neg
to pos affect
Schaffer et al., 15 (10 female) No information R Cz High vs. low BDI EEG at F3/4, P3/4 Yes ↑ BDI, ↑ RFA
1983 scores
Silva et al., 55 females No information R AR Restrained eaters (RE) EEG at F3/4, P3/4 Yes RE, ↑ RFA
2002 vs. unrestrained eaters
(UE)
Tomarken 38 (20 female) Mean = 13 R Cz, LE, AR Family history of EEG at F3/4 No F: ↓ LFA
et al., this years depression (F) vs. no ↓ SES, ↓ LFA
volume family history (NF);
socio-economic status
(SES)
Wiedemann 48 (39 female) Mean = 36.55 R Cz Panic (P) vs. control EEG at F3/4, P3/4 Yes Rest: P, ↑ RFA
et al., 1999 years groups (C); conditions:
rest (R), neutral stim A: P, ↑ RFA
(N), panic stim (Pn), P, ↓ LFA when shown
anxiety stim (A), erotic pictures
emotional stim (E),
motor task (M)

29
fects, reporting more right frontal activity (not less left frontal activity) in depressed versus
non-depressed mothers, and correspondingly similar differences in their respective infants.
Infant studies such as these are important not only because they add to the growing liter-
ature on frontal EEG asymmetry and depression, but because they hold the potential for
suggesting the origin of trait frontal EEG asymmetries. EEG spectra are highly heritable
(see Lykken et al., 1982), and though it is impossible to tell from these reports the degree
to which infant frontal EEG asymmetries derive from genetic versus environmental influ-
ences, the finding of mother/infant asymmetry similarities points to the need for research
on the heritability of frontal EEG asymmetry, in addition to research designed to identify
which maternal behaviors or other environmental factors may influence infant trait asym-
metries. To date, there is limited evidence bearing on whether frontal EEG asymmetries
are heritable (Coan, 2003; MacDhomhail et al., 1999). For example, in a small sample of
female mono- and di-zygotic twins, Coan (2003) estimated that genetic influences may
account for as much as 22% of the variance in resting mid-frontal EEG asymmetry, and that
most of this genetic influence is non-additive. Other designs would also prove informative
in addressing this question, including an adoption design comparing infants of depressed
versus non-depressed adoptive mothers.
If frontal EEG asymmetry were indeed a moderator of risk for psychopathology, one
would expect trait levels of frontal EEG asymmetry to be relatively stable, even as episodes
of depression come and go. As a moderator, trait (stable) frontal EEG asymmetry would
interact with other environmental variables to cause depressive episodes; environmental
variables, which are potentially less consistent, would serve as the co-determinants of any
particular episode. If, by contrast, frontal EEG asymmetry changes to a significant degree
with the presence or absence of an affective disorder, one would conclude that frontal
EEG asymmetry potentially acts as a mediator of psychopathology. (And a more complex
possibility exists, such that asymmetry has some trait-like predictive value in the face of
episode-dependent changes, thus potentially serving as moderator and mediator.) A re-
view of the literature suggests a somewhat inconsistent picture regarding the stability of
trait frontal EEG asymmetry in relationship to affective psychopathology. For example,
Jones and Field (1999) have found that music or massage therapy applied to depressed
adolescents resulted in the attenuation of their group level relative right frontal activity,
suggesting that relative decreases in the magnitude of psychopathology can result in corre-
sponding decreases in relative right frontal resting activity. Further, Jones et al. (1998) have
demonstrated that applying massage therapy can produce alterations in frontal EEG asym-
metry in infants. In this work, applying massage therapy to 1-month-old infants decreased
relative right frontal EEG activity from pre-test to mid-treatment and from mid-treatment
to post-test (Jones et al., 1998).
Two studies offer some insight into the stability of trait frontal EEG asymmetry across
time in adults undergoing treatment for depression. Debener et al. (2000) examined 15
medicated depressed patients on two occasions separated by 2 weeks, they found (1) that
control subjects showed relatively greater left frontal resting activity than did subjects who
had depression (this finding was anticipated) and (2) although depressed subjects exhib-
ited lower test–retest stability of frontal EEG asymmetry than did controls, no systematic
mood-dependent changes in asymmetry occurred across sessions in these depressed pa-
tients. Patients in this study received a variety of antidepressant compounds, most initiated
prior to the first EEG assessment, and 11 of the 15 additionally received benzodiazepines,
thus raising the possibility that the variability in the depressed patients could reflect the
acute effects of the initiation of a trial of medication; no evaluation of this possibility was
performed.
One study examined the stability of frontal EEG asymmetry in a non-medicated sample of
depressed patients as they progressed through a non-pharmacological treatment (Allen et al.,
2004; reported in preliminary form in Urry et al., 1999). Allen et al. (2004) found evidence
of adequate stability in resting frontal EEG asymmetry in depressed patients. Depression
and frontal EEG asymmetry were assessed at 4-week interals. Across three occasions of
measurement the median ICC at frontal sites (across three reference schemes) was 0.56,
across five assessments the comparable value was 0.61. This stability was apparent despite
rather substantial improvements in clinical status over the same interval. These values
are comparable to those reported by Debener et al. (2000) for control subjects, and by
Tomarken et al. (1992b) in unselected college students. Interestingly, just as with Debener
et al., Allen et al. found that changes in frontal asymmetry over assessments was not related
patient’s clinical status or mood. The most obvious difference between the two studies is
that patients in Allen et al. (2004) received no medication, whereas those in the study of
Debener et al. (2000) received a variety of antidepressant compounds and most additionally
received benzodiazepines. Clearly a systematic investigation of the impact of antidepressant
and antianxiety medications on frontal EEG asymmetry would be desirable, both in terms of
understanding the extent to which they may alter asymmetry, and also in terms of informing
questions related to mechanism of action.
In aggregate, these studies tentatively suggest some trait-like stability in frontal EEG
asymmetry across time in depressed subjects, but provide no evidence to suggest that varia-
tion in frontal EEG asymmetry across measurement occasions is due to changes in clinical
status. From a moderator perspective, it would be expected that test–retest be fairly high
even in clinical populations as symptoms wax and wane. While the evidence for this is strong
on one study, but not another, it is consistently the case that occasion-related variance in
resting frontal activity is not linked to clinical state.
Most of the work on frontal EEG asymmetry and psychopathology has concerned depres-
sion, but several studies have also examined anxiety disorders as well. Relatively greater
right frontal activity has been associated with panic disorder (Wiedemann et al., 1999) and
social phobia (Davidson et al., 2000), while anxious apprehension has been associated with
relatively greater left frontal activity (Heller et al., 1997). Although the general pattern is
consistent with the model suggested by Davidson (1998a,b), inconsistencies have prompted
Heller and colleagues (e.g., Heller and Nitschke, 1998) to propose a revised valence model
of frontal EEG asymmetry and anxiety; i.e., anxiety is comprised of two distinct though re-
lated processes, anxious apprehension and anxious arousal, and these processes are reflected
in frontal EEG asymmetries as relatively greater left frontal and right parietal activity, re-
spectively (see also Nitschke et al., 1999). Although there are data supportive of this position
(Heller et al., 1997; Nitschke et al., 1999), it is hard to reconcile with other findings that
place all forms, or nearly all forms, of anxiety squarely in the domain of relatively greater
right frontal activity. In an attempt to resolve this discrepancy, Heller and Nitschke (1998)
have argued that affective valence may account for the difference between their findings
and those of Davidson et al. (2000) and Wiedemann et al. (1999). In particular, Heller and
Nitschke (1998) have argued anxiety coupled with negative affective valence should be
associated with the pattern of right frontal activity that other researchers have found in their
studies of frontal EEG asymmetry and anxiety. Thus, ultimately Heller and colleagues argue
that anxiety can become manifest in frontal EEG asymmetry as either relatively greater left
frontal, relatively greater right frontal, or relatively greater right parietal activity, depending
on the relative presence or absence of anxious apprehension, anxious arousal and negative
affect.
7. Frontal EEG asymmetry as a possible mediator of emotional responding
Systematic alterations in frontal EEG asymmetry in response to specific emotional stimuli

suggest the possibility that the systems tapped by frontal EEG asymmetry may also fulfill
a mediating role in emotional responding. While this need not be true of all emotional
responding, it may well be true of the motivational properties that form one or more of the
components of emotional responding.
Modeling frontal EEG asymmetry as a mediator. Just as with modeling frontal EEG
asymmetry as a moderator, it will be useful to review the data analytic and statistical con-
siderations underlying the specification of a mediator. Fig. 2 represents a mediational model
of frontal EEG asymmetry in emotional responding, also adapted from Baron and Kenny
(1986). For this illustration, consider again the independent variable example discussed
previously, where subjects are presented with an image of either a poisonous snake (the fear
stimulus) or an elephant (a neutral stimulus).
Frontal EEG asymmetry could be said to be a mediator of emotional responding if a
measurable change in it is necessary—at least in part—for the relationship between some
emotion-eliciting stimulus and the subsequent emotional response. That is, it could be said
to mediate emotional responses to the degree that it serves as, or is highly correlated with,
the mechanism by which emotional stimuli have their effects. In the case of the example,
arguing that frontal EEG asymmetry is a mediator of fear responses is tantamount to saying
that the fear response would not occur, or would occur differently, or would occur at a
lower level of self reported intensity, if there was no change in frontal EEG asymmetry in
the direction of increased relative right activity (in accord with the approach/withdrawal
model). In this way, the mediational models refer specifically to frontal EEG activation as
opposed to activity.
In Fig. 2, this situation is represented by three causal pathways, identified as paths a,
b and c. In path a, changes in the type of stimulus (in the example, the presentation of a
Mediator
(EEG Asymmetry)
a b
Stimulus
Type Emotional
(snake vs. elephant) c Response
Fig. 2. Frontal EEG asymmetry as a mediator. Model adapted from Baron and Kenney (1986).
Table 4
Frontal EEG activation asymmetry as a state measure
Citation N Age Handedness reference scheme Independent variable Dependent variable Hem Results summary
Allen et al., 2001 18 females 18–38 years R Cz Biofeedback training to move Self report emotion, facial EMG Yes ↑ RFA caused ↓ positive
asymmetry towards greater left or affect, ↓ zygomatic, and ↑
right activity corrugator activity
Benca et al., 1999 17 (4 female) 35–63 years R LM Wakefulness vs. various sleep EEG at F3/4, F7/8, T3/4, T5/6, Yes Waking EEG correlated with
stages (REM, StgII, SWS) P3/4 O1/2 sleep (notably REM) in

frontal and temporal regions
Blackhart et al., in 77 (41 female) 16–39 years R LM Pre (PRE) and post (POST) EEG EEG at F3/4, FP1/2, F7/8, T3/4, No Women: ↓ POST mood, ↑
press hook-up mood ratings T5/6, C3/4, P3/4, O1/2 LFA
Men: ↓ POST mood, ↑ RFA
Coan and Allen, in Resting EEG: 30; No information R AR, LM Resting EEG at F3/4, F7/8, Emotional intensity reports (IR) No ↑ resting LFA, ↑ IR-A
press state EEG:31 FTC1/2; state EEG at F3/4, F7/8, following voluntary facial
and FTC1/2 during voluntary expressions of anger (IR-A), ↑ resting LFA, ↑ IR-D
facial expressions of anger (A), disgust (IR-D), fear (IR-F), joy ↑ resting LFA, ↑ IR-J
disgust (D), fear (F), joy (J) and (IR-J) and sadness (IR-S) ↑ LFA during A, ↑ IR-A
sadness (S). ↑ LFA during J, ↑ IR-J
↑ RFA during F, ↑ IR-F
Coan et al., 2001 36 (26 female) 17–24 years R Cz, LM, AR Voluntary emotional facial EEG at F3/4, F7/8, FTC1/2, P3/4 Yes W, ↓ LFA
expressions grouped according to A=C
approach (A), withdrawal (W)
and control (C) conditions
Collet and Duclaux, 24 (13 female) 18–45 years R AR Emotional expression during EEG at F3/4, T1/2, T3/4, T5/6, No No effects
1986 emotional films; happy (H), sad C3/4, P3/4 O1/2
(S) and neutral (N)
Davidson et al., 1990 11 females 17–41 years R Cz Emotional facial expressions EEG at F3/4, C3/4, T3/4, P3/4 Yes No effect of films.
during emotional film clips Disgust (face), ↑ RATA
Joy (face), ↑ LATA
Davidson and Fox, 24 infant females ∼10 months No information Cz Films of an actress performing EEG at F3/4, P3/4 Yes Happy, ↑ LFA
1982 happy vs. sad faces
Davidson et al., 2003 41 (29 female) 23–56 years R LE Meditation (M) vs. control (C); EEG at F3/4, FC7/8, T3/4, C3/4 No No frontal effects.
pre-treatment (T1), At T2 and T3, ↑ baseline
post-treatment (T2), 4 month activity in left central region
follow-up (T3); antibody titers to (C3/4) in M
the influenza vaccine (HIA) In M, greater relative left
activity in C3/4 from T1 to
T2 corresponded with greater
HIA.
33
34
Davidson et al., 1992 9 rhesus monkeys ∼12 months No information LM Benzodiazepam shot vs. vehicle EEG at F3/4, P3/4 Yes Benzodiazepam, ↑ LFA
(4 female)
Davidson et al., 1993 9 rhesus monkeys ∼12 months No information LM Benzodiazepam shot vs. vehicle EEG at F3/4, P3/4, freezing time No Those with most ↑ LFA to
(4 female) in response to challenge Benzodiazepam showed
longest duration freezing
behavior

Dawson et al., 1992 21 infants 21 months No information Cz Baseline (B) vs. “mother out” EEG at F3/4, P3/4 No ↑ overall frontal activation
(MO) conditions during MO
Ekman and 14 No information No information LM Duchenne (D) vs. unfelt smiles EEG at F3/4, F7/8, C3/4, T3/4, Yes D ↑ LFA, LATA
Davidson, 1993 (U) vs. anger face (A) T5/6, P3/4, O1/2
D ↑ LFA than A
Ekman et al., 1990 31 females 17–41 years R Cz Emotional facial expressions EEG at F3/4, C3/4, T3/4, P3/4 Yes D, ↑ LATA
during emotional film clips;
Duchenne (D) vs. unfelt (U)
smiles
U, ↑ RATA
Fox and Davidson, 35 infant females ∼10 months R (parents) Cz Stranger approach (SA), mother EEG at F3/4, P3/4 Yes MA, ↑ LFA (mother reach
1986 approach (MA), maternal sub-condition); (↑ LFA if
separation (MS) condition vocalizing)
MS + crying, ↑ RFA (↑
LFA if vocalizing)
Fox and Davidson, 35 infant females ∼10 months R (parents) Cz Stranger approach (SA) vs. EEG at F3/4, P3/4 Yes D, ↑ LFA than U
1987 mother approach (MA); facial A and S (no crying), ↑ LFA
expressions of joy (J), anger (A), A and S (crying), ↑ RFA
sadness (S); Duchenne (D) vs.
unfelt (U) smiles
Fox and Davidson, 16 infant (no sex 2–3 days R (parents) Cz Emotional facial expressions EEG at F3/4, P3/4 Yes 1–3 Hz band: H2 O, ↑ RFA
1988 information) during taste conditions (sucrose S, ↑ LFA
[S], citric acid [CA], H2 O) 6–12 Hz band: H2 O, ↑ RFA
S, ↑ LFA
Gilbert et al., 1994 32 (16 female) 21–35 years R No information Various self-report measures EEG at F3/4, T3/4, P3/4 (others) Yes ↑ BDI, ↑ RFA (in normals)
Hagemann and 31 (19 female) 19–36 No information Cz Occular artifacts vs. no occular EEG at FP1/2, F3/4, F7/8, T3/4, Yes No effects of occular artifact
Naumann, 2001 artifacts in EEG recordings C3/4, T5/6, P3/4, O1/2 in the alpha range
Harmon-Jones et al., 67 (33 female) No information R LE Anger manipulation (AM) vs. no EEG at F3/4, F7/8, FT7/8 Yes ↑ LFA during AM
2002 anger (NA), symptoms associated During AM, if ↑ HB, then ↑
with depression (D) and LFA
hypomania-plus-biphasia (HB) During AM, if ↑ D, then ↑
RFA
Harmon-Jones and 42 males No information R LM Baseline (B), insult (I), no-insult Self-reported anger (A) and Yes I produced, ↑ A, ↑ AG, ↑ LFA
Sigelman, (NI) conditions aggression (AG); EEG at F3/4, LFA correlated with anger in I,
2001 F7/8, P3/4 not NI
LFA correlated with Aggression
in I, not NI
Jones and Fox, 1992 23 females 18–22 years R Cz Emotional facial expressions EEG at F3/4, T3/4, P3/4 Yes H, ↑ LFA
during videos of anger (A), S, ↑ RFA
D, ↑ RFA

happiness (H), disgust (D), and
sadness (S); positive (P) vs. P, ↑ LFA during H
negative (N) affectivity groups N, ↑ RFA during H
Kline et al., 2000 49 females Mean = 64.2 years No information No information Odor conditions; vanilla (V), EEG at Fp1/2, F3/4, F7/8, O1/2, Yes V, ↑ LFA
neutral (N), valarian (VN). P3/4, T5/6
Miller and Tomarken, 60 (30 female) Mean = 19 L and R Cz Incentive levels: large reward EEG at F3/4, C3/4, P3/4, AF3/4 Yes ↑ R, ↑ LFA
2001 (LR), reward (R), no reward Men: HE, ↑ LFA
(NR), punish (P), large punish Women: LE, ↑ LFA
(LP); expectancy levels: high LT, ↑ RFA
(HE), medium (ME) and low RT, ↑ LFA
(LE); response levels: active (A)
and passive (PS); hand response
levels: left (LT) and right (RT)
Reeves et al., 1989 16 (7 female) 20–50 years R LM TV segments depicting positive EEG at F3/4, O1/2 Yes P, ↑ LFA
(P) and negative (N) scenes N, ↑ RFA
Sabotka et al., 1992 15 (8 female) 18–25 years R LM Reward (R) vs. punishment (P) Ratings of happiness (H) vs. Yes R, ↑ LFA
conditions sadness (S) during conditions; P, ↑ RFA
EEG at F3/4, F7/8, T3/4, C3/4,
O1/2, TP3/4; Approach (finger
press; FP) vs. withdrawal (finger
lift; FL) responses
Sanders et al., 2002 Study 1: 39 (29 Study 1: mean = 31 years No information Cz Studies 1 and 2: lavender odor (L) EEG at F3/4, P3 No Study 1: L, ↑ LFA
female), study 2: vs. rosemary odor (R); baseline Study 2: no effects
26 infants left frontal (LF) vs. baseline right
frontal (RF)
Schmidt et al., 1999 24 males 18–38 years R Cz Prednisone (P) vs. control groups; EEG at F3/4, C3/4, P3/4, O1/2 No T2 and P, ↑ RFA
pre-treatment (T1) vs.
post-treatment (T2)
Tucker and Dawson, 9 method actors (5 No information R LM Imagination condition; depressed EEG at F3/4, C3/4, P3/4, O1/2 Yes S ↑ RFA, compared to D
1984 female) (D) vs. sexually aroused (S)
35
36
Waldstein et al., 2000 30 (18 female) Mean = 24 years R Cz Imagination and film conditions; EEG at F3/4, C3/4, P3/4, O1/2 Yes H ↑ LFA compared to A
happiness (H) vs. anger (A)
Zinser et al., 1999 72 (no sex Mean = 26.3 R Cz Cigarette deprivation (D) and EEG at F3/4 No D,A ↑ LFA
information) control (C) groups by 1 cigarette Smoking itself, ↓ LFA
“anticipation” (A) and 2 cigarette
“no wait” (N) groups (2 × 2
factorial)

RFA: right frontal activation, LFA: left frontal activation; RATA: right anterior temporal activation, LATA: left anterior temporal activation; RPA: right parietal activation, LPA: left parietal activation.
snake versus an elephant) correspond to different changes in frontal EEG activity (frontal
EEG activation). In path b, frontal EEG activation corresponds to changes in emotional
responding. In path c, changes in levels of the independent variable (snake versus elephant)
correspond to changes in emotional responding. Frontal EEG asymmetry can be said to
be a mediator of emotional responding to the extent that path c—the direct relationship
between emotional stimuli and emotional responding—is attenuated when paths a and b
are statistically adjusted for. By this reasoning, frontal EEG asymmetry would be a perfect
mediator of emotional responding if statistically adjusting for paths a and b resulted in a
residual of zero for path c (thus identifying frontal EEG activation as a necessary condition
for emotional responding). This idealized scenario is unlikely. Rather, frontal EEG asym-
metry is likely to represent, if anything, one of several mediating processes in emotional
responding. If this is the case, then it would be expected that paths a and b improve the
overall fit of the model, and that the residual in path c is significantly decreased when paths
a and b are statistically adjusted for. Such a finding would suggest that, while not necessary,
frontal EEG activation may be a sufficient condition for generating emotional responses,
an idea that could in theory be tested.
In applying data analysis to this mediational model, one can start by conceptualizing
each path (a, b and c) as separate regression equations. That is, one could regress frontal
EEG activation (the mediator) on the independent variable, the emotional response (the
criterion variable) on the independent variable, and the emotional response on frontal EEG
activation. Baron and Kenny (1986) point out that coefficients from each equation can alone
be used to suggest (or, more strongly, rule out) a mediating relationship. Using the example,
by this method one would expect to find (1) that frontal EEG activation is related to the
differential presentation of a fearful or non-fearful stimulus (represented in Fig. 2 as path a),
(2) that the intensity of a fear related response will be related to the presentation of a fearful
versus a non-fearful stimulus (represented in Fig. 2 as path c), and (3) that the intensity
of the fear related response will be related to frontal EEG activation (represented in Fig. 2
as path b). If any of these three conditions are not obtained, then the possibility of EEG
activation serving a mediating role in the observed emotional responding can effectively be
ruled out. If these conditions are obtained, however, then mediation has not been ruled out
until controlling paths a and b show an observed impact on path c in Fig. 2.4
Another possible method of testing mediational models of this sort is to utilize struc-
tural equation modeling (SEM). The SEM approach is increasing in popularity, an indirect
measure of which is its conspicuous appearance as a new component of various popular
statistical programs, such as SAS, Statistica, etc. (Also useful are SEM dedicated programs
4 It should be noted that while it may be tempting to conclude, from analyses such as those described here,
that mediation can be ruled in, this is in fact not generally true. With the mediational analyses described here,
true mediation can at best only fail to be ruled out, unless statistically adjusting for paths a and b do indeed result
in a residual of zero, which is exceedingly unlikely (Patrick McKnight, personal communication). Moreover, the
Baron and Kenney method of addressing the status of a hypothesized mediator may suffer from unrealistic type I
error rates and low statistical power with small or even medium sample sizes. The length and scope of this article
precludes a detailed discussion of the many complexities involved in the determination of statistical mediation,
such as issues of sample size, attempts to model multiple mediators, etc. Thus, our treatment of these data analytic
issues are somewhat idealized. For additional information on mediation analyses, the reader is enthusiastically
referred to Kenny et al. (1998) and MacKinnon et al. (2002).
such as LISREL and EQS. EQS is particularly recommended.) SEM approaches essentially
reconstruct the three regression equations listed above as one model, where coefficients are
estimated within the context of the entire covariance matrix of the model’s variables. This
allows one to estimate the overall “fit” of the model one has constructed, using various
indices (for a thorough review of SEM approaches, see Loehlin, 1998).
7.1. Empirical support for frontal EEG asymmetry as a mediator
A number of studies provide oblique evidence that frontal EEG asymmetry may indeed
mediate emotional responses (see Table 4). Most of the evidence reviewed below simply
demonstrates that frontal EEG asymmetry can be altered by emotional or quasi-emotional
stimuli. Few studies measure other emotional responses as a correlate of changes in frontal
EEG asymmetry, where each is in response to some emotional stimulus. No studies to date
have explicitly tested the mediational hypothesis.
The approach/withdrawal model of frontal EEG asymmetry accommodates state changes
as well as individual differences in trait propensities. According to the model, stimuli in-
tended to elicit approach-oriented responses should result in an observed relative left frontal
EEG activation, while stimuli intended to elicit a withdrawal-oriented response should re-
sult in an observed relative right frontal EEG activation. Indeed, there is evidence to support
this prediction (e.g., Coan et al., 2001; Ekman et al., 1990; Davidson and Fox, 1982).
Some of the earliest work in this area was done by Davidson and Fox (1982), who found
that 10–12-month-old infants showed evidence of increased left frontal EEG activity in
response to films of an actress performing happy faces. Subsequently, Fox and Davidson
(1986) found that infants as young as 2–3 days exhibited an increase in left frontal activity
in response to drops of sugar water deposited on their tongues, while exhibiting more
right frontal activity in response to neutrally flavored drops (of water). Still later, Fox and
Davidson (1987) found that 10 month-old infants who reached for their mothers during a
mother approach task showed more concomitant left frontal activity than infants who did
not, and that babies who cried in response to maternal separation showed a similar right
frontal activity effect compared to other infants. Moreover, Fox and Davidson (1988) found
that anger and sadness in response to maternal separation corresponded with relatively
greater left frontal activity, unless the infants were crying, in which case both anger and
sadness corresponded with relatively greater right frontal activity. (This last finding presents
some interesting difficulties for both the approach/withdrawal and valence models of EEG
asymmetry, but nevertheless serves to illustrate the potential mediating role of processes
indicated by anterior EEG alpha asymmetries.)
Similar results have been obtained in studies of adults. Using emotional films to investi-
gate the relationship between emotional experience and frontal EEG asymmetry, Davidson
et al. (1990) found that, although frontal EEG recordings averaged across the entire period
of viewing emotional films did not show evidence of differences in hemispheric activity,
important differences did emerge during facially expressive emotional reactions to those
films. In particular, disgust films elicited relatively greater right anterior temporal activity
relative to baseline, while happy films elicited more left anterior temporal activity (Davidson
et al., 1990). In a reanalysis of the same data set, Ekman and colleagues (Ekman et al., 1990)
found that individuals who exhibited Duchenne smiles (smiles involving activation of the
orbicularis pars lateralis muscle) in response to happy films showed more concomitant left
anterior temporal activity than did individuals who exhibited “unfelt” smiles. Subsequently,
Ekman and Davidson (1993) asked participants to voluntarily perform Duchenne versus un-
felt smiles and again found that Duchenne smiles resulted in greater left anterior temporal,
as well as left frontal, activity.
Thus, lateralized brain activity seems to be a potentially important element in the col-
lection of properties that comprise at least some emotions or emotion families. This idea is
borne out further by other work (e.g., Coan et al., 2001; Harmon-Jones and Sigelman, 2001;
Jones and Fox, 1992). For example, Coan et al. (2001) used a voluntary directed facial action
task (cf., Levenson et al., 1990) to elicit approach (joy and anger) and withdrawal (disgust,
fear and sadness) related emotions, hypothesizing that approach-related emotions should re-
sult in left lateralized frontal activation while withdrawal-related emotions resulted in right
lateralized frontal activation. Their predictions were partially confirmed; withdrawal-related
emotions, particularly fear and sadness, did result in the expected relative right frontal ac-
tivation compared to a control condition, but approach-related emotions did not result in a
comparable relative left frontal activation (Coan et al., 2001). While Coan et al. (2001) did
measure other emotional responses, such as subjective emotional experience reports, they
did not test an explicit mediational model of frontal EEG asymmetry and emotion.
Recently, Coan and Allen (2003c) used the extant data reported in Coan et al. (2001)
to assess the relationship between state frontal EEG asymmetry and emotional experience
during voluntary emotional facial expressions. They found that anger and, marginally, joy
were more likely to be reported if their concomitant state EEG asymmetries involved greater
left activity, and that fear was more likely to be reported if its concomitant state EEG
asymmetry involved greater right activity (state EEG asymmetry by emotion interaction,
F(4, 895) = 8.17, P < 0.001). These results proved to be independent of reference scheme
or specific frontal region. Unfortunately, this data set did not include a single dependent
measure that was recorded following each emotion task, and the lack of such an outcome
measure precluded a proper mediational analysis. Had each participant been asked, for
example, to rate the degree to which they experienced fear following each emotion induction,
a mediational analysis, where emotion type would be the independent variable, frontal EEG
asymmetry would be the mediator and fear experience would be the outcome measure,
would be readily forthcoming.
Further evidence of the relationship between emotional states and concomitant changes
in frontal EEG asymmetry can be found in a series of studies conducted by Harmon-Jones
and co-workers (Harmon-Jones and Sigelman, 2001; Harmon-Jones et al., 2003). In an
investigation that probably comes closest to testing a true mediational model of frontal EEG
asymmetry and emotion, Harmon-Jones and Sigelman (2001) observed that individuals who
showed relative left frontal activation (again, change in frontal EEG asymmetry from rest) in
response to an insult were more likely to report experiencing anger. Similarly, Harmon-Jones
et al. (2003) observed that individuals showing left frontal activation under a different anger
induction procedure also displayed more aggressive and retaliatory behavior. Interestingly,
Harmon-Jones et al. (2003), also found that left frontal activation only occurred in response
to an anger elicitation when coping or retaliatory responses were possible. In their study,
college students were confronted either with a bogus radio broadcast confirming that a
tuition increase was certain or with one that suggested that such an increase was merely
under consideration. Those subjects who were led to believe that the increase was merely
under consideration (1) showed greater left frontal activation than those who believed the
increase was certain and (2) were more likely to engage in coping actions such as signing
and taking petitions (Harmon-Jones et al., 2003). Taken together, these studies suggest
that frontal EEG asymmetry, or by inference the activity of the brain systems it measures,
may mediate emotional responding, and that these systems are likely to be particularly
motivational in nature, as predicted by the approach/withdrawal model.
8. Frontal EEG asymmetry as a trait-like moderator and a state-related mediator
One important question regarding frontal EEG asymmetry’s role as either a moderator
or a mediator is its relative robustness as one or the other. That is, one could ask how ro-
bust trait-like individual differences in baseline frontal EEG asymmetry are across different
emotional states? An equally important question could be asked of state dependent frontal
EEG asymmetries: how robust are state frontal EEG asymmetries across individuals? Gen-
eralizability theory, or g-theory (Cronbach et al., 1972), provides a method of estimating
the reliability of particular facets of any given measure across other facets of that measure.
In g-theory, variance components are estimated and used to calculate specific intraclass co-
efficients, in this context referred to as generalizability or “g” coefficients. Thus, g-theory
can be applied to answer the precise questions articulated above. Indeed, for this article,
g-theory was applied to an extant data set described in Coan et al. (2001).
In this data set, frontal EEG asymmetries were recorded from 36 research participants
both at rest and during a voluntary directed facial action task wherein they were asked to
perform voluntary facial expressions denoting anger, disgust, fear, joy and sadness (see Coan
et al., 2001 for a detailed description of the methods used in this study). These emotions were
then grouped according to the approach/withdrawal motivational model of emotion. By this
scheme, frontal EEG asymmetries during anger and joy were arithmetically averaged into
an approach condition and disgust, fear and sadness were arithmetically averaged into a
withdrawal condition. An additional control condition was also employed.
Generalizability theory allowed for analyses of these data such that the following ques-
tions could be evaluated empirically: (1) were state changes in frontal EEG asymmetry
resulting from the emotional manipulation task reliably elicited in all subjects? And (2)
were trait predispositions in frontal EEG asymmetry preserved within emotional state con-
ditions? Results indicated first that trait, state and the trait by state interaction accounted
for approximately 8, 10 and 11% of the variance in frontal EEG asymmetry during state
manipulations, respectively (see Table 5). These results suggest that variations in frontal
EEG asymmetry attributable to traits, states and trait by state interactions are approximately
equal—around 10%. In addition to this information, trait and state g-coefficients were 0.42
and 0.97, respectively. Thus, the answers to questions 1 and 2 above appear to be yes and
somewhat, respectively. Indeed, it appears that state changes were strikingly robust to indi-
vidual differences in this study. Put another way, to the extent that state changes in frontal
EEG asymmetry occurred at all in response to the emotional manipulation, they occurred
in nearly all of the subjects, regardless of their trait predispositions. By contrast, trait pre-
dispositions were only moderately preserved within state manipulations. Ultimately, these
Table 5
Results of a state manipulated frontal EEG asymmetry generalizability study
N Variance component % variance
Trait 36 0.003 8.23

State 3 0.004 9.79
Trait × state 0.005 11.42
Residual 0.030 70.57
Relative error variance Generalizability coefficient
Trait 0.002 0.42

State 0.0001 0.97
results raise the possibility that frontal EEG asymmetry may function more robustly as
a mediator of emotional responses than as a moderator of emotional responses, although
different results might be obtained if one assessed frontal EEG asymmetry across several
occasions to provide a better and more stable estimate of trait asymmetry. Indeed, the
Spearman–Brown Prophecy Formula suggests that the generalizability of trait frontal EEG
asymmetry across emotional states would increase from 0.42 to 0.74 if averaged across 4
occasions of measurement. Such an approach may make it easier to assess the degree to
which trait predispositions in frontal EEG asymmetry affect state changes in the same.
9. Concluding remarks
While there is a great deal of evidence suggesting that frontal EEG asymmetry may
function as both a moderator and a mediator in various aspects of emotion, it is striking how
few studies provide explicit evidence of either moderation or mediation. Indeed, in the case
of mediation, explicit tests are entirely lacking, although extant data sets could conceivably
be used to explicitly test for both mediation and moderation. In this paper, recommendations
have been made for the rigorous evaluation of frontal EEG asymmetry as either a moderator
or a mediator.
9.1. Frontal EEG asymmetry as a moderator of emotion
Thus far, compelling evidence suggests a moderating role for frontal EEG asymmetry in
at least some emotions, supporting Davidson’s (1998a,b) theory of affective style. Never-
theless, generalizability analyses presented here suggest that while frontal EEG asymmetry
may function as a moderator, its influence may only be modestly reliable across emotional
states, and it is emotional states that trait frontal EEG asymmetries are supposed to be
moderating. Others have obliquely pointed this out in various ways. For example, Davidson
and colleagues (e.g., Davidson, 1998b; Henriques and Davidson, 1991; Tomarken et al.,
1990; Wheeler et al., 1993) have long advocated for the use of multiple measures of rest-
ing frontal EEG asymmetry in its measurement as a robust trait. This group of researchers
have taken different approaches to this, from averaging values across multiple sessions
(thereby increasing the measure’s reliability; e.g. Sutton and Davidson, 1997) to selecting
only individuals whose resting frontal EEG asymmetry remains stable over 2 or >2 weeks
(e.g., Wheeler et al., 1993). Such practices have many psychometric virtues. Indeed, the
Spearman–Brown prophecy formula would predict that with four occasions of measure-
ment, the reliability of trait frontal EEG asymmetry, even across emotional states, should
increase to a quite respectable range.
9.2. Frontal EEG asymmetry as a moderator of psychopathology
To the extent that trait frontal EEG asymmetry moderates emotional responses, it may
do the same for psychopathology. That is, as Davidson (1998a) has argued, an individual’s
particular affective style may create a predisposition to risk for psychopathology. If this is
true, the empirical data to date remain mixed in their support this proposition. While several
studies have suggested a relationship between frontal EEG asymmetry and psychopathology
(Allen et al., 1993; Bruder et al., 1997; Henriques and Davidson, 1990, 1991; Gotlib et al.,
1998; Debener et al., 2000; Davidson et al., 2000; Wiedemann et al., 1999), some have
suggested otherwise (Reid et al., 1998), and none have attempted to rigorously model
frontal EEG asymmetry as a moderator in the explicit fashion recommended by Baron
and Kenny (1986). Importantly, however, establishing a moderating effect of frontal EEG
asymmetry will require that data sets include measures of risk-related events or traits that
frontal EEG asymmetry can moderate. So for example, if it is found that a particular cognitive
vulnerability (for example, hopelessness; Abramson et al., 2002) is related to depression,
then one could ask if that relationship is especially strong for those lowest in left frontal
activity. Ideally, of course, one would obtain prospective data, such that hopeless cognitions
and frontal EEG were assessed in a relatively high-risk but euthymic population, and the
development of depression at a later timepoint would be assessed.
One might object to this last remark on the grounds that modeling moderator effects
for psychopathology is not possible given the difficulty in implementing the kind of large,
prospective studies that such an approach would require, but such declarations are probably
premature. There may be ways to model frontal EEG asymmetry as a genuine modera-
tor of psychopathology that do not require such costly commitments. For example, Allen
et al. (1993) studied participants suffering intermittently from seasonal affective disorder
(SAD)—a psychological difficulty whose course, treatment and eliciting environmental
stimulus is relatively well understood, and moreover, relatively manipulable by investiga-
tors (via techniques such as phototherapy and/or waiting for the seasons to change). In
studying psychopathology with an episodic course, of which SAD is a prime example, one
could construct a GLM that would straightforwardly test the moderator model such as the
following: SAD = season + trait frontal EEG asymmetry + season × trait frontal EEG
asymmetry. One could also substitute a phototherapy manipulation for the Season vari-
able in the case of SAD, or a psychotherapy treatment variable in the case of non-seasonal
depression.
Other possibilities no doubt exist. For example, various negative life events have been
associated with depression (e.g., Goodman, 2002). One could imagine that individuals who
have just experienced the death of a close loved one may be at greater risk for depression than
would those who have not. One could imagine further, indeed Davidson’s diathesis/stress
model predicts, that individuals with relatively greater right frontal EEG asymmetry would
be particularly likely to become depressed following the death of a close loved one. As
a general linear model, one could state this as follows. Depression = loss status (yes/no)
+ trait frontal EEG asymmetry + loss × trait frontal EEG asymmetry. Similarly, adjustment
disorders with depressed features frequently strike freshmen undergraduate students away
from home for the first time. The approach/withdrawal diathesis/stress model would predict
that individuals who show relatively greater right frontal EEG activity at rest are at greater
risk for such adjustment disorders during their freshman year of college.
9.3. Frontal EEG asymmetry as a mediator
While no study to date has explicitly modeled frontal EEG asymmetry as a mediator of
emotional responses, several studies provide evidence that this is at least a distinct possibil-
ity, and the generalizability analyses reported here suggest that if frontal EEG asymmetry
does indeed function as a mediator, its effects are quite robust to individual differences in
trait frontal EEG asymmetry.
As for modeling frontal EEG asymmetry as a mediator, it will be important for individuals
to record measures of emotional response other than frontal EEG asymmetry per se. That
is, many studies of state changes in frontal EEG asymmetry regard frontal EEG asymmetry
as a dependent variable only. In order to assess its function as a possible mediator, some
other criterion of emotional response must be established. A good example of this, though
also one in which frontal EEG asymmetry is not explicitly modeled as a mediator, was
conducted by Davidson et al. (2000). These researchers identified state changes in frontal
EEG asymmetry in social phobics as a function of anticipating giving a speech. In addition
to demonstrating changes in frontal EEG asymmetry, other measures of physiological and
self-reported distress were obtained, allowing at least the possibility of an explicit media-
tional model. Similarly, Harmon-Jones et al. (2003), in identifying state changes in frontal
EEG asymmetry resulting from bogus anger inducing radio broadcasts, also measured cop-
ing behaviors, such as signing and taking petitions, again allowing for the possibility of
an explicitly mediational model. Ultimately, if frontal EEG asymmetries prove to satisfy
criteria as a mediator of emotion, then activity in the brain systems tapped by frontal EEG
asymmetry may not simply be an output of emotion, but rather may be something that
facilitates the emotional response.
9.4. Future directions
As a sub-field of emotion and motivation, the study of frontal EEG asymmetry holds
substantial promise. In terms of basic science, this sub-field promises to inform us regarding
the fundamental properties of emotion, both in terms of how emotions occur and what
properties they entail. In more applied settings, the possibility yet remains that frontal EEG
asymmetry may serve as a useful liability marker for depression and anxiety. Regardless
of the application of this measure, it is increasingly important that theoretical predictions
surrounding frontal EEG asymmetry are put to more rigorous tests, especially those provided
by testing explicit mediational and moderational models. In the absence of such explicit
tests, the field will remain a collection of studies merely suggestive of moderating and
mediating influences, around which much exciting and potentially important speculation
and theory is generated. It is possible to more explicitly test that speculation and theory
with models that more adequately can support or refute such inferences.
The results of these explicit tests will guide the field in investigating whether and how
frontal EEG asymmetry may serve as a risk marker for psychopathology, and in investigating
what underlying physiological systems influence and are influenced by emotion. Gaining a
deeper understanding of the fundamental properties of emotion will require clear thinking
in terms of how the various components of emotion and emotional experience are related.
It is in this spirit that the present remarks are offered.
Acknowledgements
This work was supported, in part, by a Young Investigator award from NARSAD (John
Allen) and a Graduate Research Fellowship from the National Science Foundation (James
Coan). Portions of the present work appear in Coan and Allen (2003a) and appear with
permission. Address for correspondence: James A. Coan, W.M. Keck Center for Functional
Brain Imaging and Behavior, Waisman Center, University of Wisconsin, Madison, WI
53705, USA. E-mail: jacoan@wisc.edu or John J.B. Allen, Department of Psychology,
University of Arizona, Tucson, AZ 85721-0068, USA. E-mail: jallen@u.arizona.edu.
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Review
Contributions from research on anger and cognitive
dissonance to understanding the motivational
functions of asymmetrical frontal brain activity
Eddie Harmon-Jones∗
Department of Psychology, University of Wisconsin-Madison,
1202 West Johnson Street, Madison, WI 53706, USA
Abstract
Research has suggested that approach-related positive emotions are associated with greater left
frontal brain activity and that withdrawal-related negative emotions are associated with greater right
frontal brain activity. Different explanations have been proposed. One posits that frontal asymmetry
is due to emotional valence (positivity/negativity), one posits that frontal asymmetry is due to motiva-
tional direction (approach/withdrawal), and one posits that frontal asymmetry is due to a combination
of emotional valence and motivational direction (positive-approach/negative-withdrawal). Because re-
search had confounded emotional valence and motivational direction, the theoretical explanation was
muddled. Solely supporting the motivational direction model, recent research has revealed that anger
and cognitive dissonance, emotions with negative valence and approach motivational tendencies, are
related to relatively greater left frontal activity.
Keywords: Frontal EEG asymmetry; Emotion; Anger; Cognitive dissonance
1. Introduction
Over the past two decades, a variety of research approaches have pointed to the impor-
tance of the left and right frontal brain regions in emotion and motivation. Research has
suggested that left frontal brain activity is associated with positive emotions and approach
behavior and right frontal brain activity is associated with negative emotions and with-
drawal behavior. This research has created an impression that high levels of left frontal
∗ Tel.: +1-608-265-5504; fax: +1-608-262-4029.

E-mail address: eharmonj@facstaff.wisc.edu (E. Harmon-Jones).
doi:10.1016/j.biopsycho.2004.03.003
52 E. Harmon-Jones / Biological Psychology 67 (2004) 51–76
activity are preferred to low levels of left frontal activity. Several popular press articles
have appeared in the New York Times, Parade Magazine, and other sources echoing the
message advanced by several researchers (e.g., Fox et al., 2001; Davidson, 1998) that rel-
atively high left frontal brain activity is more psychologically and physically healthy than
relatively less left frontal brain activity. This theoretical model is widely accepted, even
among researchers who are not involved in research on the frontal asymmetry (e.g., Oatley
and Jenkins, 1996; Zajonc and McIntosh, 1992). Indeed, researchers have begun to use the
past findings regarding the association of left frontal activity with more positive outcomes
in creating treatment strategies such as biofeedback (e.g., Baehr et al., 1997; Rosenfeld
et al., 1995). However, in this article, I review research that casts doubt on the assumption
that increased left frontal activity is always beneficial. Although several studies have found
left frontal activity to be associated with positive emotions, recent research has indicated
that these findings resulted because the past research confounded approach motivation with
positive emotional valence. Appetitive motivations are not always associated with positive
affects. Anger, greed, lust, and mania are some examples of approach motivations that may
have deleterious consequences. In this article, I will briefly review research on the rela-
tionship between emotion/motivation and asymmetrical frontal brain activity. I will then
describe several theoretical explanations of the research results. After reviewing the vari-
ous theoretical explanations, I will review recent research on the emotion of anger and the
emotive state of cognitive dissonance that has favored the motivational direction view over
the other views. Finally, I broadly consider this recent research for theories and research on
emotion.
2. Asymmetrical frontal brain activity and emotion
Broadly speaking, research on frontal asymmetry has proceeded along three lines: (1)
examinations of the relationship between behavioral or experiential indices of trait af-
fect/motivation and resting electroencephalograph activity (EEG); (2) examinations of
the relationship between resting EEG and responses to emotion-eliciting stimuli; and (3)
examinations of EEG changes during exposure to emotionally evocative situations.1 To
begin, I will briefly review representative findings from each of these empirical
approaches.
1 Much of the research on asymmetrical frontal brain activity has assessed the activity using alpha frequency
band activity derived from the electroencephalograph (EEG). Research has revealed that alpha power is inversely
related to regional brain activity using hemodynamic measures (Cook et al., 1998) and behavioral tasks (Davidson
et al., 1990). Additional data from individuals with brain damage supports the research reviewed in this article (e.g.,
Robinson and Downhill, 1995). Because the majority of research on the frontal asymmetry has used EEG alpha
power, the review focuses on this research. In addition, in the review, I use the term brain activity to refer to the
inverse of alpha power, as is commonly done in this literature. Moreover, I reserve the use of the term activation to
refer to state-induced changes in EEG, whereas activity can refer to state or trait (baseline) EEG. Finally, the term
relative left frontal activity (or activation) is used to describe greater left than right frontal activity—a difference
or asymmetry score.
E. Harmon-Jones / Biological Psychology 67 (2004) 51–76 53
3. Examinations of the relationship between indices of trait affect/motivation and

resting EEG
3.1. Depression
Depression has been found to relate to resting frontal asymmetrical activity, with de-
pressed individuals showing relatively less left than right frontal brain activity. This rela-
tionship between depression and asymmetrical frontal activity has been found in individuals
identified by self-report indices of depression (Jacobs and Snyder, 1996; Schaffer et al.,
1983), and individuals identified through clinical interviews (Allen et al., 1993). More-
over, relatively less left frontal activity has been found in individuals who were previously
clinically depressed but were in remission status (Henriques and Davidson, 1990).
3.2. Positive and negative affect
Other research has revealed that trait positive affect is associated with greater left than
right frontal brain activity, whereas trait negative affect is associated with greater right
than left frontal brain activity (e.g., Tomarken et al., 1992a). In this past research, trait
positive affect and negative affect were assessed using the Positive and Negative Affect
Schedule (Watson et al., 1988). These affects are best described as activated positive affect
and activated negative affect (Watson et al., 1999), as the measures include words such as
interested and active on the positive affect scale, and afraid and distressed on the negative
affect scale.
3.3. Behavioral activation/behavioral inhibition
Other research has found that trait behavioral activation sensitivity (BAS) relates to greater
left than right frontal brain activity (Coan and Allen, 2003; Harmon-Jones and Allen, 1997;
Sutton and Davidson, 1997). In this research, BAS was measured by Carver and White’s
(1994) behavioral inhibition sensitivity (BIS)/BAS questionnaire, which includes items
such as “When I want something, I usually go all-out to get it.” Regarding the relationship
of behavioral inhibition sensitivity (BIS; “I worry about making mistakes.”), studies have
produced inconsistent results, with one finding a significant relationship between BIS and
greater right than left frontal activity (Sutton and Davidson, 1997) and the two others finding
a non-significant relationship (Coan and Allen, 2003; Harmon-Jones and Allen, 1997). It is
possible that BIS is not equivalent to withdrawal motivation (see Harmon-Jones and Allen,
1997).
4. Examinations of the relationship between resting EEG and responses to

emotion-eliciting stimuli
Resting baseline frontal asymmetrical activity has been found to predict emotional re-
sponses. Individuals with relatively greater right than left frontal activity exhibit larger neg-
ative affective responses to negative emotion-inducing films (fear and disgust) and smaller
positive affective responses to positive emotion-inducing films (happiness) (Tomarken et al.,

1990; Wheeler et al., 1993). In a related vein, research has found that resting baseline
frontal asymmetrical activity predicted evaluative responses to merely exposed stimuli
(Harmon-Jones and Allen, 2001). That is, individuals with relative right frontal activity
reported more favorable attitudes toward familiarized stimuli (safety) than did individuals
with relative left frontal activity. Other research has found that relative right frontal activ-
ity at baseline predicts crying in response to maternal separation in 10-month-old infants
(Davidson and Fox, 1989).
Although these effects are based on correlational evidence and hence subject to alterna-
tive explanations, recent research has more strongly suggested that the frontal asymmetry
is causally involved in the production of these emotional responses. In this experiment,
biofeedback training was used to manipulate the frontal asymmetry (Allen et al., 2001).
Participants were randomly assigned to receive biofeedback training designed to increase
right frontal relative to left frontal activity or to receive training in the opposite direc-
tion. Five consecutive days of biofeedback training provided signals of reward (300 Hz
reward tone) or nonreward (150 Hz nonreward tone) depending on whether the difference
between right and left frontal activity exceeded a criterion value. Systematic alterations of
frontal asymmetry were observed as a function of biofeedback training. Moreover, sub-
sequent self-reported affect in response to emotionally evocative film clips were signifi-
cantly influenced by the direction of biofeedback training. That is, individuals trained to
increase left frontal activity reported more positive affect in response to the happy film
clip than individuals trained to increase right frontal activity. These results suggest that
the frontal asymmetry can be altered using biofeedback training and that this alteration
can affect emotional responses. Taken together with previous research, this experiment
suggests that the frontal asymmetry is causally involved in the production of emotional
experience.
5. Examinations of EEG activity during exposure to emotionally evocative

situations
Research has also demonstrated that asymmetrical frontal brain activity is associated with
state emotional responses. For instance, Davidson and Fox (1982) found that 10-month-old
infants exhibited increased left frontal activation in response to a film clip of an actress
generating a happy facial expression as compared to responses exhibited to a film clip of
an actress generating a sad facial expression. Frontal brain activity has been found to relate
to facial expressions of positive and negative emotions, as well. For example, Ekman and
Davidson (1993) found increased left frontal activation during voluntary facial expressions
of smiles of enjoyment (i.e., activation of zygomatic major with concurrent activation of
orbicularis oculi, pars lateralis) as compared to voluntary facial expressions of smiles not
associated with enjoyment (i.e., activation of zygomatic major without orbicularis oculi,
pars lateralis). More recently, Coan et al. (2001) found that voluntary contractions of the
facial musculature to form a happy facial expression produced relatively greater left frontal
activity, and that voluntary contractions of the facial musculature to form a fearful facial
expression produced relatively less left frontal activity.
6. Explanations of the relationship between asymmetrical frontal brain activity and

emotion
Primarily, there have been three conceptual models designed to explain the observed re-
sults. The first view has posited that the left frontal brain region is involved in the experience
and expression of positive emotion and that the right frontal brain region is involved in the
expression and experience of negative emotion (e.g., Ahern and Schwartz, 1985; Gotlib
et al., 1998; Heller, 1990; Heller and Nitschke, 1998; Silberman and Weingartner, 1986).
Indeed, this theoretical model is widely accepted (e.g., Oatley and Jenkins, 1996; Zajonc
and McIntosh, 1992). Most of the results can be explained with this model, which I refer
to as the valence model.
A second view has posited that the left frontal brain region is involved in expression
of approach-related emotions and that the right frontal brain region is involved in ex-
pression withdrawal-related emotions (Davidson, 1995; Fox, 1991; Harmon-Jones and
Allen, 1997; Sutton and Davidson, 1997). Again, the obtained results can be accommo-
dated by this model, which I refer to as the motivational direction model. That is, the
affects and emotions that have been examined in the research are all associated with
approach or withdrawal motivation. The approach-related emotions have been found to
be associated with relatively greater left frontal activity, whereas the withdrawal-related
emotions have been found to be associated with relatively greater right frontal
activity.
A third view has posited that the left frontal brain region is involved in the expression
and experience of positive, approach-related emotions and that the right frontal brain re-
gion is involved in the expression and experience of negative, withdrawal-related emotions
(Davidson, 1998; Tomarken and Keener, 1998). The obtained results can also be accom-
modated by this model, which I refer to as the valenced motivation model. That is, the
positive affects and emotions that have been examined in the research are all associated
with approach motivation, and the negative affects and emotions that have been examined
are all associated with withdrawal motivation.
Because the previously conducted research confounded the valence of the emotion with
the direction of motivation, it is unable to address whether the frontal asymmetry reflects
the valence of the emotion, the direction of the motivation, or a combination of valence and
motivation. Often, positive emotion is associated with approach-related motivation, whereas
negative emotion is associated with withdrawal-related motivation. Indeed, most contem-
porary theories of emotion posit that positive emotion is always associated with approach
motivation and that negative emotion is always associated with withdrawal motivation emo-
tion (e.g., Watson, 2000; for a different point of view, see Carver, 2001). However, not all
emotions behave in accord with this presumed relationship between the valence of emotion
and direction of motivation. Anger is one of the best examples of a violation of the rela-
tionship, because anger is negative in valence (e.g., Lazarus, 1991; Watson et al., 1999), but
it often evokes approach motivation (e.g., Berkowitz, 1999; Darwin, 1872/1965; Plutchik,
1980; Young, 1943).
To address the primary emotional/motivation functions of asymmetrical frontal brain
activity, my colleagues and I have been examining the emotion of anger, as it is often con-
sidered a negative emotion that evokes approach motivational tendencies. By examining the
emotion of anger, we are in a position to answer precisely what the emotional/motivational

functions of asymmetrical frontal brain activity are.
7. Anger and approach motivation
Before reviewing the research on anger and asymmetrical frontal activity, it is important
to consider whether anger is associated with approach motivation. Several lines of research
suggest that anger elicits behavioral approach or approach motivation tendencies. In what
follows, I briefly review representative research supporting the idea that anger is associated
with approach inclinations.
7.1. Behavioral evidence
In the animal behavior literature, a distinction has been made between offensive or irritable
aggression and defensive aggression (Flynn et al., 1970; Moyer, 1976). It has been posited
that irritable aggression results from anger and that pure irritable aggression “involves attack
without attempts to escape from the object being attacked” (Moyer, 1976, p. 187). A number
of aggression researchers have suggested that offensive aggression is associated with anger,
attack, and no attempts to escape, whereas defensive aggression is associated with fear,
attempts to escape, and attack only if escape is impossible (Blanchard and Blanchard,
1984; Lagerspetz, 1969; Moyer, 1976). In demonstrating that organisms evidence offensive
aggression and that this is an approach behavior, Lagerspetz (1969) found that under certain
conditions mice would cross an electrified grid to attack another mouse.
In other research with adult humans, Baron (1977) demonstrated that angry individuals
are reinforced positively by signs of their tormentor’s pain. The participants who had been
deliberately provoked by another individual had a sanctioned opportunity to assault him in
return. Indications that their first attacks were hurting their target led to intensified aggres-
sion even though the unprovoked participants reduced the intensity of their punishment at
learning of the other’s pain. The initial signs of their victim’s suffering showed the angry
persons they were approaching their aggressive goal and thus evoked even stronger assaults
from them. Other research is consistent with these findings (e.g., Berkowitz et al., 1981).
In addition, Lewis et al. (1992) found that infants who expressed anger during extinction
maintained interest during subsequent relearning, whereas infants who expressed sadness
during extinction evidenced decreased interest during relearning. Thus, subsequent to frus-
trating events, anger may maintain and increase task engagement and approach motivation.
7.2. Subjective evidence
Additional support for the idea that anger is associated with approach motivation comes
from research testing the conceptual model that integrated reactance theory with learned
helplessness theory (Wortman and Brehm, 1975). According to this model, how individuals
respond to uncontrollable outcomes depends on their expectation of being able to control
the outcome and the importance of the outcome. When an individual expects to be able to
control outcomes that are important, and those outcomes are found to be uncontrollable,
psychological reactance should be aroused. Thus, for individuals who initially expect con-
trol, the first few bouts of uncontrollable outcomes should arouse reactance, a motivational
state aimed at restoring control. After several exposures to uncontrollable outcomes, these
individuals should become convinced that they cannot control the outcomes and should
show decreased motivation (i.e., learned helplessness). In other words, reactance will pre-
cede helplessness for individuals who initially expect control. In one study testing this
model, individuals who exhibited angry feelings in response to one unsolvable problem
had better performance and were presumably more approach motivated on a subsequent
cognitive task than did participants who exhibited less anger (Mikulincer, 1988).
Other research has revealed that state anger relates to high levels of self-assurance, phys-
ical strength, and bravery (Izard, 1991), inclinations associated with approach motivation.
Additionally, Lerner and Keltner (2001) found that anger (both trait and state) is associated
with optimistic expectations, whereas fear is associated with pessimistic expectations. More-
over, happiness was associated with optimism, making anger and happiness appear more
similar to each other in their relationship with optimism than fear and anger. Although Lerner
and Keltner (2001) interpreted their findings as being due to the appraisals associated with
anger, it seems equally plausible that it was the approach motivational character of anger that
caused the relationship of anger and optimism. That is, anger creates optimism because anger
engages the approach motivational system and produces greater optimistic expectations.
7.3. Hormonal and physiological evidence
Further evidence supporting the conceptualization of anger as involving approach and

not withdrawal comes from research on testosterone, which has been found to be associated
with anger and aggression in humans (e.g., Olweus, 1986). In this research, testosterone
treatments have been found to decrease withdrawal (fear) responses in a number of species
(e.g., Boissy and Bouissou, 1994; Vandenheede and Bouissou, 1993). Other research has
demonstrated that damage to the amygdala, a brain region involved in defensive behavior,
has no effect on offensive aggression but reduces reactivity to nonpainful threat stimuli
(Blanchard and Takahashi, 1988; Busch and Barfield, 1974).
7.4. Individual differences evidence
Other evidence supporting the idea that anger is associated with an approach-orientation
comes from research on bipolar disorder. The emotions of euphoria and anger often oc-
cur during manic phases of bipolar disorder (Cassidy et al., 1998; Depue and Iacono, 1989;
Tyrer and Shopsin, 1982). Both euphoria and anger may be approach-oriented processes, and
a dysregulated or hyperactive approach system may underlie mania (Depue and
Iacono, 1989; Fowles, 1993). Research suggests that hypomania/mania involves increased
left frontal brain activity and approach motivational tendencies. In this research, it has been
found that individuals who have suffered damage to the right frontal cortex are more likely
to evidence mania (see review by Robinson and Downhill, 1995). Thus, this research is
consistent with the view that mania may be associated with increased left frontal activity
and increased approach tendencies, because the approach motivation functions of the left
frontal cortex are released and not restrained by the withdrawal system in the right frontal
cortex. Furthermore, lithium carbonate, a treatment for bipolar disorder, reduces aggres-
sion (Malone et al., 2000), suggesting that anger and aggression correlate with the other
symptoms of bipolar disorder. In addition, trait anger has been found to relate to high lev-
els of assertiveness and competitiveness (Buss and Perry, 1992). These lines of research
suggest that anger is associated with a number of approach-related individual differences
characteristics.
Recently, two additional individual differences studies were conducted to test the hy-
pothesis that trait anger is related to trait approach motivation, or more specifically, trait
BAS (Harmon-Jones, 2003). In both studies, trait BAS, as assessed by Carver and White’s
(1994) scale, was positively related to trait anger at the simple correlation level, as assessed
by the Buss and Perry (1992) aggression questionnaire. One of the two studies found that
trait anger also related to trait behavioral inhibition sensitivity at the simple correlation
level. In both studies, general negative affect was statistically controlled. This was done
because anger’s association with general negative affect (Berkowitz, 1999, 2000; Watson,
2000) may cause the association of BIS and anger. That is, the affect of anger has two
subcomponents: a nonspecific component that reflects the contribution of general negative
affect (Berkowitz, 1999; Watson, 2000) and a more specific component that reflects the
unique qualities of anger (Watson, 2000). In other words, at the simple correlation level,
anger may be associated with BIS, but when controlling for negative affect, anger will not be
associated with BIS but will only be associated with BAS. Results supported this prediction
in both studies. Additional results in Study 2 revealed that BAS was positively correlated
with physical aggression, and simultaneously regressing aggression onto BAS, BIS, and
general negative affect revealed that physical aggression was positively related to BAS,
negatively related to BIS, and positively related to negative affect. These results support the
hypothesis that anger is related to approach motivation and strongly challenge theoretical
models that assume that approach motivation is only associated with positive affect.
7.5. Summary of section
Because of the large body of evidence suggesting that anger is often associated with
approach motivation, we examined the relationship between anger and relative left frontal
activation to test whether the frontal asymmetry is due to emotional valence, motivational
direction, or a combination of emotional valence and motivational direction.
8. Anger and asymmetrical frontal brain activity
8.1. Asymmetrical frontal activity and trait anger
In one of the first studies examining the relationship between anger and asymmetrical
frontal brain activity (Harmon-Jones and Allen, 1998), EEG of young adolescents (M age =
13 years) was recorded as they sat quietly for 6 min. Trait anger was measured using the Buss
and Perry (1992) aggression questionnaire. Results indicated that trait anger was positively
related with relatively greater left than right frontal brain activity. Moreover, additional
analyses revealed that high levels of trait anger were associated with increased left frontal
activity and decreased right frontal activity. These results suggest that the frontal asymmetry
is associated with motivational direction (approach versus withdrawal) rather than emotional
valence. In addition, in this study, general activated positive and negative affect, as assessed
by the Positive and Negative Affect Schedule—Children’s version (PANAS-C; Laurent
et al., 1994), related to the frontal asymmetry in magnitudes similar to those found in
previous research (Sutton and Davidson, 1997). That is, positive affect related to relative
left frontal activity and negative affect related to relative right frontal activity. Presumably,
positive affect and anger related to relative left frontal activity because both emotions are
approach-related. Moreover, controlling for positive and negative affect, separately and
together, did not alter the magnitude of the anger—frontal asymmetry relationship. These
results suggest that anger is related to relative left frontal activity, independent of general
activated positive and negative affect.
A second study was conducted to assess the validity of an alternative explanation for the
relationship between anger and relative left frontal brain activity (Harmon-Jones, 2004).
According to this explanation, individuals with high levels of trait anger might regard anger
as a positive emotion, and this positive feeling or attitude toward anger is responsible for
anger being associated with relative left frontal activity. To understand why anger might be
a positive emotion, it is important to consider what is meant by positivity and negativity
of emotion. Emotions can be regarded as positive or negative because of the conditions
that evoked the emotion or because of the emotion’s subjective feel. The emotion of anger
can be viewed as negative when considering the conditions that evoked the emotion, and
positive or negative when considering the subjective feel or evaluation of the emotion.
Indeed, past writers have suggested in line with this latter definition that some individuals
“take considerable pleasure in the experience of anger” (Ekman and Friesen, 1975, p. 81).
To address whether the relationship of anger with increased left frontal activation could
be explained by the fact that individuals with high levels of trait anger enjoy the experience
of anger more than individuals with low levels of trait anger, studies were conducted to first
create and assess the reliability and validity of a scale that would assess attitude toward
anger and second to examine the relationship of attitude toward anger with the resting
frontal asymmetry (Harmon-Jones, 2004). A reliable and valid measure of feelings toward
anger was created, and then it and a measure of trait anger were related to the resting
frontal asymmetry. Results indicated that trait anger related to relative left frontal activity2 ,
2 Two other studies have provided additional examinations of the association of anger with the frontal EEG
asymmetry. However, the results were not strongly supportive of an anger-left frontal activity relationship. In
one of these experiments (Dawson et al., 1992), 21-month-old infants’ facial expressions were recorded during
emotion-eliciting situations. During expressions of anger, relatively greater left than right frontal activity occurred,
and during expressions of sadness, relatively greater right than left activity occurred. However, the frontal asym-
metry was significantly different from neutral expressions only for sad expressions and not for angry expressions.
In another experiment (Fox and Davidson, 1988), 10-month-old infants evidenced greater left than right frontal
activity during angry facial expressions not accompanied by crying, and greater right than left frontal activity
during angry facial expressions accompanied by crying. Effects of identical direction occurred for sad facial ex-
pressions; that is, greater left than right frontal activity during sad facial expressions not accompanied by crying,
and greater right than left frontal activity during sad facial expressions accompanied by crying. Because sadness
and anger showed similar relations with the frontal asymmetry, it is difficult to infer from these effects whether
the frontal asymmetry reflects valence or direction. Finally, both of these studies were correlational and subject to
interpretational difficulties associated with correlational studies.
replicating the previous study (Harmon-Jones and Allen, 1998). Moreover, while trait anger
was directly associated with a more positive attitude toward anger, the attitude toward anger
did not relate to relative left frontal activity. In addition, statistically controlling for attitude
toward anger did not alter the magnitude of the relationship between trait anger and relative
left frontal activity. This study suggested that the relationship between trait anger and relative
left frontal activity was not due to relative left frontal activity being associated with a more
positive feeling toward anger. In addition, this study replicated the results of the previous
one, but with a sample of young adults, whereas the first study examined adolescents who
might be less controlled and more likely to translate anger into approach behavior. That
anger related with relative left frontal activity in young adults (M age 19 years) suggests
that the relationship is not limited to young adolescents.
8.2. Asymmetrical frontal activity and state anger
While evidence suggests that anger is a negative and approach-oriented emotion, and that
trait anger is related to relative left frontal activity, it is not known how state anger relates to
asymmetrical frontal brain activity. Moreover, the trait anger-relative left frontal evidence
presented thus far is entirely correlational and subject to the interpretational difficulties
associated with correlational results. Because past research has found asymmetrical frontal
activity to be responsive to manipulations of positive-approach and negative-withdrawal
states (see above review as well as Hagemann et al., 2002), it was therefore important to
examine whether manipulated anger would increase relative left frontal activity.
In this state anger research, we also examined the relationship between anger-related
asymmetrical frontal activity and aggression. Emotions such as anger can be conceived
of as having motivational functions and as generating action tendencies (Brehm, 1999;
Frijda, 1986). Of course, emotions may generate action tendencies that may not be mani-
fest in overt behavior. However, anger often generates approach-related action tendencies
that are generally aimed at resolving the anger-producing event. In the case of an insult,
the action tendency may be aggression. If anger-induced relative left frontal activity is
involved in approach motivational processes, then greater anger-induced left frontal activ-
ity may relate to increased aggression. Our research on trait aggression and asymmetrical
frontal activity has yielded some support for this prediction, in that relative left frontal ac-
tivity at baseline has been found to relate to somewhat greater self-reported trait aggression
(Harmon-Jones and Allen, 1998). To assess the relationship of relative left frontal activity
with aggression, we included a behavioral measure of aggression. We predicted that rel-
ative left frontal activity in response to an anger-eliciting event would relate to increased
aggression.
To test these predictions, participants were randomly assigned to a condition in which
they were insulted or not insulted (Harmon-Jones and Sigelman, 2001). They were informed
that the study concerned personality, psychophysiology, and perception. They were also told
that another participant was in another room with another experimenter, and that the study
would be conducted in connection with this other participant’s study. Then, they were told
that there were two perception studies, the first involving person perception and the second
involving taste perception. In the first ostensible study, participants wrote an essay on a
social issue that they found important and they argued in support of the side of the issue
they favored (e.g., legal drinking age). Then, the other ostensible participant supposedly
read and evaluated their essay. Finally, participants read the feedback provided by the other
participant. The feedback was designed to be insulting or not. Immediately after the feedback
manipulation, EEG was recorded.
Then, participants completed the “second perception study” that involved taste percep-
tion. This “study” allowed us to obtain a behavioral measure of aggression. In this “study,”
participants were told that it was very important for experimenters to remain blind to the
type of tastes to which participants are exposed in taste perception studies. The experimenter
explained that one way to keep experimenters blind to the tastes is to have one participant
assign the tastes to the other participant. He also explained that the other participant would
have to drink all that he is given. He then showed that participant six types of beverages,
which consisted of 11 oz of water with 1, 2, or 3 teaspoons of sugar, apple juice, lemon
juice, salt, vinegar, or hot sauce mixed into the water. Thus, each of the six types of bever-
ages had three concentration levels. It was explained that most persons find the sugar water
most pleasant and the hot sauce most unpleasant, and that the other beverages were rated
in between these two extremes, with those closer to sugar being more pleasant and those
closer to hot sauce being more unpleasant (presented in the following order: sugar, apple
juice, lemon juice, salt, vinegar, hot sauce).
Participants were told to select one of the six types of beverages for the other participant,
to pour some of each of the three concentrations into cups, and to cover the cups with
lids when done. The participants were also told to label the concentration level on the
bottom of each cup. The experimenter indicated that the participants may choose which
type of beverage to administer and how much to administer to the other participant. The
participants were also given a black sheet to cover the unused beverages when they were
finished administering the beverages, to keep the experimenter blind to the type of beverage
they chose. Aggression was calculated by assigning each beverage a value that corresponded
to its unpleasantness. This measure of aggression is similar to a technique developed by
other researchers (Lieberman et al., 1999; McGregor et al., 1998).
Results indicated that participants in the insult condition reported feeling more angry and
were more aggressive than participants in the no insult condition. More importantly, partic-
ipants in the insult condition evidenced greater relative left frontal activity than participants
in the no insult condition. Finally, within the insult condition, participants who evidenced
greater relative left frontal activity in response to the insult reported feeling more angry and
behaved more aggressively.
This research supports the prediction that manipulated anger causes increased relative
left frontal brain activity. In conjunction with trait-based research (Harmon-Jones, 2004;
Harmon-Jones and Allen, 1998), the research demonstrates that asymmetrical frontal brain
activity reflects motivational direction rather than emotional valence. In addition, results
suggested that relative left frontal activity during an anger-evoking situation related to
behavioral aggression.
In addition to the reviewed evidence, other research is consistent with the hypothesis
that anger is associated with left frontal activity.2 For example, D’Alfonso et al. (2000)
recently used slow repetitive transcranial magnetic stimulation (rTMS) to inhibit the left or
right prefrontal cortex. They found that rTMS of the right prefrontal cortex caused selective
attention towards angry faces whereas rTMS of the left prefrontal cortex caused selective
attention away from angry faces. Because slow rTMS produces inhibition of cortical ex-
citability, these results suggests that the rTMS of the right prefrontal cortex decreases its
activation and caused the left prefrontal cortex to become more active. The same holds
true for rTMS of the right prefrontal cortex and activation of the left prefrontal cortex. The
increase in activation left prefrontal led participants to attentionally approach angry faces,
as in an aggressive confrontation. In contrast, the increase in activation right prefrontal
led participants to attentionally avoid angry faces, as in a frightening confrontation. The
interpretation of these results, which d’Alfonso et al. advanced, concurs with other research
that has demonstrated that attention toward angry faces is associated with high levels of
self-reported anger and that attention away from angry faces is associated with high levels
of cortisol (van Honk et al., 1998, 1999, 2001), which is associated with fear.
8.3. Manipulating the intensity of approach motivation in an anger-evoking situation
According to the motivational direction model of asymmetrical frontal activity, approach

motivation is related to left frontal activity and withdrawal motivation is related to right
frontal activity. Thus, increased left frontal activation occurs in response to anger-inducing
situations because the increase in relative left frontal activity increases approach motiva-
tional tendencies that would assist in behavior that may rectify the anger-inducing situation.
From this perspective, it follows that if no approach behavior could be taken to deal with
the anger-provoking situation, then this increase in relative left frontal activation should
be less. In other words, if approach and withdrawal motivational tendencies do underlie
asymmetrical frontal activity, then alterations in motivational intensity should affect the
degree of activation in the frontal brain regions.
Several motivational theories posit that the expectancy of success or perceived task dif-
ficulty should affect motivational intensity (for reviews, see Brehm and Self, 1989; Wright
and Kirby, 2001). For the emotion of anger, if a situation creates anger and the individ-
ual believes that she can successfully act to alter the situation, then motivational intensity
should be relatively high. If, on the other hand, the individual believes that no action can
be taken, then motivational intensity should be relatively low. A similar prediction follows
from the idea of secondary coping (Lazarus, 1991). Negative emotions including anger, sad-
ness, guilt and fear occur when persons find themselves in aversive situations. According to
Lazarus (1991), the type of negative emotion evoked by a situation may be determined by
coping potential—how persons appraise their ability to deal with the aversive situation. If
something can be done to resolve the situation, then anger, an active and negative emotion,
should be aroused. In contrast, if nothing can be done to resolve the situation, then a pas-
sive and negative emotion, sadness, may be aroused. Theorists make similar predictions for
appraisals of power (Roseman, 1991), power and control (Scherer, 1993), and likelihood of
reinstatement of the goal state (Levine, 1995).
Unfortunately, little research has addressed whether appraisals of higher coping poten-
tial lead to more anger. However, research by Levine (1995) found that, when 5-year-old
children were presented with scenarios in which a child experienced a negative outcome,
they expected the protagonist to experience more anger and less sadness when they judged
the possibility of goal reinstatement more likely and less anger and more sadness when they
judged goal reinstatement less likely.
Based on the integration of ideas from the motivational model of asymmetrical frontal
activity with theories of motivational intensity and how coping potential relates to anger, we
predicted that greater left frontal activation would occur in response to an anger-producing
event when persons believe that action can be taken to resolve the situation as compared to
when persons believe that no action can be taken to resolve the situation.
To test these predictions, university students who paid a sizable portion of their tuition
and who were opposed to a tuition increase were invited to an experiment ostensibly con-
cerned with reactions to pilot radio broadcasts. They then heard an editorial in which the
speaker argued forcefully for a tuition increase. Immediately prior to hearing the editorial,
participants were informed that the tuition increase may occur in the future and that petitions
were being circulated to attempt to prevent the increase (action-possible condition), or they
were informed that the tuition increase would definitely occur (action-impossible condi-
tion). Immediately after listening to the editorial, EEG was recorded, and then participants
completed a self-report emotion questionnaire. Finally, participants in the action-possible
condition were given the opportunity to sign a petition and take as many petitions as they
wanted to have others sign.
Results revealed that participants in the action-possible condition evidenced greater rela-
tive left frontal activity than did participants in the action-impossible condition. Moreover,
within the action-possible condition, this increase in relative left frontal activity directly
related to self-reported anger and behaviors aimed at rectifying the anger-producing event
(i.e., whether or not they signed the petition and number of petitions taken). Interestingly,
self-reported anger did not differ between the action-possible and action-impossible con-
ditions. Both conditions reported feeling much more angry after hearing the editorial as
compared to before hearing the editorial. These results suggest that the appraisal of cop-
ing potential influenced relative left frontal activity but not angry feelings (Harmon-Jones
et al., 2003b).
8.4. Individual differences that predict increased relative left frontal activity
during anger
The research reviewed thus far suggests that trait and state anger are related to relative left
frontal activity when anger is associated with approach motivational tendencies. As men-
tioned earlier, past research has revealed that individual differences in behavioral approach
sensitivity are related to relatively greater left frontal activity (Harmon-Jones and Allen,
1997; Sutton and Davidson, 1997). Thus, greater BAS should predispose individuals to
respond with greater left frontal activity when angered. Indeed, the BAS has been posited to
be involved in predatory aggression (Depue and Iacono, 1989; Gray, 1982). In addition, the
BAS has been proposed to underlie types of psychopathology, with depression involving a
hypoactive BAS (Fowles, 1988, 1993) and mania/hypomania involving a hyperactive BAS
(Depue and Iacono, 1989; Depue et al., 1987; Meyer et al., 1999).
Based on these ideas, research examined the relationship between proneness to hypoma-
nia/mania and anger-related left frontal activity (Harmon-Jones et al., 2002). In the study,
individuals with proneness toward hypomania/mania or depression symptoms were exposed
to the anger-evoking radio broadcast used in the previously mentioned study (Harmon-Jones
et al., 2003b). Results indicated that individuals with proneness toward hypomania/mania
evidenced greater left frontal activation when confronted with the anger-evoking situation,
whereas individuals with proneness toward depression symptoms evidenced less left frontal
activation when confronted with the same anger-evoking situation. These results support
predictions derived from models relating mania/hypomania to BAS activity (Depue and
Iacono, 1989; Fowles, 1988, 1993), models of the motivational functions of asymmetrical
frontal activity (Harmon-Jones and Allen, 1997; Sutton and Davidson, 1997), and models
that consider anger as part of the BAS (Depue and Iacono, 1989; Harmon-Jones and Allen,
1998, 2001; Harmon-Jones and Sigelman, 2001; Harmon-Jones et al., 2003b).
This research extends the past research on anger and frontal brain activity by revealing
individual difference characteristics that predict who is more likely, as well as less likely, to
respond with increased left frontal activity in anger-inducing situations. That is, individuals
with proneness toward hypomania/mania symptoms evidence greater relative left frontal
activity, whereas individuals with proneness toward depressive symptoms evidence lesser
relative left frontal activity when confronted with an anger-evoking event. From these re-
sults, it seems plausible to predict that proneness toward hypomania/mania symptoms may
predispose persons toward responding with increased approach (and decreased withdrawal)
motivational tendencies given challenging or frustrating situations, whereas proneness to-
ward depressive symptoms may predispose persons toward responding with decreased ap-
proach (and increased withdrawal) motivational tendencies given these same situations. In
other words, proneness toward hypomania/mania symptoms may lead to reactance-like re-
sponses and proneness toward depressive symptoms may lead to helpless responses in the
face of challenges (e.g., Abramson et al., 1989; Mikulincer, 1988; Wortman and Brehm,
1975).
8.5. On the reduction of anger-related left frontal activity
Whereas the reviewed evidence cogently links approach anger to relative left frontal
activity, it would be important to establish that manipulations that reduce angry approach
behaviors also reduce relative left frontal activity. To address this issue, we tested whether
sympathy would reduce the relative left frontal activity typically observed during anger.
Past research has suggested that experiencing sympathy for another individual can reduce
aggression toward that individual (e.g., see review by Miller and Eisenberg, 1988). We
hypothesized that sympathy may reduce aggression by reducing the relative left frontal
activity associated with anger. To test this hypothesis, participants were told that the study
concerned personality, perception, and brain activity, and that they and another student
would be writing essays and evaluating each other based on the essays. Participants then
wrote a persuasive essay arguing either for or against a 10% tuition increase. Then, the
experimenter returned to the participants’ room and handed them a folder containing a
reading perspective, an essay, and a questionnaire.
The reading perspective instructions asked participants to remain completely objective
(low sympathy) or to try to imagine how the other person must feel (high sympathy), as in
much past sympathy research (Batson, 1991; Harmon-Jones et al., 2003a). The participant
then read the essay ostensibly written by the other participant. In the essay, the other partic-
ipant described his/her difficulties with having multiple sclerosis. Following the reading of
the essay, the participant received an evaluation of his/her essay ostensibly written by the
other participant. The evaluation contained either neutral ratings and comments (no insult)
or insulting ratings and comments (insult). Immediately after feedback manipulation, EEG
was collected. Then, the participant completed a questionnaire assessing impressions of the
other participant and a questionnaire assessing emotions.
Results indicated that the insult condition evoked greater self-reported anger than the
no-insult condition. Also, the high sympathy condition evoked greater self-reported sympa-
thy than the low-sympathy condition. No significant insult X sympathy condition interac-
tions emerged for either anger or sympathy. Moreover, no significant condition differences
emerged for self-reported sadness, happiness, fear, or distress.
More importantly, the insult condition evoked greater left frontal activity but only when
high levels of sympathy were not first evoked for the insulting person. That is, the low
sympathy/insult condition produced greater relative left frontal activity than every other
condition. In addition, the low sympathy/insult condition evoked greater left frontal activity
and lesser right frontal activity than every other condition, when separate estimates of
left and right frontal activity were examined using methods suggested by Wheeler et al.
(1993). Thus, when participants first experienced sympathy for the target person, they did
not evidence increased left frontal activity when insulted. Moreover, they expressed less
hostile attitudes toward the insulting person than did participants who did not first experience
sympathy for the insulter. That is, the low sympathy/insult condition differed from each of
the other conditions. The experiment thus suggested that the alteration of relative left frontal
activity via sympathy can reduce angry aggression.
9. Dissonance and left frontal activity
The anger research has strongly supported the motivational direction model over the
emotional valence model of the frontal asymmetry. In addition to this anger research, some
recent evidence suggests that cognitive dissonance is associated with left frontal activity.
Because cognitive dissonance is associated with negative affect (e.g., Elliot and Devine,
1994; Harmon-Jones, 2000a; Zanna and Cooper, 1974; for a review, see Harmon-Jones,
2000b), this research further supports the motivational direction model over the valence
model.
The idea that dissonance caused by commitment to a course of action might be associated
with left frontal activity was derived from the action-based model of cognitive dissonance
(Harmon-Jones, 1999; Harmon-Jones and Harmon-Jones, 2002). The action-based model
proposes that inconsistency between cognitions makes persons uncomfortable because in-
consistency has the potential to interfere with effective action. From the viewpoint of the
action-based model, cognitions are important because they guide the actions of an organ-
ism. When an individual holds two relatively important cognitions that are inconsistent,
the potential to act in accord with them is undermined. To reduce the inconsistency and
resulting negative affect, individuals engage in a variety of cognitive strategies. For exam-
ple, dissonance results when one “freely chooses” to engage in behavior that is inconsistent
with an attitude or belief. The “free choice” is subtly induced by the experimenter in ex-
perimental research. Numerous experiments have found that when individuals engage in
such behavior, they often change their attitudes to be consistent with their recent behavior.
In other research, it has been found that after making difficult decisions (which have been
found to cause dissonance), individuals value the chosen alternative and devalue the rejected
alternative more than they did prior to the decision (for reviews, see Beauvois and Joule,
1996; Brehm and Cohen, 1962; Harmon-Jones, 1999). In both of these dissonance-evoking
situations, dissonance occurs because there are cognitions that are inconsistent with a cho-
sen course of action. That is, in the former situation, the past attitude is inconsistent with
the current behavior. In the latter situation, the positive aspects of the rejected alternative
and the negative aspects of the chosen alternative are inconsistent with the decision. The
dissonance thus has the potential of interfering with the translation of the decision into
effective action. According to the action-based model, attitude change produced by disso-
nance is the result of following through with the commitment to the behavior. The attitude
change is posited to be one of a number of processes that would assist with the translation of
the commitment into effective and unconflicted action. Thus, according to the action-based
model, dissonance evokes a negative affective state that signals the organism that some-
thing is wrong and motivates the organism to engage in behavior to correct the problem.
The correction of the problem often involves following through with the commitment to the
behavior or decision. This view of dissonance is consistent with past as well as present the-
orizing on the function of dissonance and dissonance reduction (e.g., Beckmann and Kuhl,
1984; Harmon-Jones, 1999, 2000a; Jones and Gerard, 1967; McGregor et al., 1999; Newby-
Clark et al., 2002).
To assist in translating the intention into effective action, approach motivational processes
should be activated, as the individual works to successfully implement the new commitment.
Thus, the increase in approach motivation should activate the left frontal cortex. Interest-
ingly, past research findings are consistent with the idea that the left frontal cortical region
may be involved in approach motivational processes aimed at resolving inconsistency. For
example, event-related functional magnetic resonance imaging research has found that the
left dorsolateral prefrontal cortex is more active during preparation for color naming than
during preparation for word naming in a Stroop task (MacDonald et al., 2000). Moreover,
more activity in this brain region was associated with less conflict (i.e., smaller reaction time
interference effects). MacDonald et al. suggested that these findings support the hypothesis
that the left dorsolateral prefrontal cortex is involved “in the implementation of control,
by representing and actively maintaining the attentional demands of the task (p. 1837).”
They also suggested that greater activity in the left dorsolateral prefrontal cortex, which
implements control, should cause less conflict. Other research has suggested that activity
in the anterior cingulate cortex is involved in monitoring the occurrence of errors or the
presence of response conflict (e.g., Carter et al., 1998; Gerhing et al., 1993). Importantly,
recent research has found increased anterior cingulate cortex activity, as measured by the
event-related potential known as the error-related negativity, when behavior conflicts with
the self-concept (Amodio et al., 2004). This finding suggests that even higher level conflicts,
the type with which dissonance theory has been most concerned, also activate the anterior
cingulate cortex.
Based on this past research, it seems plausible that dissonance (or potential response
conflict, in action-based model terms) activates the anterior cingulate cortex, and then ac-
tivates left dorsolateral prefrontal cortex, which assists in resolving the conflict. To test the
prediction that dissonance was associated with increased left frontal cortical activity, uni-
versity students who were opposed to a tuition increase participated in a study ostensibly
concerned with attitudes and personality (Harmon-Jones et al., 2000c). They were ran-
domly assigned to one of two choice conditions. In the low-choice condition, participants
were told they were to write an essay supporting a 10% tuition increase at their univer-
sity. In the high-choice condition, participants were told that writing the essay in favor of
the tuition increase was their choice and completely voluntary. However, the instructions
subtly encouraged them to write such an essay. EEG was assessed for 1 min following
the beginning of the writing of the counterattitudinal essay, as past research has revealed
that dissonance is greatest at this point in time (Beauvois and Joule, 1996). Moreover, the
commitment alone (and not the complete essay writing) is sufficient to evoke dissonance
(e.g., Beauvois and Joule, 1996; Rabbie et al., 1959). Then, participants completed an
attitude measure. Replicating much past research, results revealed that high-choice partic-
ipants changed their attitudes more than low-choice participants. Supporting the primary
prediction, results also revealed that high-choice participants evidenced greater relative
left frontal activity than low-choice participants (main effect of choice manipulation in an
ANOVA with lateral frontal and mid-frontal asymmetry as repeated measures). It is im-
portant to note that high- and low-choice conditions did not differ in compliance rates;
that is, an equal number of high- and low-choice individuals engaged in the counterattitu-
dinal behavior (the illusion of choice is the critical variable in this paradigm). Moreover,
they did not differ in baseline resting frontal asymmetry. These results suggest that a se-
lection bias did not produce the above asymmetry results. In addition, the two conditions
did not differ in how convincing the essays were or in essay length, suggesting that the
differences observed on attitude and relative left frontal activity were not due to differ-
ences in the strength or length of the counterattitudinal statements. We have replicated this
finding using a different attitudinal issue and in this experiment, we measured EEG im-
mediately after commitment and before essay writing began (Harmon-Jones et al., 2000c,
Experiment 2).
The results of this recent research suggest that dissonance, a negative emotive state,
is associated with greater relative left frontal activity. While dissonance and left frontal
activity co-occur, it is not yet empirically clear how they relate to each other. Based on
other research, I would suggest that the initial experience of dissonance may activate the
anterior cingulate cortex, which then activates the left frontal cortex to engage the approach
motivational system, which ultimately may assist with the reduction of dissonance. Indeed,
anger may relate to left frontal cortical activity in much the same way; that is, the left
frontal cortex may become active during anger to engage the approach motivational system
to ultimately assist with the reduction of anger. The findings of Harmon-Jones et al. (2003b)
are consistent with such a view. Only when individuals expected to be able to rectify the
anger-evoking situation did increased left frontal activity result. And the left frontal activity
related directly to self-reported anger and actions taken to resolve the anger-evoking event.
However, when individuals did not expect to be able to rectify the anger-evoking situation,
increased left frontal activity did not occur. Interestingly, both experimental conditions
caused an increase in self-reported anger. Thus, while left frontal activity may relate to
the negative emotions of dissonance and anger, its relation is not due to the valence of the
emotions but is instead due to the approach motivational tendencies activated with these
emotions.
10. Discussion of some issues
The reviewed research provides strong support for the motivational direction model of
asymmetrical frontal activity and directly contradicts the other two models that have been
offered to explain the relationship between emotions and the frontal asymmetry. If asym-
metrical frontal activity reflected emotional valence, then anger and dissonance would have
directly related to relative right frontal activity. That the results of the reviewed studies
were significantly opposite to the prediction derived from emotional valence models pro-
vides particularly strong support for the motivational direction model. Before concluding,
it is important to discuss a few issues concerning the interpretations of asymmetrical frontal
brain activity and its relation to emotion and motivation, and to discuss a few broad impli-
cations these findings have for research on and theories of emotions.
10.1. On the relationship of angry feelings and relative left frontal activity
The research examining the relationship between asymmetrical frontal brain activity and
anger began with the assumption that anger is often associated with approach motivation.
Indeed, as indicated earlier, much past research has revealed that anger is associated with
approach motivation and behavior. However, it is important to note that angry feelings are
not inevitably associated with approach motivation and left frontal activity. For instance, in
the study in which we examined the relationship between coping potential and left frontal
activity (Harmon-Jones et al., 2003b), we found that regardless of whether individuals
expected to be able to potentially resolve the anger-producing event, equally intense feelings
of anger were produced by the aversive event. However, relative left frontal activity was only
increased when individuals expected to be able to potentially rectify the anger-producing
event. In addition, feelings of anger were associated with left frontal activity only in this
latter experimental condition. Thus, feelings of anger are often, but not inevitably, associated
with approach motivation and left frontal activity.
Results from another study are consistent with this interpretation. In this study, results
revealed a dissociation between angry feelings and left frontal activity when high levels of
sympathy were first aroused for the insulting person (Harmon-Jones et al., 2004). In this
case, angry feelings were equally high whether or not sympathy was aroused for the insulting
person. In contrast, left frontal activity differed between these two conditions, such that left
frontal activity was increased following an insult by a person for whom sympathy had not
previously been aroused, whereas left frontal activity was not increased when participants
first empathized with the insulting person. In fact, in this latter condition, feelings of anger
were directly associated with right frontal activity, suggesting that that the anger experienced
while sympathizing with the other person was associated with withdrawal motivation. It is
possible that individuals in this condition were motivated to withdraw so that their anger
would not lead them to harm the person with whom they had earlier sympathized.
In sum, research has revealed that whereas angry feelings are often associated with
approach motivation and relative left frontal activity, they are not inevitably associated
with these constructs, as has been revealed in recent research (Harmon-Jones et al., 2003b;
Harmon-Jones et al., 2004). Future research is needed to assess whether a type of anger that
evokes withdrawal and right frontal activity exists.
10.2. Defining emotional valence
Consistent with current theories of emotion, the perspective advanced in this paper as-
sumes that anger is a negative emotion. However, it is possible that anger could be a positive
emotion and thus the valence model of the frontal asymmetry could explain the evidence
linking anger to increased left frontal activity. Most perspectives on emotion rarely discuss
what is meant by the valence of emotion. Most scientists, like most laypersons, know that joy
and enthusiasm are positive emotions, and that anger and fear are negative emotions. On the
rare occasions when valence is discussed, emotions are defined as positive or negative (1)
because of the cause of the emotion; (2) because of the emotion’s adaptive consequences; (3)
or because of the emotion’s subjective feel (Lazarus, 1991). Indeed, Lazarus (1991) noted
that definition 1—whether the person–environment relationship is beneficial or harmful—is
“the most common, implicit, use of the terms” for positive and negative emotion (p. 6). By
this definition, anger is indeed negative. Thus, the reviewed research demonstrates that a
negative emotion with approach tendencies is associated with increased left frontal activity.
However, it is still possible that the frontal asymmetry is a function of emotional valence
when emotional valence is defined in an alternative manner. In our research, we sought
to test whether the valence model of asymmetrical frontal brain activity could explain the
relationship of anger and left frontal activity when emotional valence was defined using
the subjective feel definition. In the research, we first created a trait questionnaire that
demonstrated that there were reliable individual differences in persons’ subjective feelings
about anger. Then, we examined the relationship between the subjective feel of anger and
resting baseline left frontal activity. We found that while trait anger related to both left
frontal activity and a more positive subjective feeling about anger, the subjective feel of
anger did not relate to left frontal activity (Harmon-Jones, 2004). Thus, even when using a
more arcane definition of emotion, we were unable to find a relationship between positivity
of anger and left frontal activity.
Given the difficulties inherent in defining adaptational consequences, we have yet to
examine relationships between the adaptational consequences of anger and asymmetrical
frontal brain activity. However, in some definitions of adaptation, it does appear that anger
is associated with increased left frontal activity regardless of the adaptive consequences.
That is, regardless of whether anger is associated with constructive action (e.g., working
to prevent an injustice; Harmon-Jones et al., 2003b) or destructive action (e.g., behavioral
aggression; Harmon-Jones and Sigelman, 2001), anger has been found to relate to increased
left frontal activity. In sum, the evidence strongly suggests that anger is a negatively valenced
emotion that is related to relative left frontal activity because of its association with approach
motivation.
10.3. Evoking emotions
Of the emotions examined in the research on brain mechanisms involved in emotions,

anger has received less attention than emotions such as fear, sadness, and disgust, which can
be induced using established stimuli (e.g., pictures, films). Part of this relative neglect of
anger may be that fear, sadness, and disgust are relatively easier to evoke in the laboratory
because active, involving situations are not necessarily required to elicit the emotions.
Because the evocation of anger often requires the use of more active and involving situations,
the study of anger may require the assistance of social psychologists who are familiar with
creating such high-impact settings (see e.g., Harmon-Jones et al., in press).
On a related note, examinations of emotions other than anger should consider imple-
menting more active and involving situations, as the more active and involving situations
may elicit vastly different brain responses than the ones obtained in more passive situations.
Indeed, our research has revealed that the manipulation of coping potential (i.e., the belief
that one can take action to resolve the anger-producing situation) affects the activation of
asymmetrical frontal brain activity but not the experience of anger (Harmon-Jones et al.,
2003b). That is, the belief that one can take action to resolve the anger-producing situa-
tion produced an increase in left frontal activity and self-reported anger, whereas the belief
that one could not act to resolve the anger-producing situation produced an increase in
self-reported anger but not an increase in left frontal activity. Given that one of the primary
functions of emotions is the motivation of behavior (Brehm, 1999; Frijda, 1986), it is all
the more important for emotion researchers to consider the behavioral context in which
emotions are evoked.
10.4. The health consequences of increased left frontal cortical activity
Of course, the frontal cortex is a complex structure, and is involved in several psycholog-
ical processes. The presently reviewed research, in conjunction with past research, suggests
that the frontal cortex is also asymmetrically involved in approach and withdrawal moti-
vation. Although many have viewed left frontal cortical activity as only associated with
positive valence and positive outcomes, the reviewed research indicates that left frontal
activity is also associated with anger, at both trait and state levels of analysis. Thus, it is
most likely that left frontal cortical activity is associated with both positive and negative
outcomes. Whether left frontal activity (and approach motivation) is associated with pos-
itive or negative outcomes likely depends on a variety of factors (e.g., environment) and
perspectives (e.g., type of measure; individual versus society). That is, while left frontal
activity may be associated with heightened immune system functioning, it may also be as-
sociated with other negative consequences for the individual and society. Individuals high
in approach motivation, who have greater left frontal activity (Harmon-Jones and Allen,
1997; Sutton and Davidson, 1997), may also be grandiose, manic (Harmon-Jones et al.,
2002; Meyer et al., 2001), angry (Harmon-Jones, 2003, in press; Harmon-Jones and Allen,
1998), defensive (Kline et al., 1998; Tomarken and Davidson, 1994), and at greater risk for
cardiovascular problems (e.g., James et al., 1983). Moreover, some of the characteristics
associated with left frontal activity may provide both benefits and harms. For example,
angry approach-oriented behaviors may constitute highly effective short-term strategies for
achieving specific goals, asserting positions of social influence, and even causing positive
subjective feelings of satisfaction and accomplishment. On the other hand, those very same
strategies could contribute to a variety of problems, from domestic abuse to international
terrorism. Similarly, such putatively “left frontal” approach-oriented strategies could, over
time, harm the body, such as occurs in the relationship between trait anger and cardiovas-
cular disease or John Henryism (a pattern of active coping with adversity by trying harder
and harder against obstacles that may be insurmountable).
Most of the evidence cited by Davidson (this issue) in raising the possibility that relative
left frontal activity produces positive consequences and “may be associated with aspects
of resilience” is correlational and subject to the limitations of correlational evidence (in
particular, third variables). Given such correlational designs, it is prudent to assess the po-
tential moderating or mediating role of frontal brain asymmetry (Coan and Allen, this issue).
Davidson (this issue) argues in this regard that left frontal activity may not mediate emotional
responses but only moderate them. In support, he reviews research that has found inverse
relationships between left frontal activity and amygdala activity (as measured by startle
eyeblink response and hemodynamic imaging) during fear and disgust, withdrawal-related
emotions. In contrast, we have recently found that anger increases left frontal activity and
amydala activity (as measured by the startle eyeblink response; Harmon-Jones et al., 2004).
This evidence suggests that during an approach-related emotion, left frontal activity is not
suppressing amygdala activity but is positively covarying with it. When emotions that nat-
urally confound valence and motivational direction (e.g., fear) are used to test hypotheses,
explanations can be muddled.
The point of this review is not to suggest that anger is inevitably associated with increased
left frontal activity, or that left frontal activity is inevitably associated with negative out-
comes. Our research has indicated that anger is not inevitably associated with left frontal
activity. It does, however, suggest that approach motivation, which can involve anger and
other negative affective states, is associated with left frontal activity. Moreover, it suggests
that a valence model explanation of asymmetrical frontal cortical activity is no longer viable.
11. Conclusion
For the last few decades, several models of emotion have considered pleasant to unpleas-
ant dimension of emotion an important organizing principle—one that assists in under-
standing trait mood and situational reactions to significant stimuli at both subjective and
physiological levels of analysis. However, recent developments have suggested that this fo-
cus on the valence dimension may not adequately capture emotional space. Consideration
of motivational direction in the analysis of emotion, particularly as it relates to asymmetri-
cal frontal brain activity, seems especially important. In addition, as psychological science
focuses more attention on the empirically neglected positive aspects to psychological life,
it is important to keep in mind that approach motivations are not inevitably associated with
positive subjective feelings or positive outcomes.
Acknowledgements
The research presented in this article was funded by grants from the National Institute of
Mental Health (MH60747-01 and MH52662), by a grant from the National Science Foun-
dation (BCS-9910702), and by grants from the Wisconsin/Hilldale Undergraduate/Faculty
Research Fund. The comments John Allen (editor), Cindy Harmon-Jones, Steve Sutton,
Jim Coan, and an anonymous reviewer provided on this article are much appreciated.
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Resting frontal brain activity: linkages to

maternal depression and socio-economic
status among adolescents
Andrew J. Tomarken a,∗ , Gabriel S. Dichter a ,
Judy Garber b , Christopher Simien a
a Department of Psychology, College of Arts and Sciences, Vanderbilt University,
301 Wilson Hall, Nas hville, TN 37203, USA
b Department of Psychology and Human Development, Peabody College,
Vanderbilt University, Nashville, TN 37203, USA
Abstract
We tested the prediction that resting frontal brain asymmetry would be a marker of vulnerability
for depression among adolescents. Baseline electroencephalographic (EEG) activity was recorded
from 12 to14-year-old adolescents whose mothers had a history of depression (high risk group) and
whose mothers were lifetime-free of axis I psychopathology (low risk group). High risk adolescents
demonstrated the hypothesized pattern of relative left frontal hypo-activity on alpha-band measures.
Such effects were specific to the mid-frontal region and generally consistent across reference mon-
tages. Socio-economic status (SES) also predicted alpha asymmetry. When the effects of SES and
risk status were jointly assessed, SES contributed unique variance to the prediction of frontal brain
asymmetry. The implications of the observed relations among maternal depression, SES, and frontal
brain asymmetry are discussed.
Keywords: Frontal EEG asymmetry; Emotion; Risk for depression; Socio-economic status
1. Frontal brain asymmetry and depression
In this study, we assessed whether adolescents who are at-risk for depression differ
in patterns of resting frontal brain activity when compared to low risk adolescents. We
∗ Corresponding author. Tel.: +1-615-322-4177; fax: +1-615-343-8449.

E-mail address: andrew.j.tomarken@vanderbilt.edu (A.J. Tomarken).
doi:10.1016/j.biopsycho.2004.03.011
78 A.J. Tomarken et al. / Biological Psychology 67 (2004) 77–102
addressed this question because of evidence from a variety of sources indicating a linkage be-
tween unipolar depression and decreased activity of left relative to right hemisphere frontal
brain regions (for reviews, see Davidson, 1995, 1998b; Davidson et al., 2002; Tomarken
and Keener, 1998). Consistent with this conclusion are: (a) neurological studies indicat-
ing that the severity of depressive symptomatology is correlated with the proximity of a
left-hemisphere lesion to the frontal pole (e.g., Morris et al., 1996; Pohjasvaara et al., 2002;
Robinson and Downhill, 1995; Shimoda and Robinson, 1999); (b) regional cerebral blood
flow (rCBF) studies showing that clinically depressed participants demonstrate relative de-
creases in left frontal activity when compared to non-depressed control participants (e.g.,
Baxter et al., 1989; Bench et al., 1992; Ebert et al., 1991; Martinot et al., 1990); (c) rest-
ing electroencephalographic (EEG) studies showing that clinically depressed individuals
(Allen et al., 1993) or individuals characterized by elevated scores on the Beck Depression
Inventory (Beck and Steer, 1987) demonstrate relative left frontal hypo-activity when com-
pared to controls (Schaffer et al., 1983); and, (d) studies showing that transcranial magnetic
stimulation of the left frontal cortex (which may well increase left frontal activity) produces
clinical improvement in depressed individuals (e.g., George et al., 1997; Pascual-Leone
et al., 1996). As a cautionary note, we should add that not all findings have been consistent
in these areas (e.g., Dam et al., 1989; House et al., 1990; MacHale et al., 1998). In addition to
these empirical linkages are theoretical perspectives proposing that left frontal dysfunction
may be a neural substrate of core features of unipolar depression. For example, consis-
tent with the approach-withdrawal model of frontal asymmetry (Davidson and Tomarken,
1989; Fox, 1991), several commentators have proposed that anhedonia reflects a deficit in a
neural approach system, one component of which is the left frontal cortex (e.g., Davidson,
1998a).
2. Left frontal hypo-activity and vulnerability to depression:

children of depressed mothers
Of prime importance in the present context are EEG studies indicating that resting
frontal brain asymmetry may indicate heightened vulnerability to depression. For exam-
ple, two studies have found that currently euthymic individuals who have a history of
depression demonstrate left frontal hypo-activity relative to control participants (Allen
et al., 1993; Henriques and Davidson, 1990). Unfortunately, studies of individuals with
remitted depression cannot distinguish whether left frontal hypo-activity is a vulnerability
factor for depression or a consequence of depression (Alloy et al., 1999). An assessment
of at-risk populations who have not yet manifested depression represents a more direct
test of whether left frontal hypo-activity indicates vulnerability. One such population is
children of depressed parents. Such children exhibit a range of negative outcomes and psy-
chiatric diagnoses compared to children of parents without a psychiatric history (Downey
and Coyne, 1990; Gelfand and Teti, 1990) and appear to be at particularly heightened risk
for developing depression (Hammen, 1991; Warner et al., 1992; Weissman et al., 1992,
1997).
Several studies have found that infants of depressed mothers do in fact exhibit left frontal
hypo-activity (e.g., Dawson et al., 1997; see also Field et al., 1995; Jones et al., 1997).
A.J. Tomarken et al. / Biological Psychology 67 (2004) 77–102 79
Dawson and her colleagues also have linked left frontal hypo-activity in infants of de-
pressed mothers to decreased positive affect and increased negative affect during inter-
actions (Dawson et al., 1992a, 1999a,b). To date, studies of frontal brain asymmetry in
children of depressed mothers have concentrated on infants. One goal of the present study
was to investigate whether adolescent offspring of mothers with a history of depression
demonstrated the same pattern of relative left frontal hypo-activity that has been observed
in previous studies with currently depressed adults, adults with a history of depression,
and high risk infants. To test this hypothesis, we compared patterns of resting frontal EEG
asymmetry in young adolescent (12–14-year-old) offspring of depressed and non-depressed
mothers.
There were several reasons why we assessed children in this age range. First, the presence
of left frontal hypo-activity in adolescent offspring of depressed mothers would indicate a
continuity of risk beginning in infancy and extending into adolescence. Second, the peak
age of onset of depression in children of depressed parents ranges from 14 to 20 years
(Weissman et al., 1997). Thus, left frontal hypo-activity in adolescent offspring of depressed
mothers would indicate the presence of a potential indicator of risk at a point in time
that immediately antedates the dramatic increase in the incidence of depression. Third,
although the prevalence rate of depression in preadolescence is comparable in boys and
girls, by adulthood nearly twice as many women are diagnosed with depression as men
(Nolen-Hoeksema and Girgus, 1994). Thus, both increases in depressive symptoms and
sex differences in such symptoms first emerge during adolescence. Although prior studies
have not typically found sex differences in the linkages between frontal brain asymmetry
and depression, this is a largely unexplored area. We sought to examine the interrelations
among sex, differential risk for depression, and frontal brain asymmetry in adolescents at
high and low risk for depression.
3. Relations with socio-economic status
We also assessed the relation between socio-economic status (SES) and frontal brain
asymmetry. A number of epidemiological studies have indicated an inverse relation be-
tween social class and rates of unipolar depression (Kaplan et al., 1987; Leventhal and
Brooks-Gunn, 2000; Murphy et al., 1991; Pearlin and Johnson, 1977; Weissman and
Myers, 1978), as well as other psychiatric illnesses (Dohrenwend, 2000; Goodman, 1999;
Hollingshead and Redlich, 1958; Rushing and Ortega, 1979; Srole, 1962; Williams, 1990).
However, not all findings have been consistent (e.g., Weissman et al., 1991; Weissman and
Myers, 1978), and, in other cases, there is debate concerning the causal direction of the
linkage between social class and unipolar depression (e.g., Fox, 1990; Rodgers and Mann,
1993). Despite these caveats, the available evidence suggests that social class may often be
implicated in the etiology of depression.
If lowered socio-economic status is a risk factor, it may moderate relations that have been
observed between other risk variables (e.g., maternal history) and frontal brain asymme-
try or between frontal brain asymmetry and depression. Alternatively, from a mediational
perspective, SES could be a distal causal factor, the effects of which are mediated by
other more proximal variables (e.g., maternal history). Unfortunately, prior findings linking
frontal brain asymmetry and depression have failed to adequately examine the potential role
played by SES. First, many investigators have not reported the socio-demographic compo-
sition of their samples (e.g., Allen et al., 1993; Dam et al., 1989; Dawson et al., 1992a).
Second, among studies that have reported socio-demographic information, most have not
examined linkages between SES and both the occurrence of mood disorders and patterns
of frontal brain asymmetry (e.g., Henriques and Davidson, 1990; Morris et al., 1996;
Robinson et al., 1984; Robinson and Price, 1982; Robinson and Szetela, 1981; Starkstein
et al., 1987). Third, some samples have been characterized by restricted range on SES
measures. For example, in some EEG studies the clear majority of the participants were
economically disadvantaged mothers and their infants (e.g., Dawson et al., 1992a,b; Field
et al., 1995; Jones et al., 1997), whereas in other studies college students, a relatively ho-
mogenous group, have served as participants (Davidson et al., 1985; Schaffer et al., 1983).
To our knowledge, only one frontal EEG study has examined the correlation between frontal
brain asymmetry and SES (Henriques and Davidson, 1991). Although this study failed to
find a significant relation, a more systematic investigation of this question is necessary. The
current study used a sample recruited from a metropolitan community, and thus participants
varied widely with respect to SES. We sought to examine the main and interactive effects
of SES and risk status on frontal brain asymmetry.
4. Effects of reference montage
We assessed the relations among risk status, SES, and frontal asymmetry using three
different EEG reference montages. There is evidence that the linkages between EEG asym-
metry measures and measures of emotion or psychopathology are not always consistent
across difference referencing schemes (for reviews, see Davidson, 1998b; Hagemann et al.,
1998; Reid et al., 1998). Illustratively, Reid et al. (1998) assessed frontal brain asymme-
try in depressed and non-depressed adults and found significant group differences only
during the first 2 min of EEG recording using a linked-mastoid reference. There were no
significant between-group differences using average and Cz reference montages. Published
findings examining the relation between frontal brain asymmetry and risk for depression
in infants have typically examined Cz-referenced data (e.g., Dawson et al., 1992a,b; Field
et al., 1995), although others (e.g., Dawson et al., 1999b) have employed a linked-mastoid
reference strategy. In the present study, to attend to the consistency issue, we included three
reference montages (Cz, computer-averaged-ears, and average).
In sum, we addressed whether high and low risk adolescents differ in patterns of resting
frontal brain asymmetry. In addition, we assessed the roles of sex and SES in predicting
frontal brain asymmetry and whether these two factors moderated the effect of risk status on
frontal brain asymmetry. We predicted that adolescent offspring of mothers with a history
of depression would demonstrate relative left frontal hypo-activity compared to adolescent
offspring of non-depressed mothers. We did not have strong a priori hypotheses concerning
the link between frontal brain asymmetry and SES or sex. However, we expected that, if
relations were found, left frontal hypo-activity would be linked to female sex and to lower
SES. To test these hypotheses, we used multiple EEG reference montages.
5. Method
5.1. Participants
Participants were recruited from a larger sample of 240 adolescents and their mothers who
were already participating in a study investigating the development of depression in ado-
lescents. This larger sample was 54.2% female, 82% Caucasian, 14.7% African–American,
and 3.3% other (Hispanic, Asian, Native American). The sample was pre-dominantly
lower-middle class to middle class with a mean SES (Hollingshead, 1975) of 41.84 (S.D. =
13.25).
Participants for the larger study were recruited by letters sent to parents of children in
the fifth grade in the Nashville metropolitan public schools. Parents were invited to partic-
ipate and were asked to complete a brief health history questionnaire indicating whether
they ever experienced any of 24 medical conditions such as diabetes, cancer, heart disease,
and depression, or if they had ever taken any of 34 medications. Of the 1495 parents, who
returned these questionnaires, telephone screening interviews were conducted with the 587
who had endorsed either a history of depression, use of antidepressants, or no history of
psychopathology. Based on these screening calls, 349 mothers who reported a history of
depression or no history of psychiatric problems were interviewed in person with the struc-
tured clinical interview for DSM (SCID, Spitzer et al., 1990). To assess inter-rater reliability
of the SCID, a subset (20%) of audio-taped interviews was evaluated by a second inter-
viewer blind to the ratings of the original interviewer. The kappa coefficient (Cohen, 1960)
indicating chance–corrected agreement was 0.88 for SCID diagnoses of mood disorders..
Families were excluded if mothers indicated a history of solely non-affective psychiatric
disorders, or if a parent or child had serious medical problems. The final high risk sample
included 185 mothers who indicated a history of depressive disorders (i.e., major depres-
sion, dysthymia, depression not otherwise specified, and adjustment disorder with depressed
mood). The low risk group consisted of 55 mothers who were lifetime-free of psychiatric
diagnoses.
Research staff, unaware of the mother’s psychiatric history, administered a battery of
questionnaires to the parents and their children. Only those assessment instruments relevant
to the present study are described here. Families participated in yearly assessments after the
initial interviews. Participants were asked if they were interested in participating in future
studies, and those indicating such an interest were contacted to participate in the current
investigation. Adolescents in the current study were recruited between the first and second
yearly follow-up interviews.
Of the 50 high risk and 20 low risk participants from the larger study who were contacted
to participate in the current study, 32 high risk and 15 low risk participants agreed to
participate in the resting EEG recording. Among those who participated, two high risk
participants and one low risk participant were excluded from analyses because they were
not right-handed, as assessed by the Edinburgh inventory (Oldfield, 1971). Five high risk
participants and one low risk participant were excluded from analyses due to other issues
that compromised the validity of the resting EEG recording for the present purposes (e.g.,
excessive fatigue during the session, medication use). Thus, 25 high risk (11 male) and
13 low risk (7 male) participants were included in the current analyses. Participants were
compensated US$ 30. The relatively greater number of high risk than low risk participants
in the current study reflects the distribution of the larger participant pool from which these
participants were drawn. A primary goal of the larger ongoing study was to investigate the
conditions under which at-risk youths develop depression.
High risk adolescents included 24 Caucasians and one African American. Low risk
adolescents included 12 Caucasians and one Native American. The racial distributions of
participants in the current study and in the larger sample from which participants were
drawn did not statistically differ, χ2 (4, N = 283) = 5.08, p > 0.25.
Participants in the present study ranged in age from 12.2 to 14.0-year-old at the time
of their EEG recording, high risk Mean = 13.1 (S.D. = 0.3); low risk Mean = 13.0
(S.D. = 0.4). The two groups did not significantly differ with respect to age, F(1,37) =
2.20, P > 0.45. Among participants in the current study, the SES of the low risk group
(Mean = 53.2, S.D. = 6.9) was significantly higher than the high risk group (Mean = 37.3,
S.D. = 13.3), F(1,37) = 16.38, P < 0.001. Participants in the current study and those from
the larger cohort who did not participate in this study did not differ with respect to SES,
F(1,216) = 0.01, P > 0.90. In addition, there was no significant interaction between risk
group status and participant status (participated/did not participate) in SES, F(1,216) = 2.61,
P > 0.11.
5.2. Measures
5.2.1. Psychopathology
Adolescent psychopathology (i.e., mood disorders, anxiety disorders, behavior disor-
ders, and substance use disorders) was assessed at the first evaluation with the Schedule for
Affective Disorders and Schizophrenia for School-Age Children Epidemiological Version
(K-SADS-E, Orvaschel et al., 1982) and with the Longitudinal Interval Follow-up Evalu-
ation for Children (K-LIFE, Keller and Neilsen, 1988) at each follow-up assessment. All
interviews were audiotaped. A second interviewer who was unaware of the first interviewer’s
ratings reviewed a randomly selected 25% of the interviews. Kappas were 0.81 for mood
disorders, 0.72 for anxiety disorders, and 0.80 for behavior disorders.
5.2.1.1. Depressive symptoms. Two measures assessed adolescent depressive symptoma-

tology. At the initial interview and at each annual follow-up interview, children’s depres-
sive symptoms were assessed by the Children’s Depression Inventory (CDI), a widely
used self-report measure of depressive symptoms in children (Kovacs, 1981). The CDI
has adequate internal consistency, test–retest reliability, and convergent validity with other
self-report measures of depressive symptoms (Saylor et al., 1984; Smucker et al.,
1986). The internal consistency of the CDI in this sample was 0.81 at the initial
assessment.
Additionally, weekly adolescent depressive symptomatology was ascertained based on
the K-LIFE (Keller and Neilsen, 1988). Symptoms were dated and given a severity score
that ranged from one (no symptoms of depression) to six (severe symptoms of depression).
A score of five or six on this scale denoted that the adolescent met DSM criteria for major
depressive disorder, whereas lower scores denoted that the adolescent had not met criteria
for major depressive disorder.
5.2.2. Socio-economic status

Household SES was assessed with the four factor index of social status (Hollingshead,
1975), the most frequently used measure of SES (Cirino et al., 2002; Edwards-Hewitt
and Gray, 1995). Possible scores on this index range from 8 (lowest SES) to 66 (highest
SES). To calculate the SES score of a household, scale values for occupation (which range
from one to nine) and for education (which range from one to seven) were multiplied by
factor weights of five and three, respectively. These two products were then summed. Then,
adjustments were made for marital status and related factors (e.g., receipt of child-support or
alimony payments from an absent spouse) as outlined in Hollingshead (1975). Adolescents
were assigned the household SES score.
5.3. Procedure
Participants were told that the purpose of the study was to look at brain wave activity
in adolescents. After informed consent was obtained from both the adolescent and parent,
electrodes were applied for the measurement of EEG. Participants were then informed that:
(1) there would be eight 1 min resting baselines; (2) four baselines would be conducted with
eyes-open and four would be conducted with eyes-closed; and (3) during the resting base-
lines, they should try to minimize eye blinks and movements, but should not be so concerned
about doing so that they were distracted. In accord with previous work (e.g., Tomarken et al.,
1990, 1992), participants were not given highly specific instructions concerning the resting
baselines.
Two randomly assigned, counterbalanced orders were used for the eyes-open and eyes-
closed trials of the resting baselines (O–C–C–O–C–O–O–C and C–O–O–C–O–C–C–O).
Participants heard one tone denoting the beginning of each 60 s baseline and two tones
denoting the end of each baseline. There was a 3 min interval between the fourth and fifth
baselines. A 45 s interval occurred between all other baselines. Following the eighth and
final resting baseline, electrodes were removed.
5.4. Electroencephalographic recording and quantification
EEG recording followed standard guidelines (see Pivik et al., 1993). Recordings were
made from tin scalp electrodes sewn into a Lycra stretchable cap from Electro-Cap Inter-
national, Inc. (see Blom and Anneveldt, 1982). The cap was positioned on the head using
the 10–20 international system (American Electroencephalographic Society, 1994; Jasper,
1958). Fifteen standard scalp locations from the 10 to 20 system were used: F3, F4, F7,
F8, T3, T4, T5, T6, P3, P4, C3, CZ, C4, Pz, and Fz. In addition, a forehead ground was
used and tin drop electrodes from the cap were used to record from the left and right ear-
lobes (A1–A2). Nine millimeter tin cup electrodes were placed above and below the eyes
to record blinks and vertical eye movements and on the outer canthi to record horizontal
eye movements. The electrooculogram (EOG) was recorded using a bipolar reference, and
EOG electrode impedances were under 15 k. Electrode impedances for EEG sites were
under 5 k, and impedances for homologous sites were within 1 k of each other. Through
pre- and post-recording checks we documented that impedances changed minimally during
the course of the experiment.
Raw EEG and EOG signals were amplified and filtered using Grass Model 12 A5 AC
pre-amplifiers (bandpass at half-voltage cut-off points 1 and 100 Hz for EEG and 1 and
30 Hz for EOG; 60 Hz notch filter in, filter rolloff = 6 dB per octave). The gain was set
at 30,000 for EEG channels and 5,000 for EOG channels. Data were digitized at 1024 Hz
using an Analogue Devices RTI-815A analogue to digital converter interfaced to the sig-
nal acquisition package Snapstream (HEM Inc.). Eight 1 min resting baselines, four with
eyes-open and four with eyes-closed, were collected. All placements were referenced to
the vertex (Cz) during the initial recording. A set of 50 ␮V sine waves at several different
frequencies (e.g., 10 Hz) were used to calibrate the digitized EEG and to assess the techni-
cal integrity of the recording system. Calibration assessments were run both immediately
before and immediately after each experimental session.
Manual post-session artifact scoring with EEGEDIT software (James Long Company)
was performed to edit the EEG signals. This procedure eliminated epochs that were con-
founded by artifacts such as movement, extensive muscle tension, and saccades. Following
the artifact-reduction procedures, data were re-referenced offline using James Long Com-
pany EEG Analysis System software. In particular, we performed linear transformations of
the digitized EEG to derive a computer-averaged-ears reference and an computer-averaged
reference (see Henriques and Davidson, 1990). Averaged-ears EEG power at a given site
is the difference between activity at that site and the averaged power recorded across the
two ears. Averaged reference EEG power at a given site is the difference between power at
that site and the averaged power across all active sites. At least one of the three referencing
schemes used here (Cz, averaged-ears, or average) has been used in previous EEG studies
on the correlates of frontal asymmetry.
All artifact-free chunks that were 2.00 s in duration were extracted through a Hanning
window, used to prevent spurious estimates of spectral power. Chunks were overlapped
by 50% to counteract the differential weighting of data points attributable to the use of a
Hanning window. The EEG Analysis System software was then used to execute discrete
Fourier transforms of the digitized EEG. This process derived estimates of spectral power
(in ␮V2 ) in different half-hertz frequency bins. These power values were then averaged
across each of the artifact-free chunks of a given resting baseline trial. When a participant
had fewer than eight artifact-free chunks for a given baseline, that baseline was not included
in the computation; that is, it received a weight of zero. Power values were converted to
power density (␮V2 /Hz) in each of seven bands: delta (1.3–3.5 Hz), theta (4.0–7.0), alpha
1 (8.5–10.5 Hz), alpha 2 (11.0–12.5), alpha (8.5–12.5), beta 1 (13.5–19.5 Hz), and beta
2 (20.5–29.5 Hz). Power density was computed by summing power values across all the
half-hertz bins within a band and then dividing by the number of summed bins.
Consistent with the general procedures used in prior research on resting frontal asym-
metry (e.g., Tomarken et al., 1992), a natural log transformation was used to normalize the
distribution of power density values of a given baseline trial. We then computed weighted
means separately for the eyes-open and eyes-closed baselines for each participant. We
weighted by the number of chunks within each baseline. In the next step, we computed the
average of the eyes-open and eyes-closed baselines to generate a composite measure of EEG
power density. Such composite values were computed for each combination of site, band,
and reference montage. Finally, asymmetry scores were computed for each combination of
region, band, and reference montage by subtracting power density in the left-hemisphere
site from power density in the homologous right hemisphere site (i.e., log right minus log
left). The high risk and low risk groups did not differ in the total number of artifact-free
chunks per participant used in computations of the composite power and asymmetry mea-
sures (high risk Mean = 176.08, S.D. = 81.61; low risk Mean = 208.23, S.D. = 93.47, t
(36) = 1.10, P > 0.25).
To test hypotheses, we focused on measures of log power density in the alpha frequency
band. Because decreased alpha power in a given region has been linked to increased cor-
tical activity in that region (Davidson, 1988; Miller and Tomarken, 2001; Pfurtscheller,
1986; Pfurtscheller and Klimesch, 1991) higher values on the asymmetry metric denote
greater relative left frontal activity. The selection of the 8.5–12.5 Hz band as the focus of
hypotheses merits comment given the small number of prior asymmetry studies that have
assessed adolescents. The clear majority of prior studies indicating linkages between frontal
EEG asymmetry and emotion or psychopathology have used either adults or infants. In-
vestigations of the relation between frontal brain asymmetry and depression in adults have
defined alpha as 9–11 Hz (Schaffer et al., 1983), 9–12 Hz (Davidson et al., 1985), or 8–13 Hz
(Henriques and Davidson, 1990, 1991). Whereas the dominant EEG frequency band in very
young children is clearly lower (Marshall et al., 2002), the relative proportion of slow wave
activity in children decreases with age (Benninger et al., 1984; Colon et al., 1979; Matousek
and Petersen, 1973), until about 10 years of age (Benninger et al., 1984; Gasser et al., 1988;
Matousek and Petersen, 1973). Concomitant with the decrease in slow wave power during
childhood are increases in faster frequency activity (e.g., alpha 2 band activity, Gasser et al.,
1988; John et al., 1980; Matousek and Petersen, 1973).
Participants in the current study ranged in age from 12.2 to 14.0-year-old. Prior results
would indicate that the majority of the transition from lower to higher frequency activity
has been completed by this age (Gasser et al., 1988). For this reason, our primary focus
of analyses was the adult alpha-band of 8.5–12.5 Hz. Our decision was consistent with
the approach used by Kentgen et al. (2000), who assessed frontal EEG asymmetry among
adolescents using an alpha-band equivalent of 7.8–12.5 Hz. We also report the results of
exploratory analyses of other bands, with a particular interest in the theta band (4–7 Hz)
containing frequencies immediately below the alpha range.
6. Results
6.1. Depressive symptoms
We examined CDI scores from four of the yearly assessments to examine whether high
and low risk participants differed on symptoms of depression prior to or after the EEG
recording. Across the two yearly assessments preceding and the two yearly assessments
following the EEG session, the mean low risk CDI was 3.9 (S.D. = 3.7) and the mean high
risk CDI was 4.5 (S.D. = 3.4). Thus, both groups clearly scored in the non-depressed range.
Separate t-tests on risk status conducted at each of the four time points revealed the absence
of any differences with respect to CDI scores, all t’s < 0.50, all P’s > 0.25. Consistent
with these results, an omnibus risk status X time ANOVA failed to yield any significant
main effects or interactions, all P’s > 0.17.
During the eight weeks prior to the EEG session, the week of the EEG session, and the
eight weeks following the EEG session, all participants averaged less than 2 (i.e., possible
mild depressive symptoms) on the retrospective measure of weekly depressive symptoms
(potential range = 1–6). All low risk participants received scores of one (no depressive
symptoms) on this scale for every week during this time period. With the exception of four
adolescents, all high risk participants received scores of two or below during this time period
(i.e., mild symptoms of major depressive disorder). The remaining four received scores of
three or four on this measure (indicating some symptoms of major depressive disorder and
impairment, but falling short of the criteria for major depressive disorder). Thus, no low risk
and high risk participants met criteria for major depressive disorder during the two-months
prior to and the two months after the EEG recording. When the analyses reported below
were redone with those four individuals who demonstrated symptoms of major depressive
disorder removed, the results and conclusions were unchanged.
6.2. Lifetime criteria for mood disorders
Based on the K-SADS-E administered at baseline and K-LIFE administered at the first
yearly follow-up interview, no low risk participant met lifetime criteria for any mood dis-
order. One high risk participant met lifetime criteria for dysthymia. When the analyses
reported below were redone with this individual removed, the results and conclusions were
unchanged.
6.3. Electroencephalographic data
6.3.1. Effects of risk status on mid-frontal alpha asymmetry

As noted above, the primary focus of analyses was the alpha (8.5–12.5 Hz) frequency
band. Because the majority of prior studies linking frontal brain asymmetry to depression
have focused on the mid-frontal (F3/F4) recording sites, we focused on measures of alpha
asymmetry in this region. We predicted that high risk participants would demonstrate greater
relative left frontal hypo-activity (greater relative left versus right alpha-band power) than
low risk participants.
Table 1 shows mean log-transformed alpha power density (in ␮V) values for the mid-
frontal sites (F4 and F3) and mean asymmetry scores [ln(F4) − ln(F3)] derived from the
three reference montages for males and females. Recall that more positive asymmetry
scores indicate greater relative left frontal activity. Because of how the asymmetry metric is
computed, a main effect of risk status on asymmetry values is equivalent to an interaction
between risk status and hemisphere on log power density values. Analyses used to test
hypotheses in the current study focused on asymmetry values rather than on log power
density. When analyses were done on log power values from each of the three reference
montages with hemisphere as a factor, no main effects of risk status were observed that
would indicate between-group differences on overall power averaged across the two frontal
sites (all P’s > 0.90). In addition, no between-group differences were yielded by separate
analyses of F3 and F4 log power density (all P’s > 0.60). These results reflect the likelihood
that a high proportion of the between-subject variability in power is due to skull thickness
and other factors that are not of substantive interest. For these reasons, to simplify the
Table 1
Mid-frontal (F3/F4) alpha-band log power density (in ␮V) and asymmetry for and low risk adolescents
High Risk Low risk
F3 power F4 power F3/F4 F3 power F4 power F3/F4

asymmetry asymmetry
Averaged-ears
Male 1.200 (0.579) 1.208 (0.572) 0.009 (0.049) 1.448 (0.353) 1.496 (0.372) 0.047 (0.041)
Female 1.634 (0.540) 1.629 (0.536) −0.004 (0.067) 1.320 (0.572) 1.366 (0.551) 0.046 (0.057)
All 1.442 (0.588) 1.444 (0.581) 0.001 (0.059) 1.380 (0.451) 1.450 (0.448) 0.047 (0.047)
Average
Male 0.388 (0.589) 0.379 (0.563) −0.009 (0.094) 0.760 (0.558) 0.796 (0.579) 0.039 (0.126)
Female 0.825 (0.576) 0.824 (0.574) −0.001 (0.120) 0.509 (0.604) 0.600 (0.612) 0.091 (0.086)
All 0.633 (0.611) 0.629 (0.601) −0.004 (0.107) 0.644 (0.570) 0.706 (0.578) 0.061 (0.114)
Vertex (Cz)
Male 0.932 (0.637) 0.953 (0.598) 0.021 (0.092) 1.200 (0.553) 1.172 (0.543) −0.027 (0.082)
Female 1.059 (0.576) 1.054 (0.580) −0.005 (0.056) 0.739 (0.721) 0.844 (0.709) 0.105 (0.035)
All 1.002 (0.594) 1.010 (0.578) 0.007 (0.073) 0.987 (0.653) 0.621 (0.172) 0.034 (0.093)
Note: High risk male N = 11. High risk female N = 14. Low risk male N = 7. Low risk female N = 6. Standard
deviations are indicated in parentheses.
presentation of results, we report below only the results of analyses performed on asymmetry
values.
Fig. 1 shows the mean log-transformed mid-frontal alpha asymmetry values, derived
from three reference montages, for low risk and high risk adolescents. This figure indicates
that across all three montages, there was greater relative left frontal activity in the low risk
group compared to the high risk group. The results of risk status (low risk/high risk) X
sex (male/female) ANOVAs performed on computer-averaged-ears referenced and average
referenced mid-frontal EEG asymmetry values were consistent with these observations. The
analysis of computer-averaged-ears referenced data revealed a significant main effect of risk
status, F(1,37) = 5.49, P < 0.05, but no significant effects of sex, F(1,37) = 0.23, P > 0.50,
or the risk status X sex interaction, F(1,37) = 0.09, P > 0.50. Similarly, the analysis of
0.10 High Risk

Low Risk
Alpha Asymmetry
0.05
Mid-frontal
0.00
-0.05 Ears Average Vertex (Cz)

Reference Reference Reference
Fig. 1. Mid-frontal (F3/F4) alpha asymmetry [ln(left) − ln(right)] across three reference montages for high risk
(N = 25) and low risk (N = 13) adolescents. Error bars indicate one standard error of the mean.
0.15
High Risk
Asymmetry CZ Reference
0.10 Low Risk

Mid-frontal Alpha
0.05
0.00
-0.05
-0.10 Males Females
Fig. 2. Mid-frontal (F3/F4) vertex (Cz)-referenced alpha asymmetry [ln(left) − ln(right)] for male and female high
and low risk adolescents. Error bars indicate one standard error of the mean.
average referenced mid-frontal asymmetry revealed a significant main effect of risk status,
F(1,37) = 5.37, P < 0.05, but no significant main effect of sex, F(1,37) = 0.50, P > 0.40,
and no significant interaction between risk status and sex, F(1,37) = 1.44, P > 0.20.
Although the marginal means for vertex (Cz) referenced asymmetry values shown in
Fig. 1 indicates greater relative left frontal activity in the low risk group, Fig. 2 indicates
more complex, interactive relations with sex. As this figure indicates, high risk females,
but not high risk males, demonstrated relative left frontal hypo-activity when compared
to their low risk counterparts. The analysis of Cz asymmetry in the mid-frontal region
revealed no main effect of risk status, F(1,37) = 1.21, P > 0.20, no main effect of sex,
F(1,37) = 1.49, P > 0.20, but a significant risk status X sex interaction, F(1,37) = 10.49,
P < 0.01. Subsequent simple effects analyses indicated that, among females, high risk
adolescents demonstrated significantly greater left frontal hypo-activity when compared to
low risk participants, F(1,19) = 19.43, P < 0.01. No significant effects were yielded by the
simple effects analysis performed on males’ asymmetry values, F(1,17) = 1.20, P > 0.25.
6.3.2. Effects of risk status on mid-frontal EEG Asymmetry in other bands

We computed two-way risk status X sex ANOVAs on mid-frontal (F3/F4) EEG asymme-
try in each of the six EEG bands extracted: delta (1.5–3.5 Hz), theta (4.0–7.0 Hz), alpha 1
(i.e., low alpha; 8.5–10.5), alpha 2 (i.e., high alpha; 11.0–12.5), beta 1 (13.5–19.5 Hz), and
beta 2 (20.5–29.5 Hz). We assessed effects in alpha 1 and alpha 2 separately because: (1) in
some previous studies, differential effects have been observed in these bands (e.g., Davidson
et al., 2000); and, (2) the fact that our participants were young adolescents suggested that
such effects might be particularly likely to occur (see the discussion of band selection in
Section 5). Such analyses were computed for each of the three references. Because the
number of ANOVAs was large, we used a step-down Bonferroni procedure to control for
multiple significance tests (e.g., Westfall et al., 1999; Westfall and Young, 1992). Three sets
of corrections were used (i.e., one per reference montage).
After step-down Bonferroni correction, there were highly significant main effects for risk
status in the theta band on both computer-averaged-ears referenced [corrected P < 0.001,
low risk M (S.D.) = 0.071 (0.077); high risk (M) = −0.032 (0.060)] and average referenced
[corrected P < 0.001, low risk M (S.D.) = 0.120 (0.117); high risk (M) =−0.037 (0.090)]
mid-frontal asymmetry. We also found a significant main effect of risk status on average
referenced delta band asymmetry [corrected P < 0.025, low risk (M) S.D. = 0.110 (0.136);
high risk M = −0.017 (0.121)] and on Cz-referenced asymmetry in the low alpha-band
(corrected P < 0.02). These significant effects all indicated that high risk participants
showed greater relative power in the left relative to right frontal region for the target band.
Thus, the direction of these effects parallels that of the alpha-band (8.5–12.5 Hz) effects
reported above. No other significant effects were observed.
6.3.3. Effects of risk status on EEG alpha asymmetry in other regions

For each of the three references, we computed two-way risk status X sex ANOVAs on
EEG asymmetry in each of five regions: lateral frontal (F7/F8), parietal (P3/P4), anterior
temporal (T3/T4), posterior temporal (T5/T6), and central (C3/C4). Because the clear focus
of our predictions was alpha asymmetry in the mid-frontal sites and because the number
of ANOVAs was large, we once again used a step-down Bonferroni procedure to control
for multiple significance tests. Across all three references, the only significant effects that
emerged were main effects of region (all P’s < 0.01). These effects reflected topographic
differences in the patterning of asymmetry. Most importantly, there were no significant main
effects or interactions involving risk status (all P’s > 0.05).
Table 2 conveys the overall direction and strength of the relation between risk status and
alpha-band asymmetry across regions. Presented are point biserial correlations between the
dichotomous variable risk status (coded 0 for low risk and 1 for high risk) and measures of
brain asymmetry [ln(right − ln(left)] in a given band. Consistent with the main effects of risk
status on mid-frontal asymmetry presented above, the correlations between risk status and
ears-referenced (r = −0.37) and average-referenced (r = −0.36) mid-frontal asymme-
try are both significantly greater than 0. Although the correlation involving Cz-referenced
frontal asymmetry is not significant, recall that the ANOVAs revealed a more complex
risk status X sex interaction on this measure. Although the correlations involving lateral
Table 2
Correlations between risk status and alpha-band asymmetry across regions
Region Reference montage
Averaged-ears Average Vertex (Cz)
Mid-frontal (F3–F4) −0.37∗∗ −0.36∗∗ −0.16

Lateral frontal (F7–F8) −0.24 −0.25 −0.09
Central (C3–C4) 0.15 0.16 0.08
Anterior temporal (T3–T4) 0.25 0.06 0.08
Posterior temporal (T5–T6) −0.15 −0.19 −0.14
Parietal (P3–P4) −0.17 −0.19 −0.35∗
Note: N = 38. Point-biserial correlations are shown. Risk status coding: 0 = low risk, 1 = high risk. Mid-frontal
correlations were evaluated at a per-correlation alpha level = 0.05. Within each reference montage, step-down
Bonferroni corrections were applied to correlations involving the five other sites.
∗ Uncorrected P < 0.05, but step-down Bonferroni corrected P > 0.15.
∗∗ P < 0.05.
frontal asymmetry (F7/F8) are in the predicted direction, their magnitude is lower than that
of the mid-frontal correlations and is not statistically significant. Overall, other than the
aforementioned mid-frontal correlations, only one of the correlations shown in Table 3 was
statistically significant when considered in isolation (Cz-referenced P3/P4; P = 0.03).
Moreover, even this value was not statistically significant when step-down Bonferroni
corrections were used to account for the total number of correlations computed among
the five regions that were not of the focus of our initial hypotheses (P = 0.15).
6.3.4. Effects of socio-economic status

6.3.4.1. Zero-order correlations. One subsidiary goal was to assess the relation between
SES and frontal asymmetry. This question is particularly salient in the present context be-
cause the high risk and low risk groups differed on SES. When participants in both risk
status groups were pooled into one sample, we observed a significant overall correlation
between SES and alpha-band mid-frontal asymmetry for two of the three reference mon-
tages, computer-averaged-ears reference r = 0.57, P < 0.001, average reference r = 0.50,
P < 0.001, Cz reference r = 0.16, P > 0.30. These correlations indicate that higher SES
predicted greater relative left frontal activity. Fig. 3 shows scatter plots depicting the relation
between frontal brain asymmetry (derived from three reference montages) and SES, with
risk status symbolically indicated. Although this figure makes evident the small number of
low SES participants in the low risk group, it also clearly illustrates the relation between
relative left frontal activity and SES.
To investigate further the relation between alpha asymmetry in the mid-frontal region
and social class, correlations were computed separately for each risk group. Within the
high risk group, frontal asymmetry measures derived using the computer-averaged-ears
and average references both correlated significantly with SES, computer-averaged-ears
reference r = 0.56, P < 0.004, average reference r = 0.50, P < 0.01, Cz reference
r = 0.14, P > 0.50. Within the low risk group, there were no significant correlations
between SES and frontal brain asymmetry, computer-averaged-ears reference r = 0.04,
average reference r = 0.05, Cz reference r = −0.03, all P’s > 0.80. Clearly, however,
caution is necessary here because: (1) differences between relevant pairs of correlations
(e.g., high risk computer-averaged-ears versus low risk computer-averaged-ears) were not
statistically significant (all P’s > 0.10); (2) there was a restricted range of SES in the
low risk group that could significantly influence the magnitude of the observed correlation
(low risk M = 53.2, S.D. = 6.8; high risk M = 37.3, S.D. = 13.3) and, (3) due to the
differences in variability, comparisons of unstandardized beta weights are likely more appro-
priate than comparisons of correlations (e.g., Tukey, 1954). Such comparisons constituted
the SES X risk status interaction effects tested in the multiple regression analyses reported
below.
6.3.4.2. Multiple regression results. To investigate further the relations among SES, frontal
brain asymmetry, and risk status, we conducted multiple regression analyses in which risk
status, sex, and SES were specified as predictors of mid-frontal asymmetry in the alpha-band.
These analyses were designed to test the unique effects of each of the three predictors on
frontal asymmetry and to test for moderator effects. For example, a significant risk status X
SES two-way interaction would suggest that the magnitude of the relation between SES and
Fig. 3. Scatter plots of the relation between SES and mid-frontal (F3/F4) alpha asymmetry for each of three
reference montages. Top panel: averaged-ears reference; middle panel: average reference; bottom panel: vertex
(Cz) reference; H: high risk adolescents; L: low risk adolescents.
Table 3
Multiple regression analyses predicting mid-frontal alpha asymmetry
Predictors Mid-frontal asymmetry measure
Ears reference Average reference Vertex (Cz)
First-order
Risk status
β −0.067 −0.128 −0.122
Sr2 0.003 0.011 0.010
Sex
β 0.094 −0.096 −0.175
Sr2 0.009 0.009 0.030
SES
β 0.529∗∗ 0.432∗ 0.096
Sr2 0.191 0.128 0.006
R2 Increment (set) 0.336∗∗ 0.270∗ 0.064
Two-way interactions
Risk status × sex
β 0.005 0.136 0.631∗∗
Sr2 0.000 0.011 0.226
Risk status × SES
β 0.211 −0.069 −0.249
Sr2 0.011 0.001 0.016
Sex × SES
β −0.170 −0.243 0.120
Sr2 0.016 0.032 0.008
R2 Increment (set) 0.054 0.102 0.277∗
Three-way interaction
Risk status × sex × SES
β −0.344 0.004 0.091
Sr2 0.028 0.000 0.002
R2 Increment (set) 0.028 0.000 0.002
A hierarchical structure was used in which first-order terms were entered in an initial step, followed by
two-interaction terms, and the three-way interaction in subsequent steps. For first-order terms, the β’s are stan-
dardized coefficients. For second-order terms, the β’s are the unstandardized coefficients for terms that are the
product of standardized variables but are not standardized themselves. This procedure was followed in order to
yield test statistics and probability values that are invariant with respect to the unstandardized analyses of the
raw data values. Sr2 : squared semi-partial correlation. R2 Increment (set): the increment in proportion of variance
accounted for by the set of predictors entered in a given step.
∗ P < 0.025.
∗∗ P < 0.005.
frontal asymmetry is conditional on risk status and, conversely, that the relation between
risk status and frontal asymmetry is conditional on level of SES.
A hierarchical structure (Cohen and Cohen, 1983) was used for the three analyses (one
per reference). In the first step, the three predictors were entered simultaneously (risk status,
sex, and SES). This step was used to test for the main effects of each predictor on frontal
asymmetry removing shared variance with the other predictors. In the second step, the three
two-way interaction terms (risk status X SES, risk status X sex, sex X SES) were entered as
a set. In the third step, we entered the risk status X sex X SES three-way interaction term.
At each step, we tested the statistical significance of each of the individual regression coef-
ficients in the set just entered and the significance of the incremental variance attributable
to the set. To facilitate the interpretation of coefficients, we centered SES (i.e., expressed
it as deviations from its mean, thus resulting in a transformed mean of 0, e.g., Aiken and
West, 1991). We used dummy codes for the categorical variables of risk status (0 = low
risk, 1 = high risk) and sex (0 = females, 1 = males). It is important to note that identical
results and conclusions were yielded when alternative model-testing strategies were used
(e.g., for descriptions of alternative approaches, see, e.g., Aiken and West, 1991).
Table 3 shows the results of the regressions on alpha-band asymmetry for each of the three
references. To provide an interpretable metric, this table displays standardized regression
coefficients β’s for each first-order (i.e., main effect) term (risk status, sex, SES). The
test statistics and P values for such first-order coefficients are identical to those for the
unstandardized coefficients that were yielded by an analysis of the raw data values in their
original metric. In the case of two- and three-way interactions, the coefficients shown in
Table 3 are actually the unstandardized coefficients yielded by an analysis of interaction
terms that were the product of standardized first-order terms. Such interaction terms were
not, however, themselves standardized. By this means, we were able to present interaction
coefficients that had both a reasonably interpretable metric and test statistics and significance
levels identical to those yielded by analyses of the raw data values in their original metric
(Aiken and West, 1991; Friedrich, 1982). Also shown in Table 3 are squared semi-partial
correlations denoting the proportion of the total variance in asymmetry scores uniquely
attributable to each predictor (see, e.g., Cohen and Cohen, 1983) and R2 values indicating
the increment in variance accounted for by each set of predictors.
As indicated by Table 3, the results of the regressions of mid-frontal asymmetry on the
first-order terms (risk status, SES, and sex) were consistent across the ears referenced and
average referenced montages. In each case, SES, but not risk status or sex, contributed
significant unique variance to the prediction of alpha-band asymmetry (ears referenced
P < 0.005, average referenced P < 0.025). The squared semi-partial correlation coef-
ficients shown in Table 3 indicate that SES accounted for a notably higher proportion of
the variance in ears referenced and average referenced frontal asymmetry scores than the
other two predictors (see Table 3). We should emphasize that the effects shown for each
of the three predictors in Table 3 are adjusted for the effects of the other two predictors
in the equation (i.e., the three predictors were entered simultaneously as a set). When
Cz-referenced mid-frontal asymmetry was the outcome variable, no effects for first-order
terms were significant.
In subsequent steps testing for moderation, we entered the two-way and three-way inter-
action terms in the regression equations. As shown in Table 2, the only significant effect
across all three dependent measures was the risk status X sex interaction on Cz-referenced
mid-frontal asymmetry (P < 0.005). This effect was also yielded by the risk status X sex
ANOVA reported above and reflects greater differences between the high and low risk groups
among females relative to males. There were no significant two- or three-way interactions
involving SES (all P’s > 0.20).
6.3.4.3. Components of SES. We also examined the relations between the components of
SES and alpha-band asymmetry. Our measure of SES (Hollingshead, 1975) is derived pri-
marily from parental occupation, education, and marital status. We first calculated zero-order
correlations between risk status and these three components of SES. To orient readers to the
scaling and direction of relations, occupation ranged from 0 (unemployed) to 9 (higher pro-
fessional), education ranged from 1 (less that 6 years of schooling) to 7 (more than 18 years
of schooling), and marital status was coded as either 0 (unmarried) or (1) married. The high
and low risk groups differed on these components of SES in a manner that paralleled the
differences on the composite SES index reported above (occupation P < 0.001; education
P < 0.005; marital Status P < 0.02). Parents of low risk participants were more likely to
have attained higher occupation and educational levels and were more likely to be married.
When participants in both risk status groups were pooled into one sample, we observed a
significant overall correlation between occupation and alpha-band mid-frontal asymmetry
for two of the three reference montages, ears reference r = 0.50, P < 0.002, average
reference r = 0.45, P < 0.01, Cz reference r = 0.06, P > 0.50. We also observed a
significant overall correlation between education and alpha-band mid-frontal asymmetry for
two of the three reference montages, ears reference r = 0.33, P < 0.05, average reference
r = 0.38, P < 0.05, Cz reference r = 0.19, P > 0.20. Finally, we observed a significant
overall correlation between marital status and alpha-band mid-frontal asymmetry for one
of the three reference montages, ears reference r = 0.42, P < 0.0.01, average reference
r = 0.20, P > 0.20, Cz reference r = 0.12, P > 0.40. Thus, higher occupation, more years
of education, and being married generally predicted greater relative left frontal activity.
7. Discussion
7.1. Primary hypotheses
The primary goal of the present study was to assess whether children of mothers with
a history of depression demonstrated relative left frontal hypo-activity when compared
to low risk children. Across the three reference montages assessed, analyses supported
predictions. The risk status X sex ANOVAs performed on ears referenced and average
referenced mid-frontal asymmetry values indicated that high risk participants demonstrated
relative left frontal hypo-activity when compared to low risk participants.1 The pattern
of effects on the Cz-referenced mid-frontal asymmetry measures was more complex. The
two risk status groups differed in frontal asymmetry among females but not among males.
These latter findings are intriguing and may link up meaningfully with the evidence for sex
differences in depression that emerge during early adolescence (e.g., Heller, 1993; Hankin
et al., 1998; Nolen-Hoeksema and Girgus, 1994).
1 As indicated by Fig. 1, the low risk group on average demonstrated relative left frontal hyper-activity (i.e.,
greater alpha suppression in the left relative to right hemisphere) whereas the high risk group demonstrated a more
symmetrical pattern. In this regard, it is relevant to note that unselected adult participants typically demonstrate
relative left frontal activity on these measures (Reid et al., 1998; Tomarken et al., 1992). Thus, although the high
risk group did not demonstrate left frontal hypo-activity in an absolute sense, their pattern does appear to deviate
from the norm.
From a broad perspective, each of the three references provided support for the notion
that resting frontal asymmetry may indicate heightened vulnerability to depression. This
is an important observation because, as noted above, questions have been raised about the
degree to which mid-frontal EEG asymmetry findings are consistent across references (e.g.,
Hagemann et al., 1998; Reid et al., 1998). The degree of convergence that we found suggests
that we may have tapped into a robust phenomenon.
The present results were also generalizable across several different EEG bands. For
example, we found particularly notable effects of risk status on theta band measures of
ears referenced and averaged referenced asymmetry and additional effects on delta band
measures of average referenced asymmetry. This convergence across the lower-frequency
EEG components may be related to the fact that participants were young adolescents. Our
lower-band asymmetry effects merit replication and extension. Our alpha asymmetry effects
were, however, not generalizable across EEG sites. The only significant effects that emerged
were for the mid-frontal region.
7.2. Implications of risk status findings
Our results significantly extend previous findings indicating that relative left frontal
hypo-activity may indicate vulnerability to depression. Prior studies using adult participants
have compared non-depressed samples to either currently depressed (e.g., Schaffer et al.,
1983) or remitted samples (Henriques and Davidson, 1990). As noted above, both compar-
isons do not allow unambiguous inference concerning whether resting frontal asymmetry
indicates vulnerability. More compelling evidence has been provided by studies comparing
infants of depressed and non-depressed mothers (e.g., Dawson et al., 1997; Jones et al.,
1997). Our findings link up with these latter results and suggest that there may be continu-
ity of risk that extends beyond infancy. If frontal brain asymmetry is an indicator of risk
that demonstrates such continuity, it should be stable over time. Prior evidence suggests
that resting asymmetry is moderately stable in both adults (Tomarken et al., 1992) and in
infants and young children (e.g., Jones et al., 1997). Our findings mandate an examination
of the stability of resting frontal asymmetry among adolescents.
Of course, if frontal brain asymmetry indicates differential risk for depression, it should
predict the long-term onset and/or maintenance of depressive symptoms. In this regard,
the 12–14 year age range that we have studied is ideal because this is the point in de-
velopment immediately prior to the increased onset of depressive symptoms that occurs
in mid-adolescence (e.g., Hankin et al., 1998; Nolen-Hoeksema and Girgus, 1994). There
is a need for longitudinal studies that address whether those adolescents characterized by
relative left frontal hypo-activity are most likely to demonstrate an increase in depressive
symptoms and a higher proportion of diagnosable episodes over time. We believe that such
effects are most likely to be observed in interaction with other factors (e.g., stressful events).
7.3. Effects of socio-economic status
We assessed the effects of SES because it has been largely neglected in prior studies of
anterior brain asymmetry and because there is strong evidence for inverse relations between
SES and rates of unipolar depression (e.g., Leventhal and Brooks-Gunn, 2000; Murphy
et al., 1991). Consistent with the latter results, in the present study high and low risk groups
differed notably in mean household SES on the Hollingshead index. Our correlational results
indicated reasonably strong relations between SES and mid-frontal alpha asymmetry for
two of the three reference montages assessed. That is, higher SES predicted relative left
frontal activity. We also found a significant relation between SES and mid-frontal asymmetry
among high risk participants alone.
It is unclear precisely, why SES is correlated with mid-frontal asymmetry. The major
theories concerning the linkage between SES and psychopathology are one basis for spec-
ulation (Johnson et al., 1999). According to social causation theory, the chronic stress and
other adversities linked to low SES contribute to the onset of psychopathology. According to
social selection theory, biological, and environmental factors contribute to the onset of psy-
chopathology, which, in turn, induces downward social drift toward lower socio-economic
classes. Although current research favors the social causation hypothesis in application to
unipolar depression, there are findings that support both views (for a review, see Johnson
et al., 1999).
Extensions of both these hypotheses might provide a basis for speculation about the na-
ture of the relation between SES and frontal asymmetry. For example, a variant of the social
causation hypothesis would be the proposal that the chronic stress and other adversities as-
sociated with low SES produce long-term changes in brain asymmetry. Although no human
studies have addressed this issue, there is infrahuman evidence that stress can induce changes
in lateralization of neurotransmitter functions that appears correlated with anxiety-related
behaviors (e.g., Fride and Weinstock, 1988). In addition, there are a variety of factors other
than chronic stress per se that are correlated with SES and could conceivably produce effects
on brain asymmetry. Such factors include maternal warmth, peer group instability, social
support, and cognitive stimulation (for a review, see, e.g., Dodge et al., 1994).
7.4. Joint effects of maternal history of depression and socio-economic status
Our multiple regression analyses addressed the unique and interactive effects of maternal
history (denoted risk status), sex, and SES on measures of mid-frontal brain asymmetry
derived from the alpha-band. Somewhat surprisingly, SES but not risk status significantly
predicted asymmetry measures derived from the averaged-ears and average references. No
other main effects or interactions were significant. In contrast, we observed a significant
risk status X sex interaction on Cz-referenced frontal asymmetry values.
From a causal modeling perspective (e.g., Baron and Kenny, 1986; Bollen, 1989), the
overall pattern of correlational and multiple regression results that we observed on ears
referenced and averaged referenced frontal asymmetry might be taken to indicate that SES
has a direct causal effect on frontal brain asymmetry but that maternal history of depression
has only a weak direct effect at best. One possible model consistent with the data would
specify that SES largely mediates the effects of maternal history of depression on brain
asymmetry among children. This model would stipulate that: (1) maternal episodes of
depression or related vulnerability factors induce a downward drift in SES; and, (2) lowered
SES, in turn, is a proximal cause of changes in brain asymmetry among the children of
such mothers. This model has features of both the social causation and social selection
perspectives on the relation between SES and psychopathology.
Although such an interpretation might initially appear plausible, there are a host of reasons
why it is premature. First, this conclusion is based on data that if, not cross-sectional in a
strict sense, embody many of the features and limitations of cross-sectional data. Clearly,
a more systematic evaluation of the causal relations among these variables would require a
longitudinal design involving repeated assessments over time and across generations (see,
e.g., Johnson et al., 1999). Estimates of causal parameters can be seriously misleading when
cross-sectional designs are used to model effects that, by their very nature, occur over time
(e.g., Cole and Maxwell, 2003).
A second issue that complicates interpretation of our regression analyses is the problem
of omitted variables (e.g., Berk, 2004; Tomarken and Waller, 2003). Undoubtedly, there are
a number of relevant variables that are correlated with risk status, SES, and/or frontal brain
asymmetry and may be implicated in a complex, multi-factorial causal nexus. For example,
we did not assess chronic stress or frontal brain asymmetry in the parents of adolescents.
Both factors could well have causal linkages to the variables assessed in the present study
(e.g., Field et al., 1995; Kessler, 1997). It is well known that the omission of important
predictors from regression analyses can strongly bias estimates of coefficients and result in
highly misleading causal inferences (e.g., Gollob, 1991; Reichardt and Gollob, 1986).
There are additional factors limit that limit conclusions. Via effects on univariate and
joint distributions, the general absence of low SES participants from the low risk group
and the overall approach used to sample participants might have significantly affected the
results of the multiple regression analyses (e.g., McClelland and Judd, 1993; Sher and Trull,
1996). For example, these factors might have significantly lowered the power of tests for
moderation. In addition, risk status was treated as a dichotomous variable. A continuous
measure of maternal history might have yielded more robust effects. Finally, some prior
findings in this area may be inconsistent with a model stipulating that maternal depression
has only indirect effects on brain asymmetry that are mediated by SES. For example, this
model cannot easily accommodate evidence that infants of depressed and non-depressed
mothers can differ on frontal EEG asymmetry even when the two groups fail to differ on
measures of SES (e.g., Field et al., 1995).
In sum, although the results of our regression analyses are intriguing, they should be
viewed with caution and certainly require replication and extension in the context of a
longitudinal design that includes additional variables. We should also note that the ultimate
goal of such a research program is not simply to clarify the effects of maternal history of
depression and SES on frontal brain asymmetry. Rather, it is to examine the joint effects of
all three variables on the onset and maintenance of depression.
8. Summary and conclusions
In accord with predictions, we found that adolescent offspring of mothers with a history of
depression demonstrated relative left frontal hypo-activity relative to low risk adolescents.
At least some support for this hypothesis was found across all three reference montages
assessed. Such effects were specific to the mid-frontal region. We also found that lower
SES predicted greater relative left frontal hypo-activity. This linkage remained significant
even when we controlled for maternal history of depression. Further longitudinal studies
that include a broader array of variables are necessary to clarify the precise causal linkages
among these variables.
Acknowledgements
This project was funded in part by NIMH grant MH49759 awarded to Andrew J. Tomarken,
Ph.D., by a FIRST Award (R29-MH4545801A1) from the National Institute of Mental
Health, a Faculty Scholar Award (88-1214-88), and grant (96173096) from the William
T. Grant Foundation awarded to Judy Garber. Gabriel Dichter was supported in part from
an NIMH training grant (T32-MH18921). We appreciate the cooperation of the Nashville
Metropolitan School District, Drs. Binkley and Crouch, and we thank the parents and chil-
dren who participated in the project.
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Patterns of brain electrical activity in infants of

depressed mothers who breastfeed and bottle feed:
the mediating role of infant temperament
Nancy Aaron Jones∗ , Barbara A. McFall, Miguel A. Diego
Florida Atlantic University at Jupiter, 5353 Parkside Drive, Jupiter, FL 33458, USA
Abstract
Successful breastfeeding involves a dyadic interaction between a mother and her infant. The present
study was designed to examine the association between breastfeeding and temperament in infants of
depressed mothers. Seventy-eight mothers, 31 who were depressed, and their infants participated.
Depressed mothers who had stable breastfeeding patterns were less likely to have infants with highly
reactive temperaments. Multivariate analyses of variances (MANOVAs) showed that infants of de-
pressed mothers who breastfed did not show the frontal asymmetry patterns, i.e., left frontal hypoac-
tivity, previously reported. Moreover, breastfeeding stability, even in depressed mothers, was related
to more positive dyadic interactions. Finally, a model was supported, in which the effects of maternal
depression on infant feeding are mediated by infant frontal EEG asymmetry and infant tempera-
ment. These findings could provide a foundation for developing intervention techniques, employing
breastfeeding promotion and support, directed toward attenuating the affective and physiological
dysregulation already noted in infants of depressed mothers.
Keywords: Frontal EEG asymmetry; Emotion; Breastfeeding; Temperament; Infancy
1. Introduction
In 1997, the American Academy of Pediatrics recommended that women breastfeed their
infants for the first year of life (Gartner, 1998) increasing interest and rates of breastfeeding.
However, a substantial portion of women, especially depressed women, do not choose to

E-mail address: njones@fau.edu (N.A. Jones).
doi:10.1016/j.biopsycho.2004.03.010
104 N.A. Jones et al. / Biological Psychology 67 (2004) 103–124
breastfeed or do so for relatively short periods of time (Field et al., 2002a; Galler et al.,
1999). Investigators are now compelled to examine the factors that are associated with the
benefits of sustained breastfeeding and to examine whether breastfeeding can benefit the
physiological and affective development of infants. Moreover, it is important to investigate
whether breastfeeding has positive or negative effects on the affective development of in-
fants of depressed mothers. Previous research has consistently demonstrated that infants of
depressed mothers are at increased risk for physiological and affective dysregulation (Field,
1995; Jones et al., 1998) necessitating further inquiry into the benefits of breastfeeding for
these infants. In this study, we attempted to examine whether the dysregulated affective
and physiological development, noted in infants of depressed mothers, was also evident in
infants of depressed mothers with sustained breastfeeding patterns.
Little is know about patterns of breastfeeding in depressed mothers, and it is likely that
what may be true of other adults who breastfeed does not hold for breastfeeding depressed
mothers. Depressed mothers have been less likely than other adults to choose to breast-
feed (Galler et al., 1999; Milligan et al., 1990), making it unclear whether breastfeeding
can benefit depressed mothers and their infants. Until recently, inquiry into the benefits
of breastfeeding to infants of depressed mothers was largely precluded by a scarcity of
research participants since breastfeeding has been more prevalent among psychologically
non-symptomatic, college-educated, middle-class women whose infants are at low risk for
adverse outcomes. However, due to the resurgence of cultural acceptance of breastfeed-
ing and the enhanced understanding of the physiological importance (Newman, 1995),
depressed mothers are now choosing to breastfeed.
Besides the wealth of research that has touted the physiological benefits of breastfeeding
on infant health, a number of studies have also assessed the emotional benefits of breastfed
compared to bottle fed mother–infant pairs. In parallel with earlier findings highlighting
greater reciprocity and affection during breastfeeding (Bernal and Richards, 1970; Dunn
and Richards, 1977), recent research has also demonstrated (Lavelli and Poli, 1998) that
breastfeeding mothers provide their neonates with less auditory stimulation, but more visual
gaze and tactile stimulation. In addition, investigations probing whether the experiences
entailed by breastfeeding extend beyond the feeding context have been addressed only
rarely. One study compared dyadic interactions of breastfeeding versus bottle-feeding adult
mothers in play situation (Kuzela et al., 1990) and reported that breastfeeding mothers
touched their infants more frequently, suggesting the benefits of breastfeeding extend to
other contexts.
Previous research has typically focused on the characteristics of the mother and her likeli-
hood for continued breastfeeding (Mezzacappa and Katkin, 2002; Mezzacappa et al., 2002;
Pugh, 1998) while relative few studies have examined the effects of infant characteristics
on breastfeeding. Of those studies that have measured infant behavior, researchers have
reported that breastfed newborns are more irritable but show more optimal physiological
organization (Dipietro et al., 1987; Zeskind et al., 1992). However, later in infancy, breast-
fed infants are reported to be more active, temperamentally “easier”, less irritable, more
positive, and more sociable (Field et al., 2002a; VanDiver, 1997; Worobey, 1992, 1998).
These data suggest that breastfeeding may be beneficial to the infant, yet the newborn may
not manifest overt behavioral signs that promote continued breastfeeding. This issue is
even more important for depressed mothers because these mothers are less likely to feel
N.A. Jones et al. / Biological Psychology 67 (2004) 103–124 105
competent in caring for their infants (Field et al., 2002a). Therefore, if their newborn re-
sponds with elevated distress to breastfeeding, depressed mothers are more likely to dis-
continue breastfeeding.
Examination of the factors that promote breastfeeding and those that act as barriers to
sustained breastfeeding should also focus on the role of infant temperament. We adhere to
a definition of temperament that involves behavioral reactivity and regulation as a function
of tonic biological and/or physiological patterns. Moreover, we contend that we are able
to understand variations in temperament by analyzing the manner in which emotions are
expressed and regulated during infancy (Calkins et al., 1996; Fox, 1994; Fox et al., 1994;
Goldsmith et al., 1987). Our own studies, and those of others (Dawson et al., 1997), have
suggested that newborns and infants of depressed mothers demonstrate greater dysregulated
affective and physiological patterns (Jones et al., 1997a, 1998; Lundy et al., 1999). Findings
from these studies have consistently found that infants of depressed mothers show greater
right frontal EEG asymmetry, lower vagal tone, more dysregulated biochemical patterns,
more disorganized behavioral, and sleep patterns. Collectively, these data suggest that infant
bio-behavioral regulation patterns, associated with maternal depression, may lead to a neg-
ative temperamental bias that is likely to influence later development and may predispose
the child for later affective disorders (Field, 1995).
Early in infancy, parental behaviors are primarily focused on care taking. Opportuni-
ties for breastfeeding benefits are likely warranted to ameliorate the negative behavioral
and physiological patterns already identified in infants of depressed mothers. However, we
know of no other studies that have examined infants of depressed mothers and the potentially
positive outcomes that may be garnered by exposing them to stable breastfeeding patterns
during infancy. Within the present study, we examined whether stable breastfeeding patterns
in depressed mothers were associated with attenuated negative developmental patterns in
their infants. We also examined additional factors that may be related to the positive out-
comes, whether affective bonding was increased as a result of stable breastfeeding, whether
infants were physiologically benefited by breastfeeding, and whether mothers’ perceptions
of their infants’ temperament and their behaviors were associated with feeding stability and
depression status.
The purpose of the present study was to examine breastfeeding in infants of depressed
mothers. Specifically, we examined individual differences in infant temperament (positive
and negative) that may be related to stable breastfeeding patterns in depressed mothers,
including infant’s physiological and behavioral reactivity, and the dyads’ socio-emotional
interaction patterns. Our goal was to determine whether each factor was associated with
breastfeeding stability and whether stable breastfeeding in depressed dyads was associ-
ated with attenuated negative outcomes. We hypothesized that maternal depression and
more negatively reactive infant temperament would be associated with a shorter duration
of breastfeeding. Second, we expected that depressed mothers who discontinued breast-
feeding by 3 months of age (or never breastfed) would have infants who show the greatest
dysregulation, in affective regulation and physiological activity. Third, we expected that
depressed mothers who continued breastfeeding would report more positive perceptions
of their infants’ temperament and would demonstrate greater mutual interactive behaviors
with their infants. Finally, we tested a model that examined the direct and indirect effects
of maternal depression on infant temperament, infant EEG activity, and feeding behaviors.
Infant
Infant EEG Temperament
(positive
asymmetry
responsive-ness
during interaction)
Maternal
Depression
Score Duration
Breastfeeding
Fig. 1. Hypothesized model.
We hypothesized that the effects of maternal depression on feeding patterns are mediated
by infant frontal EEG activity and infant temperament (Fig. 1).
2. Method
2.1. Prescreening
Initially, hospital intake information (documenting demographic, feeding, and infant

health information) was used to obtain a sample of new mothers who fit the predefined
criteria. For the present study, we concentrated our efforts on obtaining middle class (mean
of 2–3 on Hollingshead scale (Hollingshead, 1975), adult (age: 20–39 years) women with
healthy (>9 on 5 min APGAR), full-term (>37 weeks gestation) infants. We choose to re-
cruit a middle-class, healthy infant sample to rule out other possible confounds (Buxton
et al., 1991; Cooper et al., 1993). In order to expedite recruitment of depressed participants,
only mothers who received high scores (>16) or low scores (<12) on the Center for Epi-
demiological Studies Depression Scale (CES-D; Radloff, 1977) were asked to participate in
laboratory assessments. Mothers who were eligible at the newborn period were interviewed
over the phone at 1 month on the CES-D to confirm their depression status and to schedule
a laboratory session. The mothers and infants who participated in this study were drawn
from 232 hospital and telephone questionnaires conducted.
2.2. Participants
Seventy-eight mothers and their infants participated in the laboratory assessments at 1

month and 62 (77.5%) returned for the 3-month visit. Families were predominantly White
(four African Americans, two Hispanic and one Asian American), middle to upper-middle
class (Hollingshead mean = 2.32, S.D. = 0.80, range = 1–3). Mothers were adult (mean
age = 32.20 years, S.D. = 5.04 years) and married (93.5%), with one to three children.
Approximately half of the mothers were employed outside the home (44.2%). Infants (39
females and 39 males) were assessed at 1 month (mean = 35.99 days, S.D. = 5.70 days)
Table 1
Mother and infant demographics
Measure Depressed Non-depressed
Breastfeedinga Bottle feedingb Breastfeedingc Bottle feedingd
Infant variables
Female (%) 26.7 68.8 51.7 55.6
Age (days)
One month 36.80 (5.87) 32.62 (4.63) 36.69 (6.23) 36.83 (4.82)
Three months 93.78 (8.32) 94.00 (2.24) 91.87(10.64) 95.30(11.05)
Maternal variables
Age (years) 33.60 (5.99) 31.06 (5.43) 32.37 (4.97) 31.78 (7.78)
SES (Hollingshead) 2.67 (0.79) 2.43 (0.81) 2.14 (0.84) 2.55 (0.70)
Marital status (percentage 93.3 93.8 96.4 94.4
of married)
Parity (percentage of 66.7 75.0 66.3 66.6
multiparous)
CES-D
One month 19.00 (2.53) 19.27 (6.11) 5.07 (3.28) 6.50 (3.45)∗∗∗
Three months 7.50 (4.32) 16.90 (6.48) 4.54 (3.44) 3.73 (3.39)∗∗∗
Note. Values represent mean scores. Standard deviations are in the parentheses.
a n = 15.
b n = 16.
c n = 29.
d n = 18.
∗∗∗ P < 0.001.
and at 3 months (28 females and 34 males, mean = 92.66 days, S.D. = 9.19 days) of age.
There were no differences between the depression and feeding groups on their demographic
characteristics (Table 1).
2.3. Measures
The CES-D is a 20-item questionnaire used to assess depressive symptoms in a community

sample. Scores range from 0 to 60 and a score of greater than 16 has been shown to differ-
entiate clinical depression from non-depressed status. The CES-D has a 6.1% false-positive
rate and a 36% false-negative rate (Myers and Weissman, 1980), however, we obtained ad-
ditional information on maternal depression status from the Diagnostic Interview Schedule
(DIS; Robins et al., 1981). The DIS was used to screen out participants who were mildly
depressed. Extensive testing has shown that the DIS has good psychometric properties
(Costello et al., 1984, 1985) and it can be used by lay persons to assess depressive symp-
toms. Participants who received high scores on the CES-D and who had elevated symptoms
(consistent with dysthymia or major depressive disorder) on the DIS were assigned to the
depressed group. Approximately 20 mothers (22% of those contacted) had elevated CES-D
scores but were not assigned a diagnosis on the DIS. These mothers were not included in
the data analyses for the present study. Non-depressed mothers were chosen based on their
low CES-D scores (<12) and a negative personal and family history of depression.
Feeding status was also assessed at the newborn, 1- and 3-month assessments. Mothers
were queried about their plans to use a specific feeding technique (and for how long), their
current manner of feeding their infant, and their rational for using that feeding technique.
2.4. Laboratory procedures at 1 and 3 months
Upon arrival at the lab, mothers signed a consent form, and completed a demographic and
feeding inventory, a CES-D, the DIS (if appropriate), and an infant temperament inventory
(Infant Behavior Questionnaire (IBQ); Rothbart, 1981). During this time, a research assistant
administered the Brazelton Neonatal Behavioral Assessment Scale (BNBAS; Brazelton and
Nugent, 1995) to examine the infant’s behavioral abilities during environmental interaction.
The Brazelton examiners were trained to 0.90 reliability. Seven infants did not complete the
entire Brazelton assessment. Following this assessment, mothers were asked to play with
her infant as she would at home. This face-to-face interaction lasted for 3 min and both
mothers and infants were videotaped during this procedure.
Baseline EEG activity was recorded from infant participants during a quiet, alert state.
The EEG activity was recorded while the infant was held by his/her mother or sitting in an
infant seat. EEG recordings were for 5–6 min in duration. Five infants (three at 1 month and
two at 3 months) would not tolerate the cap placement. In addition, five infants at 1 month
and four infants at 3 months had unusable data. Thus, a final sample of 70 infants had 1
month EEG data and 53 infants had EEG data at both 1 and 3 months.
Identical assessments were obtained at the 3-month visit, except the Infant Neurological
International Battery (Infinib; Ellison et al., 1985) was used as the developmental assessment
and an arm restraint procedure was performed at 3 months. The Infinib is designed to assess
the neurological integrity of infants based on 20 items with 5 factors (spasticity, vestibular
function, head and trunk ability, French angles, and leg function). This test is easy to
administer and has sufficient reliability for clinical and research purposes (Ellison et al.,
1985). For this study, the total score was computed and then standardized. This score used
to verify normal neurological function across groups. All groups were similar in their scores
(P > 0.05) and all infants were in above the above the abnormal cut-off score of 48.
The arm restraint task is modeled after the one described by Stifter and Braungart (1995)
and Stifter and Jain (1996). Stifter and her colleagues have used this task to examine tem-
peramental reactivity and the infant’s ability to regulate during a mildly frustrating task.
Infants are seated in an infant seat. Mothers sit in a chair facing her infant. Mothers are
instructed restrain their infant’s arms by the sides of their body for approximately 2 min.
The arm restraint is discontinued if the infant was distressed for 20 s. Mothers are also
instructed to maintain a neutral facial expression (or to look away from their infant if they
cannot remain neutral) and to remain silent during the procedure. Afterward the mother is
instructed to hold or sooth her infant. Three mothers and their infants did not complete this
task during the lab session.
2.5. Coding of mother and infant behaviors
Video recordings of 3 min, mother–infant interactions were coded on a second-by-second

basis. We modeled our coding schemes for the play interaction after ones described by
Kuzela et al. (1990). During the play interaction, both mothers and infants, were coded
separately for affect, attention, and vocalization. The scales were scored on a seven-point
graduated scale, with lower scores indicating more non-optimal affect, attention, and vo-
calizations and higher scores indicating more optimal affect, attention, and vocalizations.
Percentage of time within each scaled score was weighted and summed to obtain an index
of the infants and the mothers interactive behaviors, with higher scores indicating more
positive facial affect, more directed attention, and more positive vocalizations.
An index of mother–infant mutuality was also coded on a seven-point graded scale and
coded on a second-to-second basis. The purpose of this coding was to obtain measures
of mutually responsive play behaviors, employing similar coding systems described by
Field et al. (1990). A low score on this scale indicated fewer and more negative mutually
responsive behaviors and a high score indicated more optimal/positive interactive behaviors.
The total percentage of time spent in mutual gaze and affective state (combining facial and
vocal expressions) was obtained by observing the mother and infant interactive behaviors
simultaneously. Descriptions of the behaviors used to index the behaviors during the play
and mutuality coding can be found in Table 2.
Finally, infant behavioral responses during the arm restraint were coded to assess in-
fant reactivity using similar scales as those described by Stifter and Braungart (1995) and
Stifter and Jain (1996). This task was also scored on second-by-second basis using scales to
measure facial affect, attention and vocalization. Three, five-point scales, with low scores
associated with low behavioral responses and high scores indicating maximum behavioral
responses, were coded. Percentage scores were used to compute an index of negative re-
activity, using higher scores on vocal and facial affect. Using descriptive statistics, we
separated the infants into low, middle, and high reactive groups, using the equal percent-
ages of 33.33% to form the groups. Descriptions of the behaviors coded for this task are
also found in Table 2.
2.6. Physiological recordings at 1 and 3 months
A stretch lycra cap (Electro Cap Inc.) with the international 10–20 system was positioned
on the infant’s head to obtain a measure of EEG activity at each age. Electrode gel, used
to conduct, and Omni Prep gel, used to gently abrade, was inserted into eight sites. The
mid-frontal (F3 and F4), central (C3 and C4), parietal (P3 and P4), and occipital (O1 and
O2) sites were chosen in order to remain consistent with previous research in this area
(Jones et al., 1997a). Each site was referenced to the vertex (Cz).
Although there has been controversy concerning the appropriate reference location, the
vertex reference was used for three reasons. First in one study, this site has been shown
to be comparable to other reference sites (Tomarken et al., 1992). Although other studies
question the use of this reference with adult participants (Hagemann et al., 1998; Reid
et al., 1998) no study has resolved this issue with infant participants (Pivik et al., 1993).
Second recordings, using this site as a reference for infant participants, are more feasible
given the ease of preparing the Cz site and the possible attrition of infant participants
when employing more invasive and/or more numerous recording sites (Pivik et al., 1993).
Third, the literature on infant EEG activity has used the vertex as the reference site almost
exclusively (Field et al., 2002b; Fox et al., 1992; Jones et al., 1998). Thus, we choose to
Table 2
Mother and infant codes, descriptors, and inter-rater reliability
Coded behavior Description
Mother and infant affect, attention and vocalization (κ = 0.86 for infant and 0.89 for mother)
7 Participant shows strong interest, smiling, positive intonation of vocalizations, and positive
touch
6 Participant moderate shows interest, pleasant positive attitude, positive intonation of
vocalizations, and positive touch
5 Participant shows some interest but no variability in intonation of vocalizations, variable
stimulation, little touch or heightened physical activity or physical contact. Participant is
reactive but with little facial affect
4 Participant shows varied positive, no, and/or negative affect, no consistency in responsiveness
or attention. Mother’s touch is for grooming rather than stimulating. Infant is non-reactive or
neutral
3 Mother speaks to child but her face and voice are flat in affect, directs conversation without
being responsive. Infant displays escape motor activities and may attend but briefly,
occasionally frets
2 Mother losing interest, shows some self-interest (i.e., self-grooming). Infant is not attentive,
vocalizations are fussy in tone. Infant may achieve full cry temporarily but reverts back to a
fret or neutral affect
1 Mother shows varied interest in infant, possibly negative facial expressions or vocalizations.
Infant is crying or is negatively responsive
Mother–infant mutuality (κ = 0.91)
7 Positive mutuality: mother and child attending. Mother attending and allowing for infant
response, positive intonation in vocalization in both mother and infant smiling, mother
possibly singing
6 Intermittent positive mutuality: mother and child attending, varied intonation of vocalization,
infants eyes are attending but smiling is varied
5 Varied mutuality: mother attends most of the time with varied positive and some neutral
affect. Infant attends more than half of the time but with neutral affect
4 Neutral mutuality: mother and child attend but with little or no affect by either. Some
grooming behaviors may be present but little stimulus/response interaction
3 Mother attending/infant not responsive or negatively responsive: mother stimulating but infant
shows little interest. Mother possibly over-stimulating, infant my show negative response,
infant clearly not enjoying the interaction and mother not changing her behavior in response
2 Mother attending/infant not attending or escaping: mother attends but no response from
infant. Infant showing intermittent negative vocalization or full cry. Infant is showing signs
that clearly indicate distress at interacting and mother not responding to infant distress
1 No mutuality: neither attending to each other nor interacting negatively
Infant reactivity during arm restraint (κ = 0.92)
5 Infant in full, continuous cry and twisting, stretching and kicking is observed
4 Infant showing no positive vocalizations, steady cry, with escape-type behaviors
3 Infant showing escalated fussing, may have brief neutral tone but infant reverts to fretting
2 Infant showing brief fussing and facial negativity (frown, pout)
1 No negative vocalizations or facial expressions are observed
use the vertex as the reference site in order to compare our results to similar findings in the
literature.
Electrode impedances were brought down to less than 5 k or the sites were re-abraded.
EOG was also be obtained, to aid artifact scoring, using two mini-electrodes, one at the
outer canthus and one at the supra orbit position of one eye. The electrical signal was am-
plified at each site using SA Instrumentation Bioamps and bandpassed from 1 to 100 Hz.
EEG activity from each electrode lead was displayed on a computer acquisition mon-
itor. The EEG was digitized on-line at a rate of 512 samples/s and saved to the com-
puter hard disk using data acquisition software (Snapstream, v. 3.21, HEM Data Corp.,
1991).
EEG data were examined and scored for eye and motor movement artifact using the
EOG channel as cues. Using software developed by James Long Inc., artifact was si-
multaneously eliminated from all channels. Then data were then submitted to a discrete
Fourier transform using a Hanning window with 50% overlap. This analysis produced
power for the specified frequency band in pW (1 ␮V squared) for each channel. Pre-
vious research suggested that the commonly used (adult) frequency bands are not appro-
priate for infant EEG activity analyses (Bell, 2002). Moreover, research has shown that
there is a shift in the alpha frequency band across development (Matousek and Petersen,
1973).
EEG were analyzed in two ways: (1) using single hertz frequency bands in order to
examine the spectral characteristics of the data; and (2) using the frequency bands commonly
used for infants (3–6 Hz for 1-month olds and 6–9 Hz for the 3-month olds; Jones et al.,
1997a, 1998). To normalize the distribution, power scores for each region were submitted
to a natural log transformation (ln). Finally, EEG asymmetry scores were computed to
determine the relative contribution of each hemisphere (ln(right) − ln(left)), with negative
scores reflecting greater relative right hemisphere EEG activity and positive scores reflecting
greater relative left hemisphere EEG activity.
2.7. Data reduction and analyses
Chi-square analyses were used to examine the incidence of stable feeding patterns
across development for infants of depressed and non-depressed mothers. In addition, in-
fants were assigned to a highly reactive, mid-level reactive, and low reactive groups based
on their responses to the 3-month arm restraint procedure. Infants who were in the up-
per 33.33% of negative facial and vocal responses were classified as high reactive whereas
infants in the lower 33.33% of facial and vocal responses were classified as low
reactive.
To examine the association between mother and infant behaviors and physiology related
to depression status and feeding patterns, four groups were examined. These groups were
composed of the following: (1) depressed mothers with stable breastfeeding patterns from
newborn to 3 months of age; (2) depressed mothers with little breastfeeding and mostly
bottle feeding from newborn to 3 months; (3) non-depressed mothers with stable breastfeed
patterns across age; and (4) non-depressed mothers with little breastfeeding and mostly
bottle feeding across age.
Infant data were examined using multivariate analyses of variances (MANOVAs) for EEG
activity and dyad data were examined for their behavioral responses during interactions
(positive, neutral, negative, and mutual/synchronous responses). Follow-up analyses were
conducted using separate univariate ANOVAs for depressed versus non-depressed groups
and/or for stable breastfeeding versus bottle-feeding (and non-stable breastfeeding) groups.
3. Results
3.1. Maternal depression and infant temperament
In an attempt to determine whether reactive infant temperament and maternal depression

were related to the earlier cessation of breastfeeding, we conducted several chi-square
analyses. Infants classified as high in reactive during the arm restraint procedure were
compared to those low in reactive on the stability of their breastfeeding patterns to 3 months
of age. Results showed that 77.8% of the infants who were high reactive and had a depressed
mother were predominately bottle fed whereas only 22.2% were breastfed (χ2 (3, N =
59) = 13.45, P < 0.05). Moreover, 70% of infants of non-depressed mothers who were
reactive were stable in their breastfeeding whereas only 30% of these infants were bottle
fed, suggesting that infant temperament is associated with breastfeeding stability in infants
of depressed mothers. These results were not found when examining infants with low or
mid-level reactive groups.
Feeding patterns were related to depressed mothers’ plans to breastfeed at the new-
born period and their actual feeding duration during the first 3 months. Depressed mothers
planned to breastfed for shorter periods of time, with 94.2% planning to breastfed for less
than 6 months than non-depressed mothers, 27.6% of whom were planning to breastfed
for less than 6 months (χ2 (3, N = 78) = 45.92, P < 0.05). Further, a one-way ANOVA
comparing depressed to non-depressed mothers on their feeding duration during the course
of the study yielded a significant effect (F(1, 76) = 5.68, P < 0.05), with depressed moth-
ers breastfeeding their infants a shorter duration of time (mean = 43.81 days, S.D. =
38.20 days) compared to non-depressed mothers (mean = 64.13 days, S.D. = 35.95
days).
3.2. EEG patterns for infants of depressed who breastfeed
A group (four levels; depressed/breastfed, depressed/bottle fed, non-depressed/breastfed,

non-depressed/bottle fed) × region (four levels; frontal, central, parietal, occipital) × age
(two levels; 1 and 3 months) repeated-measures MANOVA was conducted using the infant’s
EEG asymmetry score as the dependent variable. Results yielded a significant three-way
interaction (F(9, 147) = 2.06, P < 0.05). Analyses of each region separately showed
group differences in frontal EEG asymmetry (F(3, 49) = 3.14, P < 0.05) across age but
no differences in central, parietal and occipital regions (all P > 0.05) (Fig. 2). Univariate
ANOVAs showed that frontal EEG asymmetry differed between groups at 1 month of age
(F(3, 66) = 6.48, P < 0.05) and were only marginally significant at 3 months (F(3, 55) =
2.90, P = 0.09).
In addition, an overall group (four levels) × region (four levels) × hemisphere (two
levels; right versus left) × age (two levels) MANOVA was conducted using the infant’s
ln-transformed EEG power values as the dependent variable. Results yielded several mul-
tivariate main effects and interactions, with an overall significant four-way interaction
(F(9, 147) = 2.34, P < 0.05). In order to interpret the interactions and due to the spe-
cific hypotheses about frontal region EEG activity, we confined our subsequent analyses to
examining frontal EEG activity.
Fig. 2. EEG asymmetries.
A subsequent group × hemisphere × age analysis for the infant’s frontal region, ln-
transformed power scores yielded a significant main effect for group (F(3, 49) = 2.88,
P < 0.05) and a significant group × hemisphere interaction (F(3, 49) = 3.26, P <
0.05), with less left hemisphere activity in the frontal region in the depressed bottle-feeding
group than in the other three groups, post-hoc significance (P = 0.04) (Fig. 3). The de-
pressed/breastfeeding group and the non-depressed groups did not show differences in
hemispheric EEG activity in the frontal region (P > 0.05).
3.3. Infant developmental assessments
Infant neurobehavioral responses were assessed on the Brazelton exam at 1 month and on
the Infinib at 3 months of age. Multivariate analyses were conducted to determine whether
Brazelton scores differed for feeding and depression groups. Results showed a multivariate
interaction for Brazelton items between groups (F(21, 189) = 3.60, P < 0.05). Follow-up
univariate analyses between groups showed differences between groups for habituation
(F(3, 67) = 7.66, P < 0.05), orientation (F(3, 67) = 2.70, P < 0.05), motor maturity
(F(3, 67) = 3.98, P < 0.05), regulation of state (F(3, 67) = 2.82, P < 0.05), and abnormal
reflexes (F(3, 67) = 6.32, P < 0.05). Mean scores for each measure can be found in
Table 3. Overall, results showed early benefits for infants of non-depressed mothers and
Fig. 3. EEG power (ln-transformed) scores for the frontal region.
infants of depressed mothers who were breastfed, with this latter group exhibiting increased
habituation abilities and decreased abnormal reflexes.
An ANOVA comparing scores on the Infinib for depression and feeding groups did not
reach significance, with both all groups showing similar developmental capabilities at 3
months of age (P > 0.05).
Table 3
Infant Brazelton scores
Measure Depressed Non-Depressed
Breastfeedinga Bottle feedingb Breastfeedingc Bottle feedingd
Habituation 7.73 (0.57)∗ 6.76 (1.20)+ 7.76 (0.30)∗ 7.10 (0.74)∗

Orientation 6.44 (1.06)+ 6.69 (0.93) 7.17 (0.58)∗ 6.78 (0.74)
Motor maturity 5.60 (0.31) 6.07 (0.66)+ 5.44 (0.70)∗ 5.61 (0.40)
Range of state 3.07 (1.18) 3.86 (0.82) 3.38 (1.16) 3.34 (0.96)
Regulation of state 5.45 (1.24) 5.58 (0.90) 6.38 (1.38) 6.20 (0.78)
Autonomic stability 6.19 (1.17) 6.29 (1.01) 6.70 (0.96) 6.57 (1.18)
Abnormal reflexes 1.00 (1.04)∗ 2.25 (1.06)+ 0.92 (1.15)∗ 1.00 (0.84)∗
Note. Values represent mean scores. Standard deviations are in the parentheses. Different superscripts denote
significantly different post-hoc comparisons, P < 0.05.
a n = 12.
b n = 16.
c n = 25.
d n = 18.
∗ P < 0.05.
3.4. Maternal reports of infant temperament
MANOVAs were conducted on the mother’s reports of positive and negative (activity
level, smiling and laughter, distress latency, distress to limitations, soothability and du-
ration of orienting) behaviors on the six scales of the Infant Temperament Questionnaire
(IBQ) for the four groups. Results showed that all mothers reported differences in infant
temperament on the six scales (F(5, 53) = 86.50, P < 0.05), with more reports of positive
behaviors and fewer reports of negative behaviors. In addition, maternal reports of infant
behaviors on the temperament scales increased across age (F(1, 57) = 116.52, P < 0.05).
However, no meaningful group differences in the types of behaviors reported by depressed
and non-depressed mothers nor for breastfeeding and bottle-feeding groups were apparent
from ratings of maternal perceived infant temperament.
3.5. Mother and infant behaviors during play
A group × affect (three levels; positive, neutral, negative) × age MANOVA showed that
infants were exhibiting more positive and less negative and neutral interactive behaviors
at 3 months than at 1 month (F(2, 110) = 13.88, P < 0.05) (Fig. 4 illustrates the data).
Follow-up univariate ANOVAs revealed that the infants of depressed, bottle-feeding mothers
showed more negative affect at 1 month (F(3, 72) = 2.80, P < 0.05) and these infants also
showed the least positive affect at 3 months (F(3, 55) = 3.22, P < 0.05), than the other
three groups.
A repeated-measures group × age MANOVA was conducted on the percentage of time in
mutually responsive interactions as the dependent variables. Result showed no significant
interaction effects. However, a significant main effect for age was evident (F(1, 55) = 27.80,
P < 0.05). As expected, the dyads demonstrated more mutually interactive behaviors at 3
months than at 1 month.
Examination of mutually interactive behaviors separately for the maternal depression
groups versus the feeding groups were conducted at 3 months of age. This univariate
ANOVA yielded a significant between-subjects effect for feeding group (F(1, 57) = 4.24,
P < 0.05), with mean scores indicating that dyads who did not have stable breastfeeding
patterns had less mutually interactive behaviors at the 3-month visit (mean = 61.23, S.D. =
7.04) than infants who had stable breastfeeding patterns (mean = 66.14, S.D. = 7.04).
3.6. Path analysis
Finally, a path analysis was conducted using EQS (EQS v. 5.7b, Multivariate Software,
Inc, 1998) in order to evaluate the role of infant frontal EEG asymmetry and temperament
in mediating maternal depression effects on feeding behaviors. Missing data for nine sub-
jects were replaced with mean values. Based on previous findings, we hypothesized that
maternal depression would negatively affect feeding behavior. Similarly, we hypothesized
that infant temperament would be related to feeding behavior. Furthermore, we predicted
that maternal depression would be related to infant temperament via its effects on the de-
velopment of the underlying structures of emotion and emotion regulation, reflected by
frontal EEG asymmetry patterns. As such the hypothesized model examined the direct and
116
N.A. Jones et al. / Biological Psychology 67 (2004) 103–124
Fig. 4. Infant behavioral responses during mother–infant interactions at 1 and 3 months.
Table 4
Correlations
Infant feeding Depression Frontal EEG Infant temperament
score asymmetry (positive during
interaction)
Infant feeding
N 78 78 78 78
Covariance 1637.722 −64.786 3.074 149.491
Pearson correlation 1 −0.221 0.338 0.366
Significance (two-tailed) 0.052 0.003 0.001
Depression score
N 78 78 78 78
Covariance −64.786 52.529 −0.487 −22.102
Pearson correlation −0.221 1 −0.299 −0.302
Frontal EEG asymmetry
N 78 78 78 78
Covariance 3.074 −0.487 0.051 0.801
Pearson correlation 0.338 −0.299 1 0.352
Infant temperament (positive during interaction)
N 78 78 78 78
Covariance 149.491 −22.102 0.801 102.093
Pearson correlation 0.366 −.302 0.352 1
Correlation is significant at the 0.01 level (two-tailed).
indirect effects of maternal depression on both infant temperament and feeding behaviors
(Fig. 1).
Analyses were conducted using the maximum likelihood estimation procedure on the
variance/covariance matrix (Table 4). The hypothesized model was tested revealing an
adequate fit for the model (χ2 (1, N = 78) = 3.81, P < 0.05), comparative fit index
(CFI) of 0.91, RMSEA of 0.19 (Fig. 5). Post-hoc modifications were then performed in an
R2 =0.09
Infant
Infant EEG .29* Temperament
(positive R2 =0.17
asymmetry
responsive-ness
during interaction)
-.30* -.22
.33*
Maternal
Depression .12
Score Duration
R2 =0.15
Breastfeeding
Chi Square=3.81,p=0.05, CFI=0.91, RMSEA=0.19
Fig. 5. Initial model.

R2 =0.09
Infant EEG
asymmetry
-.24*
-.30*
-.29* Duration
Maternal R2 =0.18
Breastfeeding
Depression
Score
Infant
-.28*
Temperament
-.22*
(positive
responsiveness during
interaction)
R2 =0.17
Chi Square=0.46, p=0.50, CFI=1.00, RMSEA=0.00

Fig. 6. Final model.
attempt to develop a better fitting model. The Wald test indicated that eliminating the path
between maternal depression and feeding behaviors would improve the fit of the model.
A path between infant frontal EEG asymmetry and feeding behavior was added following
results of the Lagrange multiplier test. The model was re-estimated revealing an excellent
fit (χ2 (1, N = 78) = 0.46, P = 0.50, CFI = 1.0, RMSEA = 0.0), suggesting an
improvement from the hypothesized model (Fig. 6).
This final model suggests that the effects of maternal depression on feeding are mediated
by infant frontal EEG asymmetry and temperament. Furthermore, this model suggests that
maternal depression was strongly predictive of infant frontal EEG asymmetry (standard-
ized coefficient for direct effect = −0.30, t = 2.73, P < 0.05) and infant temperament
(standardized coefficient for indirect effect = 0.30, t = 2.76, P < 0.001). Furthermore,
maternal depression effects on infant temperament (standardized coefficient for indirect
effect = 0.09, t = 1.89, P < 0.1) were marginally mediated by frontal EEG asymmetry
and the effects of frontal EEG asymmetry on feeding (standardized coefficient for indirect
effect = −0.08, t = 1.83, P < 0.1) were marginally mediated by infant temperament.
4. Discussion
The goal the present investigation was to examine the factors that promote breastfeeding
stability and to examine the physiological and affective development in infants of depressed
mothers who breastfed compared to those who bottle fed. Previous research has suggested
that depressed mothers are less likely to breastfeed (Galler et al., 1999; Milligan et al., 1990)
and infants of depressed mothers demonstrate dysregulated physiological and behavioral
patterns as early as the newborn period (Jones et al., 1997a, 1998; Lundy et al., 1996,
1999). Within the present study, we documented that maternal depression is associated
with less stable breastfeeding, that greater negative infant temperament is associated with
less stable breastfeeding in depressed dyads, and that more positive dyadic interaction is
associated with infants of non-depressed mothers and infants of depressed mothers with
a stable breastfeeding relationship than for infants of depressed mothers who bottle feed.
Our final model showed that infant temperament and frontal EEG asymmetry mediated the
association between maternal depression and feeding patterns. As a caveat to these results we
must note that this study is correlational in nature, as we could not assign dyads to depression
and feeding groups, yet these data point to potentially important future intervention studies.
4.1. Maternal depression and breastfeeding patterns
That depressed mothers in this study were less likely to intend to maintain an extended
duration of breastfeeding at the newborn period is discouraging given that numerous health
care agencies are working to increase breastfeeding rates across infancy (Department of
Health and Human Services, Blueprint for Action on Breastfeeding, 2000). However, these
data are consistent with previous research showing lower rates of breastfeeding in depressed
women (Field et al., 2002a; Galler et al., 1999). Typically studies have examined the char-
acteristics of the parents and the likelihood of breastfeeding continuity across infancy. This
is one of the few studies to show an association between infant temperament and breastfeed-
ing stability across the early months of development. Specifically, we showed that greater
negative infant reactivity was associated with more variable feeding patterns in depressed
mothers compared to non-depressed mothers. While our data are confounded, as we cannot
separate situational variables (mothers plans for breastfeeding or bottle feeding and moth-
ers depression status) and individual difference variables (infant temperament and EEG
activity patterns), this study points several important future studies that may be beneficial
to conduct. For example, breastfeeding support and promotion could be employed, using
random assignment, as a clinical intervention for depressed mothers during the prenatal
period. The findings of this study could determine more directly whether breastfeeding
can benefit the affective and physiological functioning of the dyad even though exposed to
maternal depression.
Moreover, there are many reasons that the depressed mothers may fail to establish stable
breastfeeding patterns with their infants. The more simplistic explanation is that depressed
mothers are more concerned about their own emotional state than the feeding status of their
infants. While this explanation is possible, we are suggesting that depressed mothers may
show lower rates of breastfeeding due to their lack of understanding of normative tempera-
mental changes across infancy. As noted by previous studies, newborns who breastfed are
more temperamentally irritable and more difficult to sooth (Dipietro et al., 1987). Bottle
feeding, on the other hand, has a depressive effect on infant behavior (Dipietro et al., 1987).
Therefore, newborn behavioral responses, as a result of breastfeeding, may confuse and
tax the already depleted resources of the depressed mother. However, several studies have
noted that breastfed newborns demonstrate more optimal physiological organization (e.g.,
Zeskind et al., 1992) and, later in development, mothers who maintain stable breastfeeding
patterns report that their infants exhibit “easier” temperaments (VanDiver, 1997) and more
socially responsive behaviors (Kuzela et al., 1990; Worobey, 1992, 1998), suggesting posi-
tive outcomes later in development for breastfed dyads. Therefore, depressed mothers must
be educated about the numerous benefits of breastfeeding stability and must be encouraged
to continue breastfeeding, despite the seemingly more challenging behaviors displayed by
their newborns. Moreover, these parents should be counseled that the seemingly more taxing
newborn behaviors are normative and not due to inadequate parenting skills. Currently de-
pressed mothers are discontinuing breastfeeding within the first 2 months and therefore fail
to experience the potential benefits associated with the more positive infant physiological
and behavioral responses that are the result of stable breastfeeding patterns.
Although we did demonstrate that infant temperament is related to breastfeeding sta-
bility in the depressed group, the sample size for this study is small and is limited to the
first 3 months of development. The findings presented here, however, remain an important
area for future work, primarily due to the increasing evidence that breastfeeding stability
benefits overall infant health and development. Ultimately supporting mothers during the
breastfeeding months will likely have long lasting benefits for depressed mothers and their
infants.
4.2. Physiological patterns in infants of depressed mothers who breastfeed
Our study also suggests that infant EEG activity is associated with maternal depression
and breastfeeding stability. The final path model showed a strong association between
maternal depression and infant EEG patterns and infant temperament. Specifically, infants
of depressed mothers who had been breastfed until their third month of life were less likely
to show the right frontal EEG asymmetry patterns previously associated with maternal
depression (Dawson et al., 1999, 1997; Jones et al., 1998) and linked to risk for depression in
adults (Davidson, 1994; Henriques and Davidson, 1990). Alternatively, infants of depressed
mothers who were bottle fed exhibited a bilateral decrease in frontal EEG activity that was
especially pronounced on the left side. Although the difference in EEG asymmetry scores
decreased with age, this may be due, in part to the declining depressive symptoms in both
depression groups or it may be due to the resiliency of these infants. Nonetheless, future
studies should examine the stability of EEG patterns across development and the situational
factors that may attenuate these seemingly dysregulated EEG patterns in infants of depressed
mothers.
The EEG findings related to feeding patterns are intriguing in light of the fact that previous
investigations have only rarely assessed neurophysiological patterns associated with infant
feedings. One recent study by Lehtonen et al. (2002) examined EEG activity in 3- and
6-month-old infants during feeding. While their goal was to examine EEG patterns during
normative infant feeding session, they found undifferentiated “theta” (similar frequency
band to the band we called alpha) responses to feeding and did not establish organized
EEG activity patterns associated with feeding until 6 months of age. The authors speculate
that the development of the frontal regions and the emotional arousal inherent in feeding
was directly related to their findings. While their findings are later in development than
our own, the findings do parallel our associations between emotional responses and EEG
activity. Of interest, they did not find distinct patterns of EEG activity for bottle fed and
breastfed groups, most likely due to the small number of bottle fed participants in their
study. Collectively this study and our own findings suggest that further research should
focus on feeding patterns in the infant and the association between emotional processing
and frontal lobe development.
4.3. Neurobehavioral assessments of infants of depressed mothers who breastfed
Consistent with previous studies, infants of depressed mothers also showed fewer op-
timal behaviors on the Brazelton Scales (Abrams et al., 1995; Jones et al., 1997a, 1998;
Lundy et al., 1996). Specifically infants of depressed mothers who bottle fed showed less
habituation and more abnormal reflexes. Although these results may be transitory, as these
infants did not differ on developmental assessments at 3 months of age, the findings suggest
that subtle differences in early neurobehavioral abilities are affected by maternal depression
and feeding status.
4.4. Mother–infant interactive behavior for depression and feeding groups
In separate analyses, we also demonstrated that mother–infant interactions were less

negative at 1 month of age and more positive by 3 months of age in the depressed group
with stable breastfeeding patterns but not in the depressed group who were bottle fed.
While previously we have established that infants of depressed mothers displayed greater
negative affect during interaction (Jones et al., 1997b) and Field et al. (1990) demonstrated
more negatively matched and fewer positively matched interactive patterns in depressed
groups, in the present study, infants of breastfeed, depressed mothers seemed to display
reduced dysregulated interaction patterns than the infants of depressed mothers who bottle
fed. Although these results could be due to other factors that motivate a depressed mother
to breastfeed, the fact that the depressed-breastfeeding dyads appeared to interact with
their infants like the non-depressed groups suggests that breastfeeding may benefit the
socio-emotional interactions of depressed dyads.
Breastfeeding patterns have also been examined retrospectively as a potential factor that
differentiates depressed and non-depressed groups. For example, Allen and his colleagues
(Allen et al., 1998) have also investigated the prenatal and perinatal risk factors for psy-
chopathologies in children and adolescents. Their study concluded that major depression
in childhood and adolescence was associated with not having been breastfed and having a
mother with an affective disorder during pregnancy. Given these data and the data presented
here, it may be beneficial to support breastfeeding patterns in depressed mothers to possibly
reduce the negative outcomes and the increased risk factors for affective problems noted in
previous studies (Allen et al., 1998; Field, 1995).
In conclusion, our previous research has demonstrated that infants of depressed moth-
ers exhibit risk factors that are associated with physiological and affective dysregulation
(Field, 1995; Jones et al., 1998). However, within this study we were able to demonstrate
that infants of depressed mothers who are stable in their breastfeeding patterns showed a
reduced association between physiological and affective dysregulation resulting from ex-
posure to maternal depression. Specifically, infants of depressed mothers who breastfed
did not demonstrate the greater relative right frontal EEG asymmetry (nor the left frontal
hypoactivity) compared to the bottle fed group. Moreover, increased positive affect was ap-
parent in 3-month-old infants of breastfed compared to the bottle-feeding/depressed group,
suggesting that breastfeeding should be examined further as a potential intervention factor

for depressed mother and their infants.
Acknowledgements
We would like to thank the mothers and infants who participated in this study. We would
also like to thank all the students at Florida Atlantic University at Jupiter who helped with
data collection. This research was supported by a NIMH grant (MH61888) and a FAU
Research Initiation Award to Nancy Aaron Jones, Ph.D.
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Prefrontal cortex activity differentiates processes

affecting memory in depression
Jack B. Nitschke a,∗ , Wendy Heller b , Marci A. Etienne c ,
Gregory A. Miller b,d
a W.M. Keck Laboratory for Functional Brain Imaging and Behavior, Departments of Psychiatry and
Psychology, Waisman Center, Room T229, University of Wisconsin,
1500 Highland Avenue, Madison, WI 53705-2280, USA
b Department of Psychology, Beckman Institute for Advanced Science and Technology,
University of Illinois at Urbana-Champaign, 603 East Daniel Street, Champaign, IL 61820, USA
c Department of Psychology, Mental Health Service Line,
Edward J. Hines Hospital, Hines, IL 60141-5000, USA

d Department of Psychiatry, University of Illinois at Urbana-Champaign, USA
Abstract
Deficits in the initiation and utilization of strategies contribute importantly to memory impairments
in depression. Other research on depression has documented memory biases toward negative and away
from positive material. This study investigated brain mechanisms accompanying the initiative deficit
and negative bias processes affecting memory in depressed individuals. Electroencephalography was
recorded prior to and during emotional narratives and correlated with subsequent memory recognition
of narrative material. Hypothesized to reflect strategy initiation, bilateral activity of the prefrontal
cortex (PFC) preceding a sad narrative was associated with memory performance for that narrative
in nondepressed controls only. Negative memory bias in depressed participants was inferred from
their association between right prefrontal activity during the sad narrative and memory performance,
consistent with research implicating that region in withdrawal-related unpleasant emotions. These
results highlight the importance of distinguishing processes that influence memory performance when
investigating the neural mechanisms of cognitive deficit and bias in depression.
Keywords: Frontal EEG asymmetry; Emotion; Depression; Prefrontal cortex; Memory

E-mail address: jnitschke@wisc.edu (J.B. Nitschke).
doi:10.1016/j.biopsycho.2004.03.004
126 J.B. Nitschke et al. / Biological Psychology 67 (2004) 125–143
1. Introduction
Depression has been associated with a variety of cognitive correlates, including memory
impairments and memory biases. In general, decrements have been reported for explicit
memory tasks that require effortful processing (for reviews, see Burt et al., 1995; Hartlage
et al., 1993). In an elegant set of studies, Hertel and her colleagues have shown that memory
deficits in depressed participants are eliminated when strategies are provided prior to the
start of a task (for reviews, see Hertel, 1994, 1997, 2000). These data are not consistent with
a capacity framework arguing for reduced attentional resources in depression. Instead, her
cognitive–initiative account posits that depressed individuals show diminished initiative
in allocating available attentional resources for utilizing strategies that improve memory
performance.
In other studies, biases have been reported for valenced information, with depression
accompanied by better recall for negative information and worse recall for positive material
(for reviews, see Blaney, 1986; Watkins, 2002). Such biases have been observed for explicit
memory tasks and some conceptually driven implicit memory tasks. The relationship be-
tween the initiative deficit and the negative memory bias accompanying depression has not
been systematically investigated, despite some evidence that they may be distinguished by
their temporal and neuroanatomical patterns.
Neuroimaging and neuropsychological research has shown that the prefrontal cortex
(PFC), especially dorsolateral sectors of the PFC (DLPFC), mediates the type of infor-
mation processing highlighted by Hertel (1994, 1997, 2000) as critical in depression (for
reviews, see Davidson et al., 2002; Heller and Nitschke, 1997; Miller and Cohen, 2001).
A central function of the DLPFC is thought to be the representation of goals and the
maintenance of context information that promotes the achievement of these goals. Context
information might include task demands, information regarding the results of previous be-
havior, emotional state, or any aspect of the internal or external environment that would
influence the accomplishment of the represented goals. Recruitment of the DLPFC in cog-
nitive control has been found to be central to performance on a variety of memory tasks,
including working memory (e.g., Constantinidis et al., 2001; D’Esposito et al., 1998; Levy
and Goldman-Rakic, 1999; Postle et al., 1999; Smith and Jonides, 1998, 1999) and episodic
long-term memory (e.g., Brewer et al., 1998; Buckner et al., 1999; Fletcher et al., 1998;
Petrides, 1996; Schacter, 1997), with two studies directly comparing both forms of memory
(Braver et al., 2001; Ranganath et al., 2003; for reviews, see Barch and Buckner, 2003;
Simons and Spiers, 2003). Of further relevance to the research conducted by Hertel (1994,
2000) on strategy utilization in depression, patients with DLPFC lesions show impairments
in using organization strategies during episodic memory tasks and benefit from instruction
in the use of such strategies (Gershberg and Shimamura, 1995; Incisa della Rocchetta and
Milner, 1993). Similar impairments in strategy utilization have been observed for Parkinson’s
disease (Pillon et al., 1998), schizophrenia (Iddon et al., 1998; Sengel and Lovallo, 1983),
and obsessive-compulsive disorder (Savage et al., 1999).
Research examining the neural circuitry of depression has identified abnormal activity
patterns in the DLPFC during resting states. A number of positron emission tomography
(PET) and single photon emission computerized tomography (SPECT) studies have re-
ported bilateral DLPFC decreases in blood flow and glucose metabolism (for reviews, see
J.B. Nitschke et al. / Biological Psychology 67 (2004) 125–143 127
Davidson and Henriques, 2000; Davidson et al., 2002; Dougherty and Rauch, 1997; Heller
and Nitschke, 1997, 1998). Decreased DLPFC activity has also been observed during task
performance. Consistent with Hertel’s cognitive–initiative framework (1994, 2000), de-
pressed patients showed less DLPFC activity bilaterally on a complex planning task than
nonpsychiatric controls in a PET study measuring blood flow (Elliott et al., 1997).
Other evidence suggests that the right DLPFC may also figure importantly in the negative
memory bias accompanying depression. An extensive literature has implicated right PFC
mechanisms in withdrawal-related negative emotions and in threat perception. Activity in
this region under such circumstances is likely to contribute to a negative memory bias (for
reviews, see Davidson, 1998; Heller and Nitschke, 1997; Nitschke and Heller, 2002). Fur-
thermore, numerous electroencephalography (EEG) studies have reported more right than
left PFC activity in depression (for reviews, see Davidson and Henriques, 2000; Davidson
et al., 2002; Heller and Nitschke, 1997, 1998). A similar pattern of asymmetry has also
been observed in a number of the aforementioned PET studies showing bilateral DLPFC
decreases, in which hypoactivity was more pronounced on the left.
Although these findings indicate an asymmetry in favor of the right PFC in depres-
sion, investigation into the brain mechanisms contributing specifically to the negative ex-
plicit memory bias in depressed subjects has only recently begun. An event-related brain
potential (ERP) study revealed no evidence of a negative memory bias in depressed pa-
tients, including no topographical differences for the P300 component between patients
and nonpsychiatric controls during encoding or recognition of negative words or faces
(Deldin et al., 2001b). Another ERP study examining the slow wave component for neg-
ative adjectives in a delayed-match-to-sample paradigm primarily implicated left parietal
irregularities in depressed patients, with some right PFC abnormalities observed for corre-
lations with depression severity (Deldin et al., 2001a). However, behavioral data indicated
that the paradigm was not successful in eliciting an overt negative working memory bias in
depressed patients. A recent functional magnetic resonance imaging (fMRI) study (Elliott
et al., 2002) examined another type of processing bias via an emotional go/no-go task previ-
ously shown to result in a bias toward sad stimuli in depressed patients (Murphy et al., 1999).
They reported greater right DLPFC activity for sad stimuli in patients than nonpsychiatric
controls. Finally, an earlier blood flow study using PET by George et al. (1997) assessing
attentional biases did not report DLPFC abnormalities in depressed patients for a standard
Stroop paradigm or an emotional Stroop task using four words (grief, misery, sad, and
bleak). Although results from studies examining the brain instantiation of negative memory
biases in depression have thus far been mixed, other research on emotion, depression, and
anxiety leads to predictions of right prefrontal engagement (Davidson, 1998; Davidson and
Henriques, 2000; Davidson et al., 2002; Heller and Nitschke, 1997, 1998; Nitschke and
Heller, 2002). A question arises, then, of whether this region will be recruited only under
particular conditions or sets of conditions. In the present study, it was hypothesized that
timing of the processes involved may be crucial to the degree to which different patterns of
PFC activity are seen.
The present study tested Hertel’s (1994, 2000) cognitive–initiative framework for de-
pression by assessing activity of the PFC during a narrative task using EEG. We predicted
that depressed participants would fail to initiate PFC-mediated memory-relevant strategies
shown by nondepressed participants prior to narrative presentation. More specifically, an
association between bilateral PFC activity during preparation for listening to a sad narra-
tive and subsequent memory for that material was expected for controls but not depressed
participants. In addition, in accord with Heller and Nitschke’s (1997) framework linking
right PFC activity to the negative memory biases often observed in depression, depressed
individuals should show an association between right PFC activity during a sad narrative
and subsequent memory performance. A sad narrative was selected because of the relevance
of sad material for the negative memory bias often observed in depression. For purposes
of comparison, brain activity and memory performance for three other narratives of dif-
ferent emotional content (fearful, happy, and neutral) were also analyzed. Both hypotheses
were evaluated at midfrontal sites (F3/4), which lie over the DLPFC regions implicated in
PET, SPECT, and fMRI research on depression. Moreover, the frontal asymmetry findings
observed in EEG research on depression have been most consistent at these midfrontal sites.
2. Method
2.1. Participants
Participants were selected based on their scores at an initial screening of 2203 under-
graduate students enrolled in Introductory Psychology. Students with extreme scores on
the Dysthymia scale of the General Behavior Inventory (GBI; Depue et al., 1989) and the
Trait scale of the State-Trait Anxiety Inventory (STAI; Spielberger, 1968) were classified
into four original groups. Individuals scoring below 0.5 S.D. above the mean on both the
GBI-D and STAI met criteria for the control group, whereas those scoring above the 90th
percentile on both were assigned to the mixed depression/anxiety group. The depression
group was comprised of students scoring above the 90th percentile on the GBI-D and below
0.5 S.D. above the mean on the STAI. The anxiety group was comprised of students scoring
above the 90th percentile on the STAI and below 0.5 S.D. above the mean on the GBI-D.
Of the 68 participating in the EEG study, 8 were in the depression group, and 20 were in
each of the other three groups. Participants were screened again prior to the EEG session
and only those showing stable scores across both times on both selection instruments were
included in analyses. For the GBI-D, low and high scorers had to maintain scores below and
above 10, respectively, whereas the cut-off for low and high scorers on the STAI was 50. In
order to maintain reasonable sample sizes, the following exceptions to these criteria were
made. The STAI cut-off was 45 for the anxiety and mixed depression/anxiety groups. In the
depression group, one of the three participants not meeting the GBI-D criterion endorsed
multiple items on the GBI Bipolar scale. Therefore, a cut-off of 8 was applied when com-
bining the Dysthymia and Bipolar scales, which resulted in the addition of one additional
subject in the mixed depression/anxiety group as well. Missing EEG data for one control
subject resulted in a final sample size of 54 participants: 15 control (8 female), 6 depression
(3 female), 16 anxiety (8 female), and 17 mixed depression/anxiety (10 female).
Because the hypotheses concerned depression, the two original groups with minimal
depressive symptoms (control and anxious groups) were combined into a low depression
group (n = 31), whereas the other two groups reporting high levels of depression (de-
pression and mixed depression/anxiety) comprised the high depression group (n = 23). To
examine effects of anxiety, a similar strategy was adopted. The two original groups with
minimal anxious symptoms (control and depression groups) were combined into a low anx-
iety group (n = 21), whereas the other two groups reporting high levels of anxiety (anxiety
and mixed depression/anxiety) comprised the high anxiety group (n = 33). The majority of
participants were strongly right-handed (M = 80.24, S.D. = 20.99) as determined by the
Edinburgh Handedness Inventory (EHI; Oldfield, 1971). Only two individuals scored below
45, with scores of 0 and 10 (maximum score of 100 indicates strong right-handedness, −100
corresponds to strong left-handedness, and 0 to ambidextrous). Analyses conducted without
those two participants did not alter the pattern of results. Individuals reporting hypomanic
symptoms with scores above the 90th percentile on the GBI Biphasic and Hypomania scales
combined were excluded.
2.2. Self-report screening measures
The GBI is a 73-item questionnaire that assesses subsyndromal levels of chronic depres-
sion and mania in psychiatric outpatient and nonclinical populations. Internal consistency
in a nonclinical sample was 0.96 (Depue and Klein, 1988). The test-retest reliability with a
nonclinical sample was 0.75 (Depue and Klein, 1988). The 46-item Dysthymia scale was
used to select participants with low or high levels of depression for this study, and the
Biphasic and Hypomania scales were used to exclude cyclothymic or manic students.
The STAI is a 40-item questionnaire that assesses state and trait anxiety. Internal consis-
tency is in the low 0.90’s with college students for both the state and trait forms (Spielberger,
1983). Previous studies have reported test-retest reliability with college students in the 0.70’s
(Spielberger, 1983). The 20-item Trait scale was used to classify participants.
The EHI is a 10-item questionnaire assessing hand preference as a continuum. Each item
lists a task, and the participant responds with the degree of preference for performing the task
with the right or left hand. Persons who are left-handed, ambidextrous, or ambilateral can
show different patterns of brain organization than right-handed individuals. Because degree
of right-handedness can vary among those who report being right-handed, this inventory
was used to confirm the degree of right-handedness of participants (laterality quotients
greater than zero).
2.3. Narrative script materials
Because the development of the narratives has previously been described extensively
(Heller et al., 1997), only a brief explanation is provided here. Four narrative scripts were
selected from a pilot sample of 12 narratives, three for each of the emotion categories of
sad, happy, fearful, and neutral. The narratives were designed to probe for both explicit
and implicit memory. Hence, each pilot narrative was constructed with one exemplar (e.g.,
scooter) from each of six different object categories (e.g., motor vehicle). Exemplars were
selected based on word frequency research (Battig and Montague, 1969). The range and
word frequency for exemplars in each narrative category were closely matched.
Pilot narratives were read by 19 raters (11 female) who completed an adjective checklist
after reading each narrative. Participants were asked to rate the content of the narrative along
a calm-aroused dimension and a pleasant-unpleasant dimension. In addition, raters indicated
the amount of discrete emotion present in the content of the narrative for the following
emotion descriptors: happy, sad, fear, anger, surprise, disgust, interest, and amusement. All
ratings were made by marking a slash on a 100 mm vertical bar for each dimension or
emotion adjective. Narratives were selected based on their representativeness of the target
emotion content for each of the four categories (for further details, see Heller et al., 1997;
Etienne, 2002).
To test the proposed hypotheses concerning cognitive abnormalities in depression, anal-
yses concentrated on the sad narrative due to the relevance of sad material to depression
and the negative memory biases observed in depression. All participants heard the same
sad narrative:
Steve just drove his motor scooter off of the edge. Still wearing your shorts from when
you played tennis just hours earlier, you and Karen stood stunned, as you listened to the
details of what would be called a suicide. You close your eyes and can picture him in his
denims waving good-bye to you after he dropped you off. You feel a lump build in your
throat as you touch the garnet ring he had just left with you.
2.4. Apparatus and physiological recording
During the laboratory session, participants were seated in a comfortable chair in a quiet
room connected to the adjacent equipment room via intercom. A computer-controlled tape
recorder was used to present narratives over a centrally located loudspeaker. A 500 ms
1000 Hz tone generated by a Beckman Circuitmate function generator was presented at a
comfortable listening level over the loudspeaker to signify the start and end of each narrative
period as described below.
EEG recording used the International 10–20 system (Jasper, 1958) with electrodes at
sites F3, F4, Cz, P3, P4, and right mastoid, each referenced to the left mastoid. The right
and left mastoid were algebraically linked off-line to serve as reference for the other sites
(Davidson, this issue; Miller et al., 1991; Nunez, 1981). Beckman miniature Ag–AgCl
electrodes were used for EEG recording and were placed with Grass EC2 electrode paste.
Horizontal and vertical EOG (electro-oculogram) were also recorded. Beckman miniature
Ag–AgCl electrodes were placed above and below the left eye and near the outer canthus
of each eye. Electrode impedances were below 10 k.
Stimulus presentation and physiological data collection were controlled by an LSI-11/73
based PEARL II-B microcomputer (Heffley et al., 1985). Recordings were amplified by a
Grass Model 12 Neurodata system with EOG channels set to a gain of 2 K and EEG channels
set to a gain of 10 K. Half-amplitude frequency cutoffs were set at 0.01 and 100 Hz. Analog
signals were digitized on-line at 250 Hz.
2.5. Procedure
During an initial session, a general tour of the laboratory was conducted, a detailed de-
scription of the study was presented, and informed consent was obtained. Participants were
screened for known health conditions that would affect data collection during physiological
recording (e.g., closed-head injury with post-traumatic amnesia). Participants were asked
to refrain from the use of psychoactive drugs on the day of the laboratory session (including
tobacco, alcohol, and caffeine). Participants were reassessed during this initial session for
trait anxiety with the STAI and for chronic depression with the GBI.
At the EEG session, 8 min of resting baseline EEG were collected using counter-balanced
eyes-open (O), and eyes-closed (C) 1 min trials, ordered COOCOCCO for half the partici-
pants and OCCOCOOC for the other half. Participants received instructions on the terminal
screen in front of them to either open (“eyes open”) or close (“eyes closed”) their eyes. The
start of each 1 min period was marked by a single tone, and the end of each minute was
marked by a double tone presented over the loudspeaker. These resting baseline EEG data
have been published (Heller et al., 1997) and are not presented here.
Following the collection of baseline data, the trial structure for the narrative presentation
was explained. Important for Hertel’s proposed cognitive–initiative deficit in depression
(Hertel, 1994, 2000), participants were not informed of the memory tasks that would follow
nor provided with any strategies for attending to the narratives. Four narrative trials were
presented. The order of narrative presentation was counterbalanced across participants.
The trial structure was as follows: 30 s Preparation, 30 s Listen (tape-recorded narrative),
30 s Relax. Eyes-closed EEG was collected during all three periods of all four narrative
presentations. Following each Relax period, the participant completed ratings about the
narrative.
After all four narrative scripts were presented, explicit memory recognition of the narra-
tives was assessed. The recognition test consisted of a sheet of paper with 32 words typed
in a 4 × 8 grid. Sixteen of the words were targets (four of the category targets selected from
each of the four narratives presented), and the other sixteen were semantically related dis-
tractors (e.g., Steve was a target, Larry was a distractor). One distractor was selected from
each of the 16 categories represented by the targets, and each had a word frequency count
comparable to its corresponding target. Target words were randomly distributed throughout
the grid. Participants were asked to circle any words that were in any of the four short stories
listened to at the beginning of the study. Number of hits and false positives were scored.
Because very few subjects had any false positives, analyses were conducted for hits only.
Implicit memory was assessed by a primed exemplar production task, following the
procedures outlined by Graf et al. (1985). This task was not successful in eliciting implicit
memory; therefore, group differences and relations with EEG were not assessed.
2.6. EEG data reduction and analysis
An eye-movement correction program was used off-line to remove EOG artifact from
the EEG (Gratton et al., 1983; Miller et al., 1988), with raw data processed in contiguous
5 s segments. The complete data sample was then digitally filtered for alpha frequency
(8–13 Hz) with a 501-weight filter (Cook, 1981; Cook and Miller, 1992; Nitschke et al.,
1998). Filter gain at 8.3, 10.7, and 12.7 Hz was 0.85, 0.99, and 0.85, respectively. EEG
alpha activity was quantified by first computing a root mean square (RMS) score for each
second of alpha-filtered EEG. An average RMS value was then computed separately for the
eyes-open and eyes-closed baselines, and separately for each narrative period (Preparation,
Listen, Relax). Distributions for the averaged RMS values at each EEG site were consistently
skewed; therefore, log transformations were performed to reduce skew in these distributions.
All MANOVAs and regressions were conducted using alpha = 0.05, with the directional
hypotheses following from Hertel’s (1994, 2000) cognitive–initiative model and Heller
and Nitschke’s (1997) neuropsychological framework for cognitive biases evaluated via
one-tailed distributions. Reported analyses do not include Sex as a factor because parallel
MANOVAs and regressions with Sex as an additional factor revealed no sex differences.
3. Results
3.1. Recognition memory
A Depression (Low, High) × Anxiety (Low, High) × Narrative (Sad, Fearful, Neutral,
Happy) repeated-measures MANOVA with memory performance (number of hits) as the
dependent variable revealed main effects for Depression, F(1, 50) = 5.89, P < 0.05,
η2 = 0.105; Anxiety, F(1, 50) = 8.98, P < 0.01, η2 = 0.152; and Narrative, F(3, 48) =
4.62, P < 0.01, η2 = 0.224 (see Table 1). High depression participants performed more
poorly on the recognition test than low depression participants. Conversely, high anxious
participants showed better memory performance than low anxious participants. Post hoc
analyses using the Least Significant Difference test or a Bonferroni correction for all six
possible pairwise comparisons indicated that recognition was better for the sad narrative than
the fearful or neutral narratives and no significant differences for the other four comparisons.
Whereas none of the interactions involving Narrative was significant, Depression × Anxiety
was F(1, 50) = 5.86, P < 0.05, η2 = 0.105. This interaction effect is reflected in an
analogous MANOVA using the four original groups, which revealed a main effect for
Group, F(3, 50) = 4.43, P < 0.01, η2 = 0.210. The depression group (participants with
high depression and low anxiety) recognized fewer words from the narratives than did each
of the other groups, including the mixed depression/anxiety group (Tukey’s HSD). There
were no pairwise differences among the other three groups.
Of relevance for the present report focusing on the sad narrative, the above between-sub-
jects effects were present for a comparable MANOVA conducted on memory performance
for the sad narrative alone: Depression, F(1, 50) = 9.05, P < 0.01, η2 = 0.153; Anxiety,
F(1, 50) = 7.63, P < 0.01, η2 = 0.132; and Depression × Anxiety, F(1, 50) = 7.71,
P < 0.01, η2 = 0.134.
Table 1
Means and standard deviations for memory recognition of words used in the four narratives
Narrative Low depression (n = 31) High depression (n = 23)
Low anxiety High anxiety Low anxiety High anxiety

(n = 15) (n = 16) (n = 6) (n = 17)
M S.D. M S.D. M S.D. M S.D.
Sad 3.07 1.10 3.06 0.85 1.50 0.84 3.00 0.79

Fearful 2.00 0.76 2.19 1.22 1.33 0.82 2.35 0.79
Neutral 2.33 1.18 2.12 1.26 1.83 1.47 2.06 1.03
Happy 2.27 1.10 2.69 0.87 1.67 1.37 2.65 1.06
3.2. EEG
Patterns of brain activity were assessed using a repeated-measures MANOVA with De-
pression (Low, High) and Anxiety (Low, High) as between-subjects variables and four
within-subjects variables: Narrative (Sad, Fearful, Neutral, Happy), Period (Preparation,
Listen), Region (Frontal, Parietal), and Hemisphere (Left, Right). A main effect for Depres-
sion, F(1, 48) = 5.16, P < 0.05, η2 = 0.097, revealed that high depression participants had
less activity across all frontal and parietal regions (more global alpha) than low depression
participants. There were only two other significant effects involving Depression or Anxi-
ety: Depression × Anxiety × Narrative × Period × Region, F(3, 46) = 2.93, P < 0.05,
η2 = 0.160; and Anxiety × Narrative × Period × Hemisphere, F(3, 46) = 3.22, P < 0.05,
η2 = 0.174. For a parallel MANOVA on the sad narrative alone, there were no significant
effects involving Depression or Anxiety. Following from the focus of the hypotheses on
frontal regions, another MANOVA for the sad narrative was conducted for frontal sites only.
Again, there was a main effect for Depression, F(1, 50) = 4.28, P < 0.05, η2 = 0.079,
indicating less bilateral frontal activity (more alpha) in high depression than low depres-
sion participants. The only other significant effect involving Depression or Anxiety was a
Hemisphere × Anxiety interaction, F(1, 50) = 7.24, P < 0.05, η2 = 0.126, indicating
greater left than right activity in high than low anxiety participants (see Heller et al., 1997).
Also of relevance to the current report was a marginally significant Depression × Period
× Hemisphere interaction, F(1, 48) = 3.73, P < 0.06, η2 = 0.069, due to greater left
than right activity in low than high depression participants during preparation for the sad
narrative, F(1, 50) = 4.01, P < 0.06, η2 = 0.074.
3.3. Recognition memory and EEG
Hierarchical regression analyses evaluating the two hypotheses under investigation were
conducted on the EEG and memory data for the sad narrative. The omnibus model predicting
recognition memory performance for the sad narrative included Depression (Low, High),
Anxiety (Low, High), frontal and parietal sites during the preparation and listen periods,
and interactions between Depression and each EEG variable. The predicted effect based on
Hertel’s (1994, 2000) model was an interaction between Depression and bilateral frontal
activity during the preparation period. The predicted effect based on Heller and Nitschke’s
(1997) framework for negative memory bias was an interaction between Depression and
right frontal activity during the listen period. In this and subsequent regression models,
parietal sites were entered before frontal sites for two reasons: to test that neither right nor
left parietal activity was associated with subsequent memory performance and as a means
of removing variance associated with global EEG power prior to testing hypotheses for
frontal regions. Results for parallel regressions omitting parietal sites replicated the effects
reported below and are therefore not reported to avoid redundancy. When left and right sites
were added on different steps, left were routinely entered first for the results presented here.
The pattern of results did not change if right sites were entered first. Anxiety status was
included in the model to account for variance associated with anxiety; however, interaction
terms involving Anxiety were omitted from the model due to the high number of predictors
(18) already included.
Depression and Anxiety entered on the first step were significant predictors of mem-
ory performance for the sad narrative, R2 = 0.12, F(2, 51) = 3.39, P < 0.05. As for
the MANOVAs conducted on memory performance above, high depression was associ-
ated with poorer memory performance, t(51) = −2.11, P < 0.05, and high anxiety
was associated with better memory performance, t(51) = 1.96, P < 0.06. Entering all
eight frontal and parietal values for the preparation and listen periods on the second step
did not result in a statistically significant increment in variance explained, R2 = 0.15,
F(8, 43) = 1.06, P > 0.40. The interaction of depression and each parietal site during
the preparation period was not significant when entered next, R2 = 0.00, F(2, 41) =
0.08, P > 0.92. As predicted, the interaction of depression and each frontal site dur-
ing the preparation period was significant, R2 = 0.10, F(2, 39) = 3.18, P < 0.05.
The Depression × Left Frontal interaction and the Depression × Right Frontal interac-
tion each were significant predictors of memory performance if entered alone at this step,
R2 = 0.10, t(40) = 2.49, P < 0.01, and R2 = 0.08, t(27) = 2.22, P < 0.05, re-
spectively. Interaction terms involving Depression and EEG during the listen period were
not significant when entered on subsequent steps. Contrary to prediction, the Depression
× Right Frontal interaction when entered last did not significantly predict memory per-
formance for the sad narrative, R2 = 0.02, t(36) = −1.07, P < 0.15. Given that the
inclusion of 18 variables in this model limits the statistical power to detect an effect for
the last variables included in the model, an alternative model was tested by not includ-
ing the eight EEG variables on the second step. For this model, the critical Depression ×
Right Frontal interaction entered on the final step was significant, R2 = 0.05, t(43) =
−1.70, P < 0.05, indicating that low and high depression are accompanied by different
relationships between right frontal alpha during the sad narrative and subsequent memory
performance.
To examine the above significant interactions involving depression status and EEG alpha,
which are central to the hypotheses of this study, the low and high depression participants
were assessed separately. A similar hierarchical regression approach was employed with
Anxiety (Low, High) entered on the first step. As a direct test of Hertel’s (1994, 2000)
cognitive–initiative model, left and right frontal alpha during the preparation period were
added to the regression model after left and right parietal alpha during that period. The
low depression group showed an association between less alpha (more activity) frontally
and better memory performance, R2 = 0.23, F(2, 25) = 4.51, P < 0.01, whereas no
significant relationship was observed for participants reporting high levels of Depression,
R2 = 0.05, F(2, 17) = 0.79, P > 0.23 (see Table 2, Fig. 1). For the low depression
group, each frontal site contributed equivalently to the prediction of memory performance
when entered alone: left frontal, R2 = 0.21, t(26) = −2.90, P < 0.01, and right frontal,
R2 = 0.17, t(26) = −2.52, P < 0.01.
Alpha during the listen period was then added to the model to assess Heller and Nitschke’s
(1997) neuropsychological framework for cognitive biases in depression. Right frontal al-
pha during the listen period added on the final step (after left and right parietal and left
frontal alpha during listen and all four sites during preparation) resulted in no change for
the low depression participants, R2 = 0.00, t(21) = 0.12, P > 0.98, but produced a
further increment in variance explained among high depression participants, R2 = 0.18,
t(13) = −2.99, P < 0.01. As predicted for depression, less right frontal alpha (more ac-
J.B. Nitschke et al. / Biological Psychology 67 (2004) 125–143
Table 2
Hierarchical regressions for EEG prior to and during sad narrative predicting subsequent memory recognition for that narrative
Variable Low depression (n = 31) High depression (n = 23)
R2 R2 Test P R2 R2 Test P
1. Anxiety 0.000 F(1, 29) = 0.00 <1.00 0.425 F(1, 21) = 15.52 <0.002
EEG alpha during preparation period
2. Left and right parietal 0.151 F(2, 27) = 2.40 <0.12 0.015 F(2, 19) = 0.25 <0.79
3. Left and right frontal 0.225 F(2, 25) = 4.51 <0.02 0.047 F(2, 17) = 0.79 <0.24
EEG alpha during listen period
4. Left and right parietal 0.020 F(2, 23) = 0.37 <0.70 0.076 F(2, 15) = 1.30 <0.31
5. Left frontal 0.000 F(1, 22) = 0.00 <0.97 0.003 F(1, 14) = 0.08 <0.79
6. Right frontal 0.000 F(1, 21) = 0.00 <1.00 0.177 F(1, 13) = 8.91 <0.01
Full model 0.396 F(9, 21) = 1.53 <0.21 0.742 F(9, 13) = 4.15 <0.02
Note: Numbered rows (1–5) indicate the order in which variables were entered into the regression equations. Rows 3 and 6 provide tests of hypotheses, and therefore
corresponding probability levels are one-tailed. All other probability levels are two-tailed.
135
Fig. 1. Bilateral frontal activity (decreased alpha) during the preparation period preceding the sad narrative predicted
improved memory performance for that narrative in low depression but not high depression participants. All values
have parietal activity during the preparation period partialled out, consistent with the main regressions reported
in text. Regression slopes and individual participants’ values are plotted, and corresponding partial correlations
are shown. Filled squares are low anxiety participants. Open circles are high anxiety participants. Removing the
low depression outlier with the lowest memory score resulted in very similar results for the low depression group,
rp = −0.41, P < 0.02 (one-tailed).
tivity) while listening to the narrative was associated with better memory performance, as
illustrated in Fig. 2.
Supplemental analyses provided further support for the hypotheses. Similar hierarchical
regressions were conducted for alpha values averaging across left and right EEG sites. When
added to the model after bilateral parietal alpha, the averaged frontal alpha showed the same
Fig. 2. Right frontal activity (decreased alpha) during the sad narrative predicted improved memory performance
for that narrative in high depression but not low depression participants. All values have bilateral parietal and
frontal activity preceding the narrative and bilateral parietal and left frontal activity during the narrative partialled
out, consistent with the main regressions reported in text. Regression slopes and individual participants’ values
are plotted, and corresponding partial correlations are shown. Filled squares are low anxiety participants. Open
circles are high anxiety participants.
relationship mentioned above for low depression participants, R2 = 0.13, t(27) = −2.08,
P < 0.05, and again no significant relationship for high depression, R2 = 0.02, t(19) =
0.75, P > 0.46. The averaged frontal alpha during the listen period added on the final step
did not predict memory performance for either group, both P > 0.58.
Hierarchical regression models were also conducted on asymmetry scores predicting
memory performance for the sad narrative. For the low depression participants, the only
significant effect to emerge was for frontal asymmetry was during the preparation period
entered after anxiety status and parietal asymmetry during that period, R2 = 0.15, t(27) =
2.34, P < 0.05, indicating that the association between increased bilateral frontal activity
and better memory recognition is particularly pronounced on the left. Conversely, for the
high depression participants, the only effect observed for frontal asymmetry was during the
listen period entered on the final step of the model, R2 = 0.08, t(17) = −1.87, P < 0.05.
The direction of this effect is consistent with the above findings of more right frontal activity
predicting better memory performance for the high depression participants. Taken together,
these results indicate a bilateral frontal effect immediately prior to presentation of the nar-
rative as expected for Hertel’s (1994, 2000) model and additionally a unilateral right-sided
frontal effect while listening to the narrative as predicted by Heller and Nitschke (1997).
Follow-up analyses revealed that the results of the above regressions for the low depres-
sion group were equally strong for both the control and anxiety original groups, and neither
group showed a right frontal effect during the listen period. The effects for the high depres-
sion group were observed when the original mixed depression/anxiety group was analyzed
alone, but the n of 8 for the depression group was insufficient for the regression analyses
conducted. The specificity of the findings to depression was further assessed by dividing
the sample into a low and a high anxiety group. No frontal effects emerged for EEG during
the preparation period for either of the two omnibus models testing interactions of anxiety
status and EEG activity, P > 0.60. However, there was an effect for right frontal activity
during the listen period entered on the final step of the omnibus regression model includ-
ing the eight EEG variables on the second step, R2 = 0.06, t(36) = −1.95, P < 0.03
(one-tailed). This effect was largely driven by an association between right frontal activity
in response to the sad narrative and subsequent memory performance for that narrative in
the high anxious participants, R2 = 0.08, t(23) = −1.71, P < 0.06 (one-tailed), as
determined by separate regressions conducted for the low and high anxious participants as
done above for low and high depression participants.
The frontal effects observed for the sad narrative were not obtained for parietal sites or
the other three narratives (fearful, happy, and neutral). Analogous omnibus regressions with
parietal sites entered after the frontal sites resulted in no significant parietal effects during
the preparation or listen periods, all P > 0.26. Regression predicting memory performance
for each of the other three narratives revealed no frontal effects during either period, all
P > 0.23.
4. Discussion
This study builds on prior research examining cognitive correlates of depression by in-
vestigating brain mechanisms associated with two distinct cognitive abnormalities often
accompanying depression. EEG was collected immediately prior to and during the auditory
presentation of a sad narrative in a sample of college students with extreme levels (low and
high) of depression and anxiety. Bilateral activity recorded over the PFC during a prepara-
tory period immediately preceding the sad narrative was associated with better memory
performance in participants reporting low levels of depression but not in those with high
levels of depression. This finding is consistent with behavioral studies conducted by Hertel
and colleagues (for reviews, see Hertel, 1994, 2000) suggesting that depressed individuals
do not initiate task-relevant cognitive processes unless concrete strategies are provided. Cor-
roborating other research implicating the right PFC in withdrawal-related negative emotions
and threat perception, factors that may play a role in negative cognitive biases (Heller and
Nitschke, 1997; Nitschke and Heller, 2002), high depression participants showed an associ-
ation between right PFC activity when exposed to the sad narrative and improved subsequent
recognition of words used in that narrative. Although the experimental design employed
does not allow indisputable conclusions about the precise aspects of memory differentially
associated with distinct patterns of brain activity in low and high depression, these data are
consistent with previous research attributing these cognitive functions to the PFC (Heller
and Nitschke, 1997; Miller and Cohen, 2001; Nitschke and Heller, 2002) and investigating
the cognitive neuroscience of depression (Davidson et al., 2002; Heller and Nitschke, 1997).
Previous research on asymmetries in emotion and memory are germane to these data. As
alluded to above, the right PFC findings are highly consistent with prior studies investigating
various forms of withdrawal-related negative emotions (Davidson et al., 2002, 2003; Heller
and Nitschke, 1997; Nitschke and Heller, 2002). On the other hand, the bilateral frontal
effect supporting Hertel’s (1994, 2000) model was particularly pronounced on the left, as
indicated by the analysis on asymmetry scores. Such a pattern would be expected to the
extent that initiating cognitive strategies is approach-related (e.g., Davidson et al., 2003) or
involves verbal processing. In addition, the analyses for EEG data (regardless of memory
performance) replicated previous findings in the literature. During preparation for the sad
narrative, there was a trend for high depression subjects to show relatively less left than
right frontal activity compared to the low depression subjects (for review, see Davidson
et al., 2002). The finding of relatively more left than right activity in high than low anxi-
ety participants has been reported previously for this same sample subdivided differently
(Heller et al., 1997) and is consistent with findings for anxious apprehension (for review,
see Nitschke et al., 2000).
One model of episodic memory has accorded different memory-related functions to
the left and right PFC (Habib et al., 2003; Tulving et al., 1994), a position that has met
with considerable controversy (Fletcher and Henson, 2001; Lee et al., 2000; Owen, 2003;
Shallice, 2003; Simons and Spiers, 2003). Although it is feasible that the association between
right frontal EEG and memory in the high depression participants might be due to right
PFC involvement in episodic memory retrieval, as proposed in Tulving’s model, it seems
unlikely this would be more true for high than low depression participants. The differential
involvement of the left PFC in retrieving information from semantic memory and encoding
novel material is not a likely contributor to the finding of greater left than right activity since
that was observed during the preparation period prior to the presentation of material to be
encoded or retrieved. Furthermore, it is important to note that their model is largely based
on earlier PET studies, none of which employed a rigorous test of asymmetry (Davidson
and Irwin, 1999). Taken together, the asymmetry findings are most consistent with previous
work on the neural correlates of emotion.
The study design afforded the possibility of testing the specificity of the findings in several
respects. First, the predicted associations between brain activity and memory performance
were restricted to the sad narrative. This was expected for the right PFC findings indicative of
a negative memory bias, because of the relevance of sadness to depression. We predicted that
the bilateral PFC effect, however, would be seen in preparation for all narratives. The poorer
memory performance for the other three narratives may explain why the effect was not also
observed for them. Second, careful measurement of anxiety revealed that the results obtained
for depression could not be explained by co-occurrence with anxiety. Although there was a
right frontal effect observed across participants reporting high levels of anxiety, that effect
was carried by the subset of participants also showing high depression. Third, with regard
to the specificity of the effects to the sites over the PFC, analyses revealed no significant
results for parietal sites. Further claims about spatial localization are not possible due to the
limited number of electrode sites sampled. For example, the EEG methods employed were
not able to differentiate between sectors of the right PFC subserving cognitive–initiative and
memory bias functions. Finally, these findings point to an important temporal distinction
between the two cognitive abnormalities assessed, with the putative cognitive–initiative
deficit associated with bilateral PFC hypoactivity immediately preceding the narrative and
the negative memory bias related to right PFC hyperactivity during the narrative.
The observed associations between brain activity and subsequent memory performance is
consistent with two seemingly conflicting literatures, one documenting memory deficits in
depression and the other reporting better memory performance for negative material. Those
studies finding memory deficits in depressed samples have either not used negative stimuli
or have not systematically assessed the emotional content of the material tested. The present
study provides a neurocognitive account for why memory performance in depression might
be impaired in some circumstances and enhanced in others. Furthermore, the confluence
of the cognitive–initiative deficit producing memory impairment and the negative memory
bias producing selective memory enhancement may result in no apparent memory effects
in depressed individuals under certain circumstances. In line with this position, there was
some indication of a memory deficit in depression across all four narratives, but only in the
small sample of depressed participants reporting low anxiety.
This initial study on the brain instantiation of cognitive–initiative and memory bias abnor-
malities points to a number of future research directions. One limitation of the current study
is that it did not include an experimental manipulation or behavioral measure of strategy
initiation or utilization (Gershberg and Shimamura, 1995; Hertel, 1994, 1997, 2000; Incisa
della Rocchetta and Milner, 1993). Second, selecting narratives or other stimuli eliciting
comparable levels of memory performance across emotion categories will be important
in assessing the relative contributions of the cognitive–initiative deficit and the negative
memory bias to memory performance in depression. Finally, other physiological recording
methods such as dense-array EEG using source localization tools or hemodynamic neu-
roimaging methodologies will be important in distinguishing the specific sectors of the
PFC contributing to the cognitive–initiative deficit and to the negative memory bias.
This study investigated neural mechanisms that may account for the behavioral data
supporting Hertel’s (1994, 2000) model of memory performance in depression. Present
findings support that model and suggest that the failure to recruit the PFC in preparation
for information processing may result in poorer performance on memory tasks. In addition,
these data support Heller and Nitschke’s (1997) claim that recruiting the right PFC under
conditions of negative emotion or threat may be associated with better memory performance.
These results highlight the importance of distinguishing different processes influencing
memory performance when investigating the neural mechanisms of cognitive deficit and
bias in depression.
Acknowledgements
The authors wish to thank E. Keolani Taitano and Tara Cecola for their help in collecting
these data and Krystal Cleven, Kristen Mackiewicz, Alissa Possin, and Emily Seidler for
assistance with manuscript preparation. This research was supported by NIH grants R21
DA14111, R01 MH39628, R03 MH52079, and R01 MH61358 and a University of Illinois
Research Board Award. JBN was also supported by K08 MH63984, T32 MH14257 (Larry
Jones, Director), T32 MH18931 (Richard J. Davidson, Director), and a HealthEmotions
Research Institute Fellowship. WH was also supported by MH19664. A portion of this
work contributed to the dissertation of MAE.
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Relative left-frontal activity is associated with

increased depression in high reassurance-seekers
Jennifer A. Minnix∗ , John P. Kline, Ginette C. Blackhart,
Jeremy W. Pettit, Marisol Perez, Thomas E. Joiner
Department of Psychology, Florida State University, Tallahassee, FL 32306-1270, USA
Abstract
Excessive reassurance-seeking, which has been associated with depression in many studies, can be
defined as the relatively stable tendency to seek assurance perseveratively from others. We hypothe-
sized that although depression has been associated with left-frontal EEG hypoactivity, reassurance-
seekers may possess a unique diathesis that is more likely to be associated with increased left-frontal
activity. Data were collected from 12 volunteers who were receiving therapeutic services from a
University Clinic. EEG asymmetry scores were averaged over two measurement occasions at least
3 weeks apart. As predicted, stable relative right-frontal activity was associated with increased de-
pression in those who were low on reassurance-seeking, while stable relative left-frontal activity was
associated with increased depression among high reassurance-seekers. Perhaps those who seek reas-
surance excessively do so because of their inability to alter their behavior even when environmental
cues are no longer reinforcing, which can maintain or exacerbate their depressive symptoms.
Keywords: Depression; EEG; Reassurance-seeking; Interpersonal style
1. Introduction
Depression research has focused on a range of possible diatheses that run the gamut from
the biological to the interpersonal. The present study provides a possible avenue toward a
rapprochement between two heretofore-separate literatures on interpersonal and biological
vulnerabilities namely, excessive reassurance-seeking and asymmetrical frontal lobe activ-
ity. Frijda (1986) contends that emotions are outcomes of the process of assessing the world
∗ Corresponding author. Tel.: +1-850-321-3298.

E-mail address: minnix@psy.fsu.edu (J.A. Minnix).
doi:10.1016/j.biopsycho.2004.03.005
146 J.A. Minnix et al. / Biological Psychology 67 (2004) 145–155
in terms of one’s own goals that, in turn, modify behavioral tendencies. Because of the im-
portance of the frontal lobes for the expression and regulation of both emotional and social
behavior, the integration of these separate lines of research provides a possible means for
the explanation of previous discrepancies in the literature on frontal asymmetry/depression
relations.
1.1. Reassurance-seeking and depression
With Coyne’s (1976) interactional description of depression as a starting point, Joiner

and coworkers have theorized that depression-prone individuals display interpersonal be-
haviors that increase their vulnerability to future depression (Joiner, 2000; Joiner and
Metalsky, 2001). Specifically, these individuals are more likely to engage in excessive
reassurance-seeking, or perseverative attempts to elicit feedback from others to assure them
that they are cared for and loved. Although this information is affectively pleasing, it con-
flicts with the individuals’ negative self-views and leads them to doubt the veracity of the
information (Swann et al., 1987; Joiner et al., 1993; Joiner and Metalsky, 1995). Conse-
quently, this doubt compels them again to seek reassurance from others and results in a
downward interpersonal spiral, including interpersonal rejection (Joiner et al., 1992), ‘con-
tagious depression’ (Joiner, 1994), and exacerbated depression (Joiner and Metalsky, 2001;
Joiner et al., 2001).
Accordingly, excessive reassurance-seeking can be defined as the relatively stable ten-
dency to seek assurance persistently from others that one is loved, regardless of how many
times these assurances have already been provided (Joiner et al., 1999). Studies have shown
reassurance-seeking to be a cohesive, valid, and reliable factor that is relatively specific to
depression and relatively distinct from other aspects of interpersonal style (such as general
dependency or doubt in others’ sincerity; Joiner and Metalsky, 2001). Multiple studies have
demonstrated a reliable association (median value of 0.36) between reassurance-seeking
and depression in a variety of samples, including college students, US Air Force cadets,
various clinical samples, and women in heterosexual dating relationships (see Joiner et al.,
1999; Katz and Joiner, 2001, for a review). At least six studies have demonstrated that ex-
cessive reassurance-seeking is a contributory cause to depression (Katz and Joiner, 2001).
Studies based on the diathesis-stress model have shown that excessive reassurance-seeking
and stress serve as interactive, contributory causes to the later development of depressive
symptoms (Joiner and Metalsky, 1995; Katz et al., 1998).
Habitual and excessive reassurance-seeking creates many problems in the interpersonal
world of depressed individuals (Pothoff et al., 1995). Because reassurance-seeking initially
elicits positive feedback from others, it is not inherently a maladaptive behavior. It is only
because some depressed individuals continue to solicit this feedback when it is clearly
creating difficulties within their interpersonal relationships that it becomes problematic. It
is possible that the negative consequences of excessive reassurance-seeking are secondary
in importance to the immediate relief experienced by the depressed individual when he/she
receives this reassurance, particularly if the depressed individual is convinced that this
behavior is necessary to provide relief. In these situations, the negative consequences may
be dismissed altogether (Schmidt et al., 1999). In essence, these persons neglect to regulate
their own behavior in response to external social cues that typically guide social interactions
J.A. Minnix et al. / Biological Psychology 67 (2004) 145–155 147
(Hamilton and Deemer, 1999). They fail to adapt their behaviors based on environmental
contingencies, which may lead to a perseverative questioning of others that ultimately leads
to rejection and may maintain their depressive symptoms (Joiner et al., 1999). Biological
factors have also been related to an increased vulnerability for the presence and maintenance
of depressive symptoms.
1.2. Frontal asymmetry and depression
Asymmetrical activity in the frontal lobes of the brain has been related to emotional and
motivational factors, as well as cognitive and behavioral ones. It has been hypothesized
that relative left-frontal activity is related to behavioral approach motivation and positive
emotion, whereas the right-frontal region is related to behavioral withdrawal motivation
and negative emotion (Davidson, 1995; Davidson et al., 2000). Positive, approach-related
emotion, is typically associated with relative left-frontal and anterior-temporal activity,
while negative, withdrawal-related emotion has been associated with higher relative activity
of the right-frontal and anterior-temporal regions (Ahern and Schwartz, 1985; Davidson,
1995; Harmon-Jones and Allen, 1997; Heller, 1990; Tomarken et al., 1990). However,
evidence for these relations is not always consistent (Hagemann et al., 1998, 1999).
Several studies have found that depression is associated with less left-frontal activity
and/or more right-frontal activity (Bell et al., 1998; Gotlib et al., 1998; Henriques and
Davidson, 1991; Roemer et al., 1992). Resting anterior asymmetry has been reported to
distinguish depressed from non-depressed individuals during both episodes and remission
(Allen et al., 1993; Bell et al., 1998; Henriques and Davidson, 1991), although some evidence
for this finding is inconsistent. For example, Reid et al. (1998) largely failed to replicate
these previous studies finding decreased left-frontal activity in depressed individuals relative
to non-depressed controls across two samples, suggesting the need to identify intervening
factors. The asymmetry model may have difficulty accounting for emotions that potentially
involve both withdrawal and approach-related strategies, such as anger or sadness. For
example, sadness can evoke an approach strategy geared towards retrieving a lost object as
well as a withdrawal strategy reflecting the desire to escape from the noxious environment,
depending on the context (see Shackman, 2000). As such, there may be factors involved
that predict which kinds of strategies individuals may employ.
1.3. Frontal lobe damage and social behavior
The frontal lobes of the brain seem to facilitate the ability to navigate a complex social
landscape, and are responsible for action selection based on internal and external cues (Kolb
and Whishaw, 1995; Kolb and Taylor, 1999). Studies have shown that the frontal cortex
plays an important role in the regulation of arousal with respect to behavioral demands
(Tucker et al., 1995; Stuss et al., 2000). Because emotions are directly tied into reinforc-
ing and punishing events, a failure to respond to changing environmental cues may lead
to inappropriate social and emotional behavior (Rolls et al., 1994). Patients with frontal
lobe damage seem to have difficulty using feedback from environmental cues to change or
regulate their behavior, such that they are impaired at developing novel strategies to deal
with problems (Kolb and Whishaw, 1995). Patients with frontal lobe lesions seem to be
unable to alter their behavior based on changes in previously learned associations between
environmental stimuli and rewards (Rolls et al., 1994). Perseveration errors, or errors re-
sulting from the failure to modify behavior based on changes in environmental cues, are
relatively specific to frontal lobe damage. In addition, research suggests that these types
of errors may be more common in patients with right-frontal lobe lesions than those with
left-frontal lobe lesions (Haut et al., 1996; Stuss et al., 2000).
Similar to patients with right-frontal lesions, those who seek reassurance excessively
may do so because of an inability to alter their behavior even when environmental cues are
no longer reinforcing. However, this is not to imply that those high in reassurance-seeking
behaviors also evince frontal lobe damage. Rather, the research involving patients with
frontal lobe damage serves to implicate a particular area in the cortex that might reflect a
tendency towards certain behaviors in ‘normal’ individuals similar in nature, though not
as severe, to those with lesions in the area. Specifically, when their reassurance-seeking
behaviors fail to provide desired positive feedback, and instead lead to interpersonal rejec-
tion, high reassurance-seekers continue to persist in seeking this feedback. This behavior
may ultimately lead to rejection of the depressed individual and an increase in depressive
symptoms.
1.4. Summary and hypotheses
Based on research regarding reassurance-seeking and depression, one might expect that
reassurance-seeking will moderate the relation between frontal brain asymmetry and depres-
sion. Individuals who seek reassurance excessively may behave in a perseverative manner,
much like what is seen in patients with right-frontal lesions. This hypothesis is consistent
with the motivational model in that proactively seeking feedback from the environment
can be considered an ‘approach’ behavior. It is possible that reassurance-seeking repre-
sents a unique diathesis for developing depressive symptoms, reflected in frontal brain
wave patterns, that is inherently different from the diathesis usually associated with relative
left-frontal hypoactivity.
Accordingly, we predicted that reassurance-seeking moderates the relation between de-
pression and frontal asymmetry, such that, in low reassurance-seekers, the usual pattern is
found (i.e. relative right-frontal activity is associated with increased depression), but that in
high reassurance-seekers, the opposite pattern is found (i.e. relative left-frontal activity is
associated with increased depression).
2. Method
2.1. Participants
Data were collected from 12 (six males, six females) right-handed volunteers aged 19–52
(M = 32, S.D. = 14.47) who were receiving therapeutic services from the Psychology
Clinic at Florida State University. Upon application, patients agreed in writing to the re-
search and training nature of the clinic; in addition, they signed a separate and additional
informed consent form for this study. Diagnoses were formulated by a trained clinician
through a combination of symptom measures and a clinical interview, based on the Diag-
nostic and Statistical Manual of Mental Disorders (4th edition, 1994). This sample included
individuals who experienced substantial depressive symptoms (mean Beck Depression In-
ventory (BDI) score was 23.5); diagnoses were Dysthymic Disorder (3), Major Depression
(2), Social Phobia (3), and Bipolar I Disorder (1), depressed phase. Three individuals had
no diagnosable Axis I mood or anxiety disorder. Co-morbid diagnoses included Alcohol
Abuse (2) and Bulimia Nervosa (1). All indices were averaged across two measurement
occasions approximately 4 weeks apart (M = 4.25, S.D. = 1.42).
2.2. Questionnaire administration and scoring
Participants completed all questionnaires prior to EEG recording. Handedness was as-
sessed with the Edinburgh Handedness Inventory (Oldfield, 1971). Level of depressive
symptoms was assessed using the Beck Depression Inventory, a 21-item self-report in-
ventory (Beck et al., 1961). Coefficient alphas (Cronbach, 1951) of 0.80 and above have
been reported for this measure when used with a variety of clinical and other samples (Beck
et al., 1988). A subscale of the Depressive Interpersonal Relationships Inventory (DIRI-RS;
Joiner et al., 1992) was used to assess excessive reassurance-seeking. This four-item sub-
scale (DIRI-RS) measures the tendency to seek reassurance excessively from others as to
whether they ‘truly’ care. Each item is rated on a seven-point Likert scale and averaged
across items. Coefficient alpha of 0.88 has been reported for this subscale (Joiner et al.,
1992). Scores from the BDI and DIRI-RS were averaged across both measurement sessions
for each participant.
2.3. EEG recording and quantification
Resting EEG was recorded with a stretch-lycra electrode cap (Electrocap International,
Eaton, OH) from a standard International 10–20 system of 19 channels referenced to linked
ears. Data collection and reduction were accomplished with Neurolex software, and a
Neurosearch 24C (Lexicor, Boulder, CO). Electrolytic gel was applied and each site gen-
tly abraded until impedances were below 10 k. Homologous leads (EEG and auricular
leads) were within 1 k of each other. EEG records were visually examined for artifact
by a trained technician, and epochs containing bioelectric artifact in any channel were
rejected.
Data were digitized on-line at 256 Hz (60 Hz notch filter enabled) during 60-s baselines:
three with eyes open and three with eyes closed. High-pass filters were set at 2 Hz, and had
a rolloff of 6 dB per octave (first order), while low-pass filters set at 64 Hz had a rolloff of
48 dB per octave (eighth order). Artifact-free epochs of 256 samples (i.e. 1-s epochs for
256 Hz) were extracted through a Hanning window and submitted to fast Fourier trans-
form. Average alpha (8–13 Hz) power (microvolts squared) was natural log transformed
for normalization, as these power values tend to be positively skewed. Asymmetry scores
were computed (log[right] − log[left]), with higher values indicating relative left-frontal
activity, for mid-frontal (F4-F3), frontal pole (Fp2-Fp1), lateral-frontal (F8-F7), central
(C4-C3), anterior-temporal (T4-T3), posterior-temporal (T6-T5), parietal (P4-P3), and oc-
cipital (O2-O1) homologous pairs.
2.4. Design and analysis
Reassurance-seeking scores (DIRI), BDI scores, and asymmetry scores were averaged
across both sessions. A general linear model analysis was used to test the hypothesis that
reassurance-seeking scores would moderate the relation between depression and anterior
asymmetry, using continuous measures of DIRI, BDI, and asymmetry. As a follow-up
procedure, a BDI × DIRI analysis of variance (ANOVA) was conducted for each of the
anterior sites found to be significantly related to BDI and DIRI in the general linear model
analysis. High and low BDI and DIRI groups were formed for the ANOVA analysis using a
median split. To assess specificity to the frontal region, posterior sites were also tested using
a general linear model analysis with continuous measures. Because of the small sample size
and lack of power, a multivariate analysis of variance (MANOVA) would have provided an
unacceptable Type II error rate.
3. Results
Means and standard deviations for each of the dependent measures are as follows. F4-F3
time 1: −0.03 (0.14), F4-F3 time 2: −0.02 (0.20), F8-F7 time 1: −0.09 (0.23), and F8-F7
time 2: −0.19 (0.10). Descriptive statistics for the independent measures are presented in
Table 1. BDI and DIRI were not significantly correlated in this sample, although the mag-
nitude and direction of the observed relation in the depressed individuals was comparable
to that which has been observed in previous samples (r = 0.31), suggesting that the present
sample was too small to have the power to detect this relation.
Continuous analyses revealed that main effects of BDI, F(1, 8) = 7.55, P < 0.05, and
DIRI, F(1, 8) = 12.47, P < 0.01 were found at F4-F3 as well as F8-F7: BDI, F(1, 8) =
10.42, P < 0.05; DIRI, F(1, 8) = 12.46, P = 0.01. A significant BDI × DIRI inter-
action emerged for the two frontal sites: F4-F3, F(1, 8) = 11.45, P = 0.01 and F8-F7,
F(1, 8) = 16.83, P < 0.01. As predicted, there were no main or interaction effects for
C4-C3, F(1, 8) = 1.65, P > 0.2; T4-T3, F(1, 8) = 3.65, P = 0.09; T6-T5, F(1, 8) =
0.196, P > 0.6; or P4-P3, F(1, 8) = 0.073, P > 0.7, suggesting that the effects found were
specific to frontal sites. In addition, no significant difference in asymmetry as a function
of diagnostic group was found (i.e. Mood Disorder, Anxiety Disorder, or Other) at F4-F3,
F(2, 9) = 0.89, P > 0.4; F8-F7, F(2, 9) = 1.54, P > 0.2; or T4-T3, F(2, 9) = 4.19,
P < 0.06.
In order to investigate the nature of the interaction, participants were divided into high
and low BDI groups (high > 24, M = 27.8; low < 24, M = 12.8) and high and low
Table 1
Distributions of independent measures across both sessions
M S.D. Range Skewness Kurtosis
BDI 23.5 13.3 38 0.023 −1.3

DIRI 11.0 6.2 18 0.60 −0.96
Fig. 1. Interactive effects of high/low depressive symptoms (BDI) and high/low reassurance-seeking (DIRI) on
frontal asymmetry at mid-frontal and lateral-frontal sites.
DIRI groups (high > 9, M = 15.7; low > 9, M = 10) using median splits. Those in-
dividuals with high DIRI scores and high BDI scores were more likely to be relatively
left-frontally active at F8-F7 and F4-F3, while those with high BDI scores and low DIRI
scores were more likely to be relatively right-frontally active F(2, 7) = 16.20, P = 0.001)
(see Fig. 1).
4. Discussion
As was predicted, results showed that reassurance-seeking moderated the relation be-
tween depressive symptoms and anterior asymmetry at two anterior sites: mid-frontal and
lateral-frontal. This relationship was such that depressive symptoms were related to less left
relative to right-frontal activity in low reassurance-seekers, while depression was related
to greater left relative to right-anterior activity in high reassurance-seekers. These results
suggest that reassurance-seeking and relative left-frontal hypoactivation may constitute sep-
arate diatheses for developing depressive symptoms in a clinic population, as both have been
reliably related to depression in the past (Gotlib et al., 1998; Joiner and Metalsky, 2001).
Lane et al. (1999) (p. 3) suggest that emotion can be conceptualized as “the outcome
of an evaluation of the extent to which one’s goals are being met in interaction with the
environment.” Individuals who engage in reassurance-seeking presumably take an ‘active’
role in the maintenance of their depressive symptoms, such that they are motivated by their
desire for assurance to interact with the environment in ways that eventually backfire.Studies
have shown that some depressed individuals generate distress within their environments
(Davila et al., 1995; Hammen, 1991) that can exacerbate their symptoms. Specifically,
studies suggest that many of the interpersonal stressors in the lives of depressed individuals
are not accidental events, but rather, self-generated consequences of a depressive lifestyle
(Pothoff et al., 1995). Similar behavior patterns, though to a much greater degree, have
been documented in patients who have lesions in their right-frontal lobes. These patients
often fail to respond appropriately to environmental demands (Stuss et al., 2000). In addi-
tion, this behavior is consistent with the motivational model of frontal asymmetry, which
relates ‘approach’ behaviors to relative left-frontal activation and ‘withdrawal’ behaviors
to right-frontal activation (see Davidson, 1995). Reassurance-seeking can be considered
an approach behavior, which is consistent with the current findings that found a relation
between depression and left-frontal activation in these individuals. These individuals may
represent a potential caveat of the Davidson (1995) model, namely, that left-frontal activity
may not be beneficial in every context. Here, if relative left-frontal activation reflects the
‘approach’ motivation associated with reassurance-seeking, it can actually enable folks to
facilitate the maintenance of their own depressive symptomatology.
Though these results suggest an interesting relation between frontal asymmetry, depres-
sion, and reassurance-seeking, the nature of the interactions between these variables needs
further exploration. In this study, baseline EEG was recorded using a linked-ears montage,
though some research suggests that this strategy may be problematic (Hagemann et al.,
2001). However, other studies have reported that linked-ear references made no signifi-
cant difference in measured asymmetries (Senulis and Davidson, 1989). In addition, the
measurement of electrical activity from the scalp does not allow for the kind of spatial
resolution that is necessary to make distinctions between frontal subregions. The current
sample was taken from a clinic population and measured across two separate occasions
separated by at least 3 weeks. However, the sample size was small and included multiple
diagnostic categories (although the average depressive symptom score was substantial).
Accordingly, the participants also differed in their individual medication status, both in
type and amount prescribed. In addition, the participants varied in the amount of therapy
they had received, both from the clinic and in the past. Because of the small sample size,
we lacked the statistical power needed to conduct a more comprehensive analysis of the
boundary conditions of the observed effect. Because there was no comparison group, the
results do not provide enough information to conclude that the effects found in the study
are specific to individuals experiencing relatively serious psychopathological symptoms.
This study represents a modest test of a potentially important concept. Though the results
should be considered with appropriate caution, they serve as a starting point for interesting
future research and a better understanding of the complex relationships between biological
function, social behavior, and psychopathology.
Despite these points of consideration, this study provides a potential extension to cur-
rent theories of frontal asymmetry and depression by framing these relations from within
an interpersonal context. Future research might examine such interpersonal moderators of
frontal asymmetry/emotion relations in non-clinical samples, as well as within more homo-
geneous diagnostic categories within clinical populations. Dismantling the nature of these
relations may help to explain some past inconsistencies in the frontal asymmetry/depression
literature (Reid et al., 1998), as well as elucidate further some of the multiple factors that
contribute to depression and its harmful effects on the lives of many.
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Methodology
Individual differences in anterior EEG asymmetry:
methodological problems and solutions
Dirk Hagemann∗
Department of Psychology, Fachbereich I—Psychologie, Universität Trier,
Universitätsring 15, 54286 Trier, Germany
Abstract
In the last two decades, a substantive body of empirical work investigated the association between
individual differences of electroencephalogram (EEG) alpha asymmetry and affective/motivational
dispositions. Recent work indicated that several methodological problems persist in this field. The
present paper reviews these problems with a focus on the reliability and validity of measures of anterior
resting EEG asymmetry, which serve as a proxy for trait-like asymmetries of cortical activity. These
issues include the treatment of ocular and muscle artifacts, the choice of the EEG reference, the use of
current source density (CSD) measures, the state–trait nature of resting asymmetry, and the treatment
of state-like fluctuations of the measures. In addition, the statistical problem of inflated type-I error due
to multiple testing is also considered and different approaches to counteract this problem are suggested.
Keywords: Frontal EEG asymmetry; Emotion; Methodology
1. Introduction
More than two decades ago, several researchers started to investigate electroencephalo-
gram (EEG) asymmetry during emotional states (Davidson and Fox, 1982; Davidson and
Schwartz, 1976; Harman and Ray, 1977; Tucker et al., 1981). A few years later, some studies
began to investigate the relationship between individual differences in resting asymmetry
and affective dispositions (Davidson and Fox, 1989; Schaffer et al., 1983). This research led
to the proposal that frontal EEG asymmetry in a resting state reflects a trait-like asymmetry
of anterior cortical activity, which acts as a diathesis for emotion-elicitors and is a contrib-
∗ Tel.: +49-651-201-2896; fax: +49-651-201-3956.

E-mail address: hagemann@uni-trier.de (D. Hagemann).
doi:10.1016/j.biopsycho.2004.03.006
158 D. Hagemann / Biological Psychology 67 (2004) 157–182
utory factor for individual differences in affective/motivational behaviors (e.g. Davidson,

1992, 1998b).
This hypothesis stimulated empirical research in several laboratories. In the typical study,
the spontaneous EEG in a resting state is recorded, the difference of alpha activity at con-
tralateral homologous sites serves as a measure of anterior asymmetry of cortical activity,
facets of affective style are measured with experimental procedures or questionnaires, and
the statistical analysis is focused on the associations between asymmetry and affect (e.g.
Hagemann et al., 1999; Harmon-Jones and Allen, 1998; Kline et al., 2001; Nitschke et al.,
1999; Tomarken et al., 1990). Many findings supported the hypothesis (for recent reviews,
see Coan and Allen, 2003b; Davidson, 1998a; Hagemann et al., 2002), but several au-
thors noted substantial inconsistencies in the evidence (Hagemann et al., 1998; Heller and
Nitschke, 1998; Reid et al., 1998). Recently, this situation stimulated a search for method-
ological factors that may contribute to the divergence of findings (Blackhart et al., 2002;
Davidson, 1998b; Hagemann et al., 1998; Reid et al., 1998). The present review gives an
overview of some of the methodological obstacles that persist in this field of research and
will suggest some prospective solutions.
2. EEG recording
The first step in each study is the recording of the resting EEG. In addition to the general
issues like appropriate electrode placement, filter settings, AD rate, and the like (for recom-
mendations, see Pivik et al., 1993), one important factor may be the length of the recording
in order to obtain reliable asymmetry measures. Some studies showed that alpha power at
single sites shows acceptable reliability estimates even for EEG segments as short as 20 or
30 s (Gasser et al., 1985, reported annual retest correlations of 0.70/0.80 for EEG segments
of 20 s length; Hagemann et al., 1998, reported parallel test correlations of 0.80/0.90 for
EEG segments of 30 s length). However, this observation may not generalize to asymmetry
measures, because difference scores are less reliable than their constituent scores (especially
if the constituent scores are correlated; see Cohen and Cohen, 1983). Several studies inves-
tigated the reliability of EEG asymmetry in a resting state. Hagemann et al. (1998) analyzed
the effect of resting EEG length on the reliability of asymmetry measures. They reported
that the reliability was low for a database of 30 s (with parallel test correlations of about
0.50), good for a database of 4 min (with Cronbach’s alpha in a range of 0.80/0.90), and
excellent for a database of 8 min (with most Cronbach’s alphas in the 0.90 s). Other studies
reported on similar reliability estimates for a database of 8 min (Reid et al., 1998; Sutton and
Davidson, 1997; Tomarken et al., 1992). In a recent study, Hagemann et al. (2002) reported
on an excellent reliability for a database of 12 min (estimated with a combined parallel and
retest approach via structural equation modeling (SEM), reliability coefficients were close
to 1). To sum up, good reliability of the asymmetry measure in a resting state can only be
achieved if the EEG is recorded for a sufficient length in time (e.g. at least 4 min). However,
it is not known at present if these reliability estimates, and the respective recommendation
for EEG recording, can be generalized to affective and motivational states.
Another factor that might be suspected to affect the asymmetry measures is the instruction
to keep the eyes open or closed while the resting EEG is recorded. However, several studies
D. Hagemann / Biological Psychology 67 (2004) 157–182 159
could consistently demonstrate excellent internal consistencies of EEG baselines that were
recorded with subjects keeping their eyes open and closed, irrespective of EEG references
such as Cz, A1 + A2, and average reference (AR) (Hagemann et al., 1998; Reid et al.,
1998; Sutton and Davidson, 1997; Tomarken et al., 1992). Thus, this procedural factor is
not likely to affect individual differences of resting asymmetry in a substantive size.
3. EEG artifacts
After the recording of the EEG, the next analysis step is usually the rejection of/correction
for artifacts in the EEG to ensure a compelling interpretation of the data (e.g. Gevins,
1987). Several technical artifacts (e.g. the electrode-pop artifact, lead sway artifact, electro
smog) may be effectively prevented with adequate care in the EEG laboratory (e.g. use
of appropriate electrode/electrolyte combinations, fixation of the leads, shielding of the
subject; see Barlow, 1986).1 Biological artifacts and in particular ocular and muscle artifacts,
however, may pose a serious problem.
Spontaneous movements of the eyes and blinks generate potentials that are conducted to
the scalp where they may produce large distortions in the EEG, which are the ocular artifacts
(see Elbert et al., 1985 for details). Unfortunately, these distorting effects are greatest at
the anterior sites, which is the region of interest in frontal asymmetry research. In a recent
study, Hagemann and Naumann (2001) analyzed the effects of ocular activity on the EOG
and the (lateralized) EEG alpha activity in a resting state while subjects were allowed for
spontaneous eye movements. One crucial finding was that in the EOG, blinks and eye
movements may generate substantial power in the alpha and even the beta range. However,
if no blinks and eye movements are present, then alpha power in the EOG appears to be
primarily of neural origin. Moreover, there were significant general effects of ocular artifacts
on anterior EEG alpha activity (i.e. mean shifts due to artifacts). Ocular activity produced
a bilateral increase of mean anterior EEG alpha, which was accompanied by asymmetrical
distortions, in particular at frontopolar and midfrontal sites where the effect sizes were
largest. However, there were almost no differential effects of ocular artifacts (i.e. no shifts
of individuals in the sample distribution of asymmetry due to artifacts, with the exception
of frontopolar asymmetry). For example, midfrontal asymmetry measures that were based
on data portions that were selected for the absence of ocular artifacts (artifact-free EEG) or
that were not screened for ocular artifacts (uncorrected EEG) showed correlations of 0.82
and 0.95 (for eyes closed and eyes open, respectively). Taken together, ocular activity may
generate substantial power in the alpha range, which may distort mean anterior EEG alpha
asymmetry, and thus, may mimic general asymmetries of cortical activity; however, ocular
artifacts hardly effect measures of individual differences of alpha asymmetry.
1 Electrode-pop artifacts result from sudden changes in the DC potential between electrode and skin, and have
a typical waveform with a sharp rise and an exponential decay (similar to a calibration waveform). Lead sway
artifacts result from movements of the leads that connect the electrodes and the (pre-) amplifier, and show slow
waves. Electro smog refers to electromagnetic pollution due to AC power cables, lights, transformers, radio and
television transmitters, and cellular phones, and may result in peak-like artifacts in the power spectrum. For details
on technical artifacts, see Barlow (1986), and the literature cited there.
These findings may have some implications for the treatment of ocular artifacts in asym-
metry research. One common procedure to control for ocular artifacts is the rejection of
EEG segments that show contamination with ocular activity (for an overview, see Barlow,
1986). If the identification of the artifacts is based on visual inspection, the method has
the disadvantages that the criteria to classify the artifacts are somewhat subjective and that
the procedure is time consuming. However, one advantage of this approach is that other
types of artifacts (muscle, drift, technical artifacts) may be readily rejected as well. If the
identification of the artifacts is done in an automatic fashion based on quantitative thresh-
olds (such as amplitude or variance criteria of the EOG), however, the setting of thresholds
is somewhat arbitrary, different subjects may show different artifact amplitudes, and thus,
may need individually matched thresholds, and other types of artifacts may be missed.
On the other side, this method can be very time effective. Taken together, the problem
of identifying artifacts with subjective criteria or quantitative thresholds may constitute
one major disadvantage of the rejection approach, and both methods have the additional
disadvantage that contaminated data are lost, small artifacts may be missed, and that the
accepted data portions are biased towards a brain state that is associated with low visual
activity. However, the findings of Hagemann and Naumann (2001) suggest that these lim-
itations may be of lesser concern for resting asymmetry research. As noted above, there
were hardly differential effects of ocular artifacts on the alpha asymmetry in a resting
state, which suggests that even considerable differences in the criteria used to identify the
artifacts would result in psychometrically parallel asymmetry measures. Thus, the specifi-
cation of rejection criteria and even minor ocular artifacts would hardly affect the outcome
of a study.
In another approach, ocular activity is removed from the EEG with a regression proce-
dure (for a general overview, see Gratton, 1998). In principle, the actual EEG time series
is regressed on the EOG time series, and the resulting residual time series represent a new
EEG from which the influence of the ocular activity is statistically removed (for a review
of several types of this approach, see Brunia et al., 1989). This method has the great ad-
vantages that is does not rely on subjective criteria or arbitrarily selected thresholds for
rejection, it does not discard EEG data in particular if ocular activity is induced by the
very task of interest (such as in visual tasks), and it can be performed automatically, and
is thus, time efficient. However, one major disadvantage of the method is that its valid-
ity depends crucially on the assumption that there is no brain activity in the EOG data,
or otherwise these procedures would give biased results, and thus, introduce a secondary
artifact (e.g. Berg, 1989; Berg and Scherg, 1994; Gratton and Coles, 1989; Pham, 1989).
Unfortunately, there is ample evidence for the presence of neural alpha activity in the EOG,
in particular when gross eye movements and blinks are absent. For example when ana-
lyzing data portions that were selected for the absence of ocular activity, Hagemann and
Naumann (2001) observed a protuberance in the EOG alpha band that corresponded to
the EEG alpha peak (this finding corroborates results of Iacono and Lykken, 1981, who
demonstrated that alpha activity of neural origin can be seen in the EOG). Moreover, there
was a correlation between EOG alpha power and occipital alpha power of r = 0.42, which
also suggests a neural origin of the EOG alpha protuberance (this finding corroborates
results of Gasser et al., 1985; Möcks et al., 1989; van Driel et al., 1989, and others; see
Hagemann and Naumann, 2001). Therefore, the regression approach of artifact removal is
in the danger of removing also anterior alpha activity, which is of course the very activity of
interest.2
In a very recent study, Barz (2003) investigated whether different methods for the removal
of ocular artifacts would yield different topographies of alpha activity in a resting state. In
particular, she compared the rejection procedure and the Gratton and Coles (1989) regression
method, and observed a significant reduction of anterior alpha due to the regression. This
finding is consistent with the presumed disadvantage of the latter method. However, this
decrease of alpha did not effect individual differences in frontal resting asymmetry. The
correlation of midfrontal asymmetry measures between both methods was r = 0.97. This
preliminary finding suggests that both methods might be used interchangeably in research
of frontal brain asymmetry, and indicates that the specific disadvantages of both methods
might be unlikely to have implications of practical significance.
A third method for the removal of ocular activity from the EEG is the multiple source eye
correction (MSEC) method of Berg and Scherg (1994). This approach rests on a modeling of
the EEG in terms of multiple overlapping electric sources within the head. In particular, the
method decomposes the EEG activity into two distinct source classes. First, ocular sources
describe the topography of eye activity; these sources may be estimated empirically from
calibration trials. Second, brain sources account for the EEG components which are due to
neural activity; these sources may be estimated with a dipole modeling approach.
Since the cortex is anatomically organized as a highly convoluted layer of billions of
neurons, the activity of cortical neurons that are distributed over wide areas results in a
dipole layer of complex geometry. This dipole layer induces electric currents that finally
give rise to the surface EEG (Nunez, 1981). The dipole modeling approach aims to explain
the surface EEG in terms of brain dipole sources. Because the true dipole layer is too
complex in geometry, it must be replaced by a manageable set of point dipoles such that
these dipoles would give rise to a surface EEG that is similar to the observed data. Thus,
this approach “explains” the EEG in terms of hypothetical dipole sources, similar to factor
analysis which explains the covariances of an item set in terms of factor components, and
similar to structural equation modeling which explains the covariance structure of measured
variables in terms of latent variables. If previous knowledge allows for an a priori location
of the dipoles in specific brain areas, then these dipoles may be denoted as “anatomically
correct” (e.g. it is known that the auditory N100 is generated in the temporal lobes; see
Scherg and von Cramon, 1985). However, if such prior knowledge does not exist or if the
signal of interest is not generated by circumscribed brain areas (as it may be the case for
spontaneous resting EEG), then these dipoles may be placed in strategic brain regions (not
necessarily the ones that generate the EEG signal) and thus, serve only as “surrogates” for
the real dipole layer.
The practical implementation of this method for the correction of resting EEG would
consist of several steps. First, EOG and EEG are recorded while the subject performs ocular
2 It may be noted that Gasser et al. (1992) suggested a modified regression approach to counteract this problem.
They proposed a filtering of the EOG with a low-pass of 7.5 Hz before the application of the regression procedure.
Although this filtering may prevent the distortion of EEG alpha due to neural activity in the EOG, such a filtering
would also remove all ocular activity in the alpha band from the EOG, which in turn may prevent an effective
removal of ocular activity in this frequency band from the EEG.
calibration movements. These data allows to estimate the ocular source of electric activity
on the head in an empirical (i.e. data-driven) fashion. In a second step, EOG and EEG are
recorded in the resting situation. These data are decomposed into the previously identified
ocular sources plus a set of surrogate dipoles within the head that account for brain activity.
In a typical application of this method, four surrogate dipoles are introduced (each one for
the anterior and posterior brain compartment of each hemisphere; see Berg and Scherg,
1994). Finally, a forward calculation of the brain surrogate dipoles (excluding the ocular
sources) yields an EEG with all ocular activity removed. Although this method overcomes
the limitations of the rejection and the regression approach, its accuracy is limited by several
factors. For example the optimal number and location of brain surrogate dipoles is unknown,
there is a dissimilarity between voluntary ocular calibration movements and involuntary
ocular activity, and the inaccuracy of electrode placement may increase modeling errors.
Moreover, inherent in this method is that any EEG modeling is only approximate. Another
problem is that the application of this method is not only time-consuming but also demanding
in terms of dipole modeling expertise and the availability of the required software. At the
time of this writing, the MSEC method appears to be a viable alternative to the more
traditional approaches, but its advantage for the measurement of anterior EEG asymmetry
is not established empirically yet.3
A final note should address another approach to minimize ocular artifacts, which is to in-
struct the subjects not to blink and not to move their eyes but to fixate a point. This approach
may be problematic, because blinks and spontaneous eye movements are controlled by sev-
eral brain systems in a highly automatic fashion (e.g. Brodal, 1992), and the instruction
to suppress these systems may act as a secondary task (see Verleger, 1991, for a discus-
sion). For example there is evidence that the instruction to refrain from blinking affects the
auditory P3 and N1 amplitude (Verleger, 1991), and that a fixation of the eyes affects the
contingent negative variation (Weerts and Lang, 1973). With respect to frontal asymmetry
research, it is important to note that the frontal eye field is of particular importance for
voluntary saccades (e.g. Brodal, 1992), and has been implied as part of a neural subsys-
tem for visuospatial selective attention and attention shifting (Chelazzi and Corbetta, 2000;
Kosslyn and Thompson, 2000; see also Robertson and Rafael, 2000, for the effects of frontal
eye field lesions on visual attention). Therefore, the instruction not to move the eyes may
result in unwanted change of activity in the frontal eye fields, which may interfere with or
override the anterior resting asymmetry.
Another type of biological artifact is due to pericranial muscle activity. The largest part
of power of the surface EMG lies in a range between 10 and 200 Hz and shows a maximal
energy between 20 and 100 Hz (Hayes, 1960; van Boxtel, 2001; van Boxtel et al., 1984),
although firing rates of motor units of the pericranial muscles may produce considerable
activity in the lower frequency range down to 10 Hz (Basmajian and De Luca, 1985).
Accordingly, contraction of pericranial muscles may result in an appreciable increase of
EEG power in the alpha range for sites that are directly located over the contracting muscle
3 In an unpublished diploma thesis of my group, Klingmann (2003) compared the event-related potentials of
affective slides after correcting the data with a regression procedure (Gratton and Coles, 1989) and the MSEC (Berg
and Scherg, 1994). There was virtually no difference in the evoked potentials between both methods, suggesting
that the regression approach might be an economic but valid alternative to the costly MSEC at least in this paradigm.
(O’Donnell et al., 1974; see also Gotman et al., 1981; Friedman and Thayer, 1991). Because
facial muscle activity tends to be asymmetric (e.g. Borod et al., 1997, 1998), such muscle
activity (e.g. of the frontalis or master/temporalis muscles) may mimic anterior EEG alpha
asymmetry (e.g. at frontopolar or anterior temporal sites).
A low-pass filtering of the EEG would naturally not remove the contamination in the
lower frequency range (such as alpha) and cannot be recommended as a tool for muscle
artifact reduction. However, two approaches may counteract this contamination. First, EEG
segments that show contamination with muscle artifacts may be rejected from analysis. Like
the rejection procedure for ocular artifacts, this approach has the disadvantage that defining
the subjective criteria or numerical thresholds for the identification of artifacts is difficult,
that data portions are lost, small artifacts may be missed, and that the accepted data portions
are biased towards a brain state that coincides with low muscular activity (and thus, might
be biased towards periods of lesser emotion).
A second approach is based on a regression procedure (Davidson, 1988; Henriques and
Davidson, 1990, 1991). In a first step, the power of a high-frequency band between 70
and 80 Hz is extracted from the data of each channel, which presumably reflects muscular
but not neural activity. In a second step, the EMG power measure may be introduced into
the statistical analysis as a covariate. In its most simple form, all statistical analyses of
alpha activity may be rerun with the EMG measure; a null finding of the latter analysis
would eliminate the possibility that significant findings of the former analysis are due
to muscle activity. Alternatively, the EMG measure may be introduced as a covariate in
an analysis of covariance (ANCOVA) of non-residualized alpha activity. More generally,
simple regressions of EEG alpha on the EMG measure would yield a residual that represents
alpha activity from which systematic muscle activity is statistically removed. This residual
may be introduced into any further analysis, or used for the computation of asymmetry
metrics.
Although this approach avoids all disadvantages of the rejection procedure, it rests on
the assumptions that (1) the EMG measure does not reflect neural activity but indicates
muscle activity and (2) that muscle activity in the alpha band is a linear function of the
muscle activity in the high-frequency EMG band. To satisfy the first condition, the EMG
band must be selected carefully. Because the frequency range of the EEG has a fuzzy upper
limit that lies somewhere between 70 and 100 Hz (Niedermeyer, 1998) but the EMG band
should also be set in a range where pericranial muscles produce maximal spectral power
(i.e. between 20 and 100 Hz), a EMG frequency band around 100 Hz (e.g. 90–100 Hz) may
be an appropriate compromise. The second assumption that supposes linearity is not strictly
met, because the lower and upper range of the EMG spectrum reflects different properties
of muscle activity. In particular, the power between 10 and 30 Hz is mostly due to the firing
rates of motor units and beyond 30 Hz it is due to the shape of the aggregated motor unit
action potentials (Basmajian and De Luca, 1985). Recent experimental work has suggested
that an individual’s lower end of the envelope of the EMG spectrum (i.e. the presence or
absence of a firing rate peak) cannot be predicted in a specific situation (van Boxtel, 2001).
At present, it is not known how severely the regression approach is limited by this problem.
Taken together, several methods allow a treatment of ocular artifacts, and in theory, all
have their own advantages and limitations. The rejection procedure is the most commonly
used method, but it has the limitation that some criteria for the presence of artifacts must be
specified and that small artifacts may remain in the data. Fortunately, empirical evidence
suggests that the method is rather robust because even great variations of these criteria do
not substantially affect individual differences in measures of anterior EEG asymmetry. The
regression procedure has the disadvantage that it may remove brain activity from the data,
but preliminary evidence suggests that this problem does not cause a distortion of frontal
EEG asymmetry. The MSEC method is limited by its approximate nature, and its value
for the measurement of anterior EEG asymmetry has not been established yet. Therefore,
it appears that the rejection approach (and possibly the regression approach) may be an
appropriate choice for the purpose of ocular artifact treatment. In contrast, the treatment
of muscle artifacts poses a more serious difficulty. Here, the rejection approach has the
same limitations but its robustness has not been established yet. Moreover, the regression
approach rests on the assumption that a high-frequency EMG band is indicative for low
frequency muscle activity but the extend to which this assumption holds is not known in
practice. It appears that both methods may be recommended on comparable grounds.
4. EEG reference
Another classical issue in quantitative EEG research is the EEG reference problem
(Katznelson, 1981; Lehmann, 1987). This problem is based on the dilemma that the quan-
tification of asymmetries of cortical activity requires the measurement of electrical activity
at single sites, but each EEG channel only yields information about the difference of electri-
cal activity between two sites—usually between a cephalic target site and a reference site.
Thus, the recording reflects the activity at the target and the reference site (Nunez, 1981),
and as a consequence, the derivation of one particular target site to different reference sites
may result in quite distinct EEG data (e.g. Katznelson, 1981; Lehmann and Skrandies,
1984; Lehmann, 1984). This problem is of particular importance for the measurement of
EEG asymmetry, because such a measurement requires—like all topographical analysis—a
non-ambiguous registration of single site activity.
The effects of typically used reference schemes for the measurement of frontal EEG
asymmetry have been analyzed in three recent studies (Hagemann et al., 1998, 2001; Reid
et al., 1998), and the findings were rather troublesome. Across four samples, the mean cor-
relation between the common vertex and the mathematically linked ears/mastoids reference
(which are the two most commonly used montages in asymmetry research) was r = −0.004
for the midfrontal asymmetry measures (range between −0.30 and 0.33). Because the re-
liability of these measures was good (reliability estimates were typically in the 0.80 and
0.90 s), this finding indicates that the common variance of the true scores of the two ref-
erences was virtually zero. Therefore, the different reference schemes appear to measure
psychometrically distinct properties of brain activity, i.e. there is no convergent validity for
these measures. Thus, treating them as interchangeable might be inappropriate, and several
consequences may arise from this problem with regard to the construct validity of EEG
asymmetry measures.
According to Cronbach and Meehl (1955), construct validity is faced with the problem
of what constructs account for variance in test performance. Only a nomological network,
which is a system of laws that relate different constructs to one another and which relates
constructs with observables, can imply construct validity for a given measure. Because there
may be multiple constructs that account for variance in a particular EEG asymmetry measure
(such as genetic, neurochemical, neurophysiological, psychological/behavioral, and social
factors), a complete account of the construct validity of a particular EEG asymmetry measure
must ultimately link the measure to both the biological and also the behavioral constructs. In
this sense, a particular EEG asymmetry measure may have a neurophysiological construct
validity (if there is a link between the measure and an underlying asymmetry in brain activity)
and it may have a psychological/behavioral construct validity (if the measure is related to
behavioral activation, approach motivation, and affective style). Most important, one kind
of construct validity does not imply the other; therefore, an EEG asymmetry measure that
is based on a particular reference may have good neurophysiological construct validity but
insufficient psychological/behavioral construct validity, or vice versa.
A somewhat different account on construct validity was fostered by Cook and Campbell
(1979), who based inference about constructs more on the fit between operations and con-
ceptual definitions than on the fit between obtained data patterns and theoretical predictions
about such data patterns. In this sense, construct validity can already bee implied by parts of
the nomological network, which relate constructs with observables (rather than considering
the links between a multitude of constructs). Thus, an EEG measure of the construct “asym-
metry of cortical activity” has good construct validity sensu Cook and Campbell (1979) if
there is a link between the measure and an underlying asymmetry in brain activity, which
corresponds to the idea of neurophysiological construct validity noted above.
Within the framework of Cook and Campbell (1979), construct validity may be inves-
tigated with the multitrait-multimethod matrix (Campbell and Fiske, 1959). This method-
ology requires that different traits are measured with different methods. If different mea-
surement methods of the same trait show convergence and the same measurement methods
of different traits show divergence, then good construct validity is established. Thus, a low
convergence between different reference schemes for measures of frontal alpha asymmetry
constitutes a problem of construct validity. As noted above, the correlation between the
common vertex and the mathematically linked ears/mastoids reference is about zero for
the midfrontal asymmetry measure, thus, implying that different constructs are measured
with these montages. However, other reference schemes may yield measures with a more
convergent validity. Across three samples, the mean correlation between the mathematically
linked ears/mastoids reference and an average reference was r = 0.81 for the midfrontal
asymmetry measures (Hagemann et al., 2001; Reid et al., 1998). In light of the high reli-
ability of these measures, this latter finding suggests that both references yield measures
with a common factor that contributes shared variance (e.g. due to the asymmetry construct)
and specific factors that contribute unique variance (e.g. due to method factors) in addition
to measurement errors. Thus, construct validity comes in gradations but is never perfect
because each method of measurement contributes at least some unique variance.
In what follows, a closer look at the most frequently used reference schemes might illumi-
nate their relative utilities and downsides for the measurement of the construct “asymmetry
of cortical activity” and thus, may shed some light on the construct validity of the measures
(for a tutorial on the reference issue and a more comprehensive comparison, see Hagemann
et al., 2001). Since the target site activity is the signal of interest, the reference site activity
may be denoted as noise; thus, the greater the amplitude of the target site activity becomes
in relation to the amplitude of the reference site, the higher the signal-to-noise ratio will be-
come, and the topographic validity of the reference scheme will increase. For an application
of this principle to different reference schemes one must bear in mind that the topography of
alpha activity in a resting state is commonly presumed to have a rather monotonic increase
from anterior to posterior (Creutzfeldt, 1995; Zschocke, 1995; see Hagemann et al., 2001,
for a discussion of this assumption).
The common vertex (Cz) reference is one of the most frequently used reference schemes
in asymmetry research, but it may have a most unfavorable signal-to-noise ratio. The vertex
is certainly an electrically active site, and it may be presumed that the frontal sites have a
lower alpha activity than vertex; thus, the derivations of F3 and F4 against vertex hardly
reflect the activity of prefrontal structures but mostly vertex activity. Moreover, it can be
shown that, depending on the amplitude and phase relations between the two target sites
and the reference site, the true amplitude asymmetry of the target sites may be enhanced,
mitigated, or even reverted (Hagemann et al., 2001). Therefore, if the (asymmetry of) local
alpha activity at the left and right frontal lobes needs to be measured, then the common
vertex reference appears to be less appropriate.
One prospective solution to this problem might be the (mathematically) linked ear-
lobes/mastoids (A1 + A2) reference, which is another commonly used montage. The topo-
graphic validity of this reference scheme rests on the assumption that the actual reference
site (the average of A1 and A2) is substantially less active than the cephalic target sites
(e.g. Hagemann et al., 1998). Thus, the signal-to-noise ratio would be quite favorable for
the derivations of all scalp electrodes to this reference. Unfortunately, empirical data do
not support this assumption. Earlier studies could demonstrate substantial event-related ac-
tivity at A1 and A2 in a variety of paradigms (Curran et al., 1993; Dien, 1998; Lehtonen
and Koivikko, 1971). A more recent study of Hagemann et al. (2001) demonstrated that the
bipolar derivation of the ears (A1–A2) in a resting state shows highly significant alpha activ-
ity, which was greater than the alpha activity of bipolar derivation between the frontopolar
(Fp1–Fp2) and midfrontal (F3–F4) sites, but smaller than activity of a central derivation
(C3–C4). This finding appears to be difficult to reconcile with the assumed inactivity of the
A1 and A2 reference sites, but the data also suggests that the earlobes/mastoids may have
lower activity than vertex. Thus, the signal-to-noise ratio of the A1 + A2 reference for the
measurement of anterior resting activity might be less favorable than one may wish, but it
appears to be greater than for the Cz reference. Therefore, the A1 + A2 reference may be
more appropriate for the measurement of frontal resting asymmetry than the Cz reference.
For practical applications of the A1 + A2 reference, it must be noted that physically
linking the ears/mastoids may result in an electrical shunt across the head if the electrode
impedances at A1 and A2 are very low (Katznelson, 1981; see also Miller et al., 1991), and
may also distort the EEG if the impedances at A1 and A2 are high but asymmetrical (see
Miller et al., 1991; Nunez, 1991).4 To avoid this problem effectively, all scalp electrodes may
4 In general, the pre-existing biological resistance is quite low compared to the linked earlobes or mastoids if
the electrode impedance is within a typical range (e.g. between 1 and 10 K). Thus, the effects of linking the ears
or mastoids are not likely to be of practical significance. However, if the electrode impedances are unusually low
(i.e. less than 1 K), then linking the ears or mastoids may create an effective shunt across the head (for detailed
model calculations, see Miller et al., 1991).
be recorded to a common and arbitrary reference site, and rereferenced to a mathematically

A1+A2 reference (for a comprehensive discussion of this issue, see Lehmann, 1987; Miller
et al., 1991; Nunez, 1991; Nunez et al., 1991). Such a common reference scheme for EEG
recording has the additional advantage that any other montage may be computed subsequent
to the data acquisition.
One different and quite promising solution to the EEG reference problem is the aver-
age reference, although this montage is less frequently applied in the context of frontal
asymmetry research. In theory, Bertrand et al. (1985) could demonstrate that under certain
conditions, the integral of the potential on the surface of a sphere is zero, and therefore,
this integral would be a perfect (inactive) EEG reference. In practice, the surface integral of
the head may be approximated by the average of the potentials across all scalp electrodes.
However, this average reference will be electrically null only if the head is sampled with a
high spatial electrode density and if the whole head is sampled (Bertrand et al., 1985). If this
condition is not met, then a distortion of the alpha topography may occur, which has been
described as the frontal mirroring of the alpha rhythm (Zschocke, 1995). Because alpha
tends to be synchronous across broad areas of the scalp with small amplitudes at anterior
and large amplitudes at posterior sites (e.g. Creutzfeldt, 1995), the average across the sites
that are located within the limited area of the 10–20 system will not result in a zero poten-
tial, but in an alpha activity of medium magnitude. Referencing the low-amplitude activity
of anterior sites to the medium-amplitude activity of the AR scheme will then result in a
medium-amplitude activity (which is largely due to the activity of the virtual AR “site”).
Effectively, the posterior alpha activity appears to be mirrored at the central coronal line
(for empirical demonstrations, see Hagemann et al., 2001; Hjorth, 1975; Katznelson, 1981;
Maurer and Dierks, 1991; for a computer simulation, see Mac Gillivray and Sawyers, 1988).
Although there is no scarcity of discussion about the electrode density and head coverage
that are necessary to obtain unambiguous EEG results with the AR approach (Chung et al.,
1996; Curran et al., 1993; Desmed et al., 1990; Junghöfer et al., 1999; Srinivasan et al.,
1998; Tomberg et al., 1990), no consensus has emerged so far. Nonetheless, the occurrence
of artifactual frontal alpha activity due to the mirror phenomenon suggests that the use of
an AR, which is based on 32 electrodes of the 10–10 system, must be discouraged for the
measurement of frontal resting asymmetry.
A totally different approach that seeks to overcome the dilemma of the EEG reference
problem is the use of current source density (CSD) measures. This approach aims to es-
timate the radial current density of the sources and sinks on the scalp that are generated
by the electrical activity of the brain. Because the current source density is proportional to
the curvature of the surface potential field (i.e. the rate of change of the rate of change
of the scalp potential when moving along the scalp; Hjorth, 1975; Nunez, 1981), the
CSD measures can be computed by suitable difference operations of EEG potential data
(Hjorth, 1975; for further computational procedures, see Hjorth, 1980; Perrin et al., 1989,
1990). It might be noted that this measure can be conceptualized as the second spatial
derivative of the potential field at a specific electrode with respect to each surrounding
electrode.
The resulting measures are strictly reference-free, i.e. they are invariant with respect to
the reference site that was used for EEG recording. Moreover, the CSD transformation has
also the property to act as a spatial high-pass filter, i.e. broadly distributed sources and sinks
will be attenuated. This latter property may be beneficial for research on alpha asymmetry,
because activity of one hemisphere or region that is introduced via volume conduction
to the other hemisphere or region would be considerably reduced with a CSD transform.
However, this same property might also have an unfavorable effect for the measurement
of alpha activity. Because alpha tends to be broadly distributed, the transformation of EEG
potential data into CSD measures might eliminate—at least in theory—the very activity of
interest. Fortunately, recent empirical findings suggest that this nuisance might be of little
practical concern.
First, CSD alpha in a resting state shows the expected scalp topography with a monotonic
increase from anterior to posterior and with greater right-sided activity (Hagemann et al.,
2001). Second, a structural equation modeling analysis of CSD based resting asymmetry
measures revealed an excellent reliability of these measures, with coefficients in the upper
0.90; moreover, these measures also showed a mediocre trait specificity with coefficients
of about 0.60, and an excellent temporal stability of the latent trait component with retest
correlations close to 1 (Hagemann et al., 2002). It may be interesting to note that the same
analysis, when performed with A1 + A2 based asymmetry measures, revealed a somewhat
lower trait specificity of resting asymmetry. Third, the CSD alpha asymmetry measures
showed excellent convergent validity with Cz, A1 + A2, and AR derived asymmetry mea-
sures for the posterior region, with most correlations in the 0.90 s (Hagemann et al., 2001).
It should be noted that posterior asymmetry measures appear to be rather invariant with
respect to the EEG reference, which may be due to the greater signal-to-noise ratio for
posterior sites (where alpha tends to be maximal). Fourth, CSD measures of resting alpha
activity show convergent validity with another neuroimaging modality. Cook et al. (1998)
obtained EEG and H2 15 O positron emission tomography data simultaneously from normal
subjects in a resting state and during a motor task. Across conditions, scalp/cortex positions,
and reference montages (ears or CSD), alpha band activity was inversely related to cortical
perfusion. Taken together, none of these observations can easily be reconciled with the as-
sumption that (the asymmetry of) resting alpha activity is eliminated by the CSD approach.
Thus, the CSD approach might be a prospective solution to the EEG reference problem
for research on resting asymmetry, in particular if the integration of EEG data with other
neuroimaging modalities is desired.
To sum up, some evidence suggests that there is only low convergent validity for anterior
asymmetry measures that are based on different EEG reference schemes for at least some
references, and the choice of the EEG reference may affect the outcome of the study.
From the perspective of psychological/behavioral construct validity, it might be prudent to
continue to use different reference schemes in each study, and to compare the relationships
between the asymmetry measures and the psychological/behavioral variables of interest (i.e.
emotion, motivation). Such a comparison may be facilitated by a data analytic approach that
uses general linear model (GLM) analysis, which allows inclusion of a repeated measures
factor for reference scheme (see Coan and Allen, 2003a, for an example). A significant
interaction involving this reference factor would indicate that the asymmetry–behavior
relationship is moderated by the reference, and thus, allows for a selection of the reference
with the strongest link between the variables. If conducted over several years, this type
of research would eventually establish good psychological/behavioral construct validity of
EEG asymmetry measures.
From the perspective of neurophysiological construct validity, however, a pre-selection

of a particular reference scheme might be desired, and such a selection may consider the
relative advantages and disadvantages of each method for the measurement of the asym-
metry construct. The common Cz reference appears to be the least recommended montage
because the alpha activity at Cz tends to be greater than at anterior sites, which may severely
distort the measurement of anterior alpha activity. The AR—if based on a limited head cov-
erage as with the 10–20 system—may result in an increased anterior alpha activity, which
might be an artifact of the reference scheme; thus, this method may be very problematic
for the measurement of frontal alpha activity as well. The A1 + A2 reference sites show
alpha activity, the magnitude of which may approach the activity at anterior sites, which is
a disadvantage of this method. However, some data suggest that the A1 + A2 reference may
yield greater signal-to-noise ratios for anterior sites than the Cz and AR montages. Thus, the
A1 + A2 reference appears to be more appropriate for the measurement of anterior alpha
activity than the other two schemes. Finally, an entirely different approach is the use of
CSD measures, which are reference-free and enhance the spatial resolution by attenuating
broadly distributed activity. Although this method has some shortcomings such as the need
for large electrode arrays and the problem that the estimation of the field curvature at the
edge of the electrode system may be inaccurate (e.g. at lateral frontal or frontopolar sites),
this approach may be recommended as a prospective solution to the reference problem. Be-
cause CSD and potential data measure different properties of the electrical field of the head,
a research approach that utilizes the CSD and the A1 + A2 reference as alternative meth-
ods within one study might be a viable route for frontal asymmetry research. This type of
research allows—at least conceptually—a direct operationalization of the theoretical con-
struct “asymmetry of cortical activity”, and thus, facilitates an empirical test of theories that
operate with this construct. The comparison between the CSD and A1 + A2 reference may
again be facilitated by a GLM analysis that includes a repeated measures factor for method.
If the asymmetry–behavior relationship is moderated by method, then these relationships
can be interpreted only with uttermost caution—the discussion of the A1 + A2 reference
and the CSD should have made clear that no definite conclusion can be drawn concerning
the neurophysiological construct validity of both methods. If the asymmetry–behavior re-
lationship is not moderated by method, however, then this association might be interpreted
with some confidence in terms of the intended construct.
5. State- and trait-composition of resting asymmetry
After artifact treatment and rereferencing of the EEG, the next analysis step is the extrac-
tion of alpha activity via a spectral analysis of the data (see Dummermuth and Molinari,
1987; Pivik et al., 1993, for guidelines). The resulting alpha power values may be used as
a proxy for cortical activity, with high values of alpha indicating a low level of cortical ac-
tivity (e.g. Shagass, 1972; see also Davidson, 1998b), and asymmetry measures of cortical
activity may be computed as the difference of alpha power of contralateral homologous
sites. Unfortunately, the resulting measures are not trait variables, which is mainly due to
the distinct state-dependence of the spontaneous EEG. This state-dependence is evidenced
by rather low temporal stability of resting asymmetry.
It is well established that resting asymmetry measures of healthy subjects show retest
correlations in the 0.50 or 0.60 s for time intervals between 2 and 6 weeks for a variety of
reference schemes such as Cz, A1 + A2, nose, the average reference, and CSD measures
(Allen et al., in press; Debener et al., 2000; Hagemann et al., 2002; Papoussek and Schulter,
1998; Sutton and Davidson, 1997; Tomarken et al., 1992). In contrast, most personality
measures, corrected for unreliability, have annual stability coefficients of 0.98–0.99 (see
Costa and McCrae, 1992). To explain this difference in stability, Tomarken et al. (1992)
suggested that resting EEG asymmetry might reflect the joint contribution of a trait that is
superimposed on state-like factors (see also Davidson, 1992, 1993; Wheeler et al., 1993).
Only recently Hagemann et al. (2002) provided direct evidence in support of the proposed
dual nature of resting asymmetry. They recorded EEG for 12 min in four occasions of
measurement each 4 weeks apart, transformed the data into CSD measures, and used a
structural equation modeling approach to decompose asymmetry measures into latent state
and trait components within the framework of latent state–trait (LST) theory (Steyer et al.,
1992). As noted above, the authors found that about 60% of the variance of the resting
asymmetry measure was due to a latent trait and that about 40% was due to state-like
fluctuations (effected by the situation or the interaction between person and situation). The
variance due to measurement errors was rather negligible. The authors obtained similar
results when they repeated their analysis with EEG data referenced to A1 + A2, although
the trait specificity was now somewhat lower and the occasion specificity was somewhat
higher.
The trait component of the resting asymmetry measure is the variable of interest but the
additional occasion-specific fluctuation is unwanted and needs to be explained. Fortunately,
several studies could shed light on the impact of situational factors that affect resting EEG
asymmetry. For example some evidence suggests that states of positive and negative affect or
approach and withdrawal motivation might be associated with shifts of anterior asymmetry
(based on EEG references such as Cz or A1 + A2; e.g. Davidson et al., 1990; Sobotka
et al., 1992; Tucker et al., 1981). Thus, transient mood state during the recording of the
resting EEG may contribute to its state variance. Earlier studies investigated this issue and
provided null findings. Tomarken et al. (1990) recorded a resting EEG with a Cz reference
and obtained mood ratings for the recording period after it was terminated. There was no
association between mood and resting asymmetry. In a similar fashion, three more studies
assessed transient mood before and after EEG recording, and found no correlation between
the average of the mood ratings and resting asymmetry for Cz and A1 + A2 references
(Hagemann et al., 1998, 1999; Wheeler et al., 1993). In addition, Henriques and Davidson
(1991) reported that the severity of depressive states (as measured with the Beck Depression
Inventory, Beck et al., 1961) was unrelated to frontal resting asymmetry for a Cz and an
average reference, both in a group of depressed and control subjects (although this finding
may be due to restricted range).
In contrast to these findings, Blackhart et al. (2002) suggested that the mood before the
EEG recording might be more predictive, because the EEG preparation procedure (fitting
of an EEG cap, abrasion of the scalp, application of gel) is somewhat aversive, and thus,
may induce a negative affective state. To test this hypothesis, they assessed mood before
and after the EEG preparation, followed by the recording of the EEG with an A1 + A2
reference. There was a significant mood shift during EEG preparation, with less pleasant
mood after the procedure was over. In addition, there were significant associations between
mood after EEG preparation and resting asymmetry if the mood before the EEG preparation
was partialed out. Women who reported greater unpleasant mood showed greater relative
right fontal activity, but men who reported greater unpleasant mood showed greater relative
left fontal activity. This finding suggests that differences in transient mood may contribute
to the state-like variance of resting asymmetry.
Another factor that may contribute to the state variance of resting asymmetry is the tran-
sient motivational state during the preparation and recording of the EEG. Kline et al. (2002)
investigated this issue recently. They pointed out that defensiveness is conceptually and
empirically related to self-presentation motives (e.g. Baumeister and Cairns, 1992), it may
moderate physiological responses to social stimuli (e.g. Newton and Contrada, 1992), and
some evidence suggests that defensiveness may be associated with anterior resting asym-
metry (Kline et al., 1998, 2001; Tomarken and Davidson, 1994). Because opposite-sex
encounters can efficiently affect self-presentation motives (see Leary et al., 1994), Kline
et al. (2002) suggested that the defensiveness of a subject might interact with the presence of
an opposite-sex experimenter, and thus, induce a shift of anterior asymmetry. To test this hy-
pothesis, Kline et al. (2002) recorded a resting EEG while a same-sex or opposite-sex exper-
imenter was present. During the presence of an opposite-sex experimenter, high-defensive
subjects showed greater left frontal activity but low-defensive subjects showed greater right
frontal activity, whereas no group effect occurred in the presence of a same-sex experimenter.
This finding suggests that complex situational factors (such as the sex of the experimenter in
relation to the sex of the subject), if not held constant, may contribute to the occasion-specific
variance.
Perhaps, a further factor that might contribute to the state variance of resting asymmetry
is a transient state of approach and withdrawal motivation. Several studies have manipulated
approach and withdrawal states, and provided evidence for a systematic association between
this experimental manipulation and frontal EEG asymmetry as measured with the A1 + A2
reference (Harmon-Jones et al., 2002, 2003; Harmon-Jones and Sigelman, 2001; Sobotka
et al., 1992). However, it is not known at present if such an association also exists for
unprovoked states of approach and withdrawal motivation, thus, the contribution of this
factor to the state variance of resting asymmetry remains uncertain.
Because the supposed dual nature of resting EEG asymmetry may contribute to the in-
consistency of findings, Davidson (1998b) suggested that it might be imperative to employ
a method for the control/reduction of state-like variability in the measures. Several proce-
dures have been used for this purpose. For example Wheeler et al. (1993) endeavored a
selection of stable subjects. The authors selected those participants from a larger sample
whose standardized resting asymmetry measures on two occasions of measurement showed
no difference greater than one third of a standard deviation. These participants were sup-
posed to have a stable asymmetry, and the asymmetry measures were averaged across both
occasions to further reduce its state variance. One grave limitation of this approach is that
the selection of participants with similar asymmetry measures on two occasions does not
necessarily imply that these participants have a stable asymmetry. Alternatively, the asym-
metry of these persons may show a fluctuation across time similar to the asymmetry of
“unstable” persons, but just happened to be similar on two occasions by chance. This ob-
jection found empirical support in the study of Hagemann et al. (2002) who analyzed data
from four occasions of measurement. Subjects who showed similar asymmetry measures
in the first two sessions showed dissimilar asymmetry measures in the last two sessions; the
retest correlation of a “stability” index across the first two sessions was uncorrelated with a
“stability” index across the last two sessions (r = 0.03 for the stability index of midfrontal
asymmetry). In total, these findings suggest that the similarity of asymmetry measures in
two occasions is no stable characteristic of the person, and thus, appears not to be a suitable
criterion for subject selection.
A related approach is the selection of extreme and stable subjects. For example Tomarken
and Davidson (1994) selected those persons from a larger sample whose asymmetry measure
scored in the top or bottom 25 percentile in two occasions of measurement (for a similar
approach, see Tomarken et al., 1992). A major limitation of this method is that each extreme
group selection suffers from the problem of a regression to the mean, which is a hazard for
any specific substantive interpretation of the data (see Cohen and Cohen, 1983, for a full
discussion of this problem). Moreover, the objections against the selection of stable subjects
also apply to the selection of subjects that are extreme on two separate occasions (which
implies relative similarity in both occasions). Therefore, this selection procedure may be
less appropriate.
A very different approach is the aggregation of data across occasions. For example Sutton
and Davidson (1997) averaged the EEG data of two occasions in an attempt to reduce the
state-like variability of the asymmetry measures (for other examples of an aggregation
across two occasions, see Debener et al., 2000; Tomarken and Davidson, 1994). The ra-
tionale of this approach leads back to work of Epstein (1983). If any measure reflects the
joint contribution of a trait and occasion-specific state-like factors, then aggregation across
several occasions may reduce the state and increase the trait variance (see also Schmitt and
Steyer, 1990). A limitation of this method is that it may reduce the state-flux contamination
of the asymmetry measures, but it does not eliminate it. In particular, it is not self-evident
that an aggregation across only two occasions would yield asymmetry measures with suf-
ficiently reduced state-variance. To estimate the effects of aggregation Hagemann et al.
(2002) performed latent state–trait model calculations for the EEG asymmetry measures
(these calculations are similar to the Spearman–Brown formula for prolonging scales; see
Steyer and Schmitt, 1990, for theoretical foundations). For the case that the data were ag-
gregated across two, three, and four occasions the median of the trait specificity across the
whole head was estimated to be 0.76, 0.83, and 0.86, respectively. This finding suggests
that an aggregation across two or three occasions may yield an asymmetry measure with
mediocre or good trait specificity, respectively, but an aggregation across four occasions
would provide only little further improvement.
Finally, it may be mentioned that an elimination of unsystematic effects of the situation
may be achieved with simultaneous latent state–trait modeling. In this approach, two or
more latent traits may be represented with separate LST models within one simultaneous
analysis, and the correlation of the latent traits or the latent state residuals may be assessed
directly (see Eid et al., 1994; Steyer et al., 1990, for applications). Unfortunately, this type
of analysis involves complex structural equation models, which require larger sample sizes
for a reliable identification of the latent variables than those that are usually available.
Taken together, the resting EEG asymmetry is not a trait variable, but about half of its
true score variance may be attributed to a latent trait and the other half may be due to
occasion specific factors. Some evidence suggests that transient mood states and the social
context may contribute to the state-like variations of the measure, but there is no doubt
that a plethora of specific factors are at work that are not known at present. Nonetheless,
these factors need to be controlled to ensure that the trait component of the measure is
enhanced. Several procedures aimed to reduce the occasion-specific variance, but not all
may be suited equally well. Some researchers selected subjects with similar (or extreme)
asymmetry measures on two occasions and trusted that these subjects have a rather stable
asymmetry, i.e. an asymmetry that is not likely to respond to situational factors. However,
recent empirical evidence suggests that this selection procedure does not result in a group
of stable subjects, because the similarity of the asymmetry in two subsequent occasions is
no stable characteristic of the person. Other researchers aggregated the EEG data across
two occasions of measurement. This approach appears to be far more appropriate, because
70–80% of the variance of these measures may be due to the latent trait. A more favorable
aggregation would include even three occasions, but four occasions would hardly improve
the measures. Alternatively, the latent trait variable of the asymmetry measure might be
correlated directly with the behavioral indicators in a structural equation modeling approach,
but the necessary models are rather complex and require probably large sample sizes.
6. Statistical issues
No matter how the alpha power measures of the resting EEG were acquired and pro-
cessed, the final step of the empirical endeavor is the statistical analysis of the data. Here,
a first problem is the positively skewed distribution of alpha power, which makes a nor-
malization of the data necessary. For this purpose, Gasser et al. (1982) compared several
transformations, and found that the natural logarithm yields the closest approximation to the
normal distribution. Thus, this transformation should be applied before further statistical
analyses take place.
The associations between the topography of alpha activity and behavioral traits may
be statistically evaluated in a multivariate fashion, either with a correlation analysis or
with a general linear model approach. Both approaches may have several advantages and
disadvantages that should be considered.
For the correlation analysis, the asymmetry measures for anterior and posterior regions are
correlated with the behavioral variables (the posterior asymmetry needs to be introduced
into this analysis to secure that the associations under question are really specific to the
anterior sites). The directional hypotheses allow one-tailed t-tests of significance for each
correlation involving the anterior sites, which will yield greater statistical test power than
the usual two-tailed tests (see Hays, 1994). However, the null hypotheses for posterior sites
are non-directional and allow only the use of two-tailed tests.
The major drawback of the correlation approach is the hazard of an inflation of type-I
error rate due to multiple testing. In the typical study, several correlations need to be tested,
and it is common practice to test each correlation separately. However, this must inevitably
result in an increase of type-I error rate for the whole set of tests, i.e. the probability of
making at least one type-I error (the familywise error rate) is greater than the nominal alpha
level of each test. For example, if a total of only eight correlations is tested with a nominal
level of alpha = 0.05 for each test, the familywise error rate will amount to 0.34 (Hays,
1994, Eq. (11.13.1))—which appears to be rather unacceptable. Fortunately, there are two
ways to counteract this inflation and the danger of erroneous decisions.
First, the Bonferroni approach allows an adjustment of the testwise error rate such that
the familywise error rate will not exceed the desired nominal alpha level. For the classical
Bonferroni approach, the nominal error rate is divided by the number of tests, which yields
the adjusted testwise error rate. For the example just given above, a familywise error rate
of not greater than alpha = 0.05 will be achieved if the testwise error rate is set to 0.006
(=0.05/8). The major disadvantage of this method is its conservative nature, i.e. this method
will yield significant results only if the population correlations are large. However, a less
problematic version of this approach is the sequentially rejective Bonferroni approach of
Holm (1979). For this procedure, the correlations must be organized in a rank order, starting
with the highest correlation. The first correlation is tested with the classical Bonferroni
method. If it is significant, then the second correlation is tested with the Bonferroni method,
but the number of tests is now reduced by 1. If this correlation is also significant, then the
next correlation is tested, always reducing stepwise the number of tests for the Bonferroni
correction. The procedure finally stops when the first non-significant test result occurs. This
approach has an intuitively appealing logic, it is easy to apply, and it is considerably less
conservative than the classical approach.
Second, the correlation pattern analysis developed by Steiger (1980) allows the omnibus
test of the hypothesis that all correlations in a set are zero. For the application to the present
problem, the correlations between asymmetry and affect indices might be divided into two
subsets, one containing the associations for anterior and one for posterior sites. Then both
subsets may be tested for significance using Steiger’s (1980) Eq. (22) (which essentially
yields a chi-square model test). If the proposed association between alpha topography and
affect holds, then the statistical null hypothesis should be rejected for the anterior but not
the posterior set. This approach has the advantage to reduce the total number of tests to two,
and thus, minimizes type-I error inflation. However, in case of a rejected null hypothesis, the
question is open which of the correlations contribute to the overall association and which do
not (the sequentially rejective Bonferroni approach might serve as a follow-up procedure).
Another problem is that the employed test statistic approaches the chi-square distribution
only in medium to large samples (Steiger, 1980). Finally, the underlying chi-square test
statistic is usually rather low in power, and may be associated with substantial type-II error
in small to medium sized samples (Cohen, 1988). Thus, in small samples, this test may not
have adequate statistical power to detect a relationship between anterior asymmetry and
affective dispositions that is present in the population.
A totally different avenue than the correlation analysis is provided by the general linear
model approach, which offers a hierarchical set of repeated measurement omnibus tests.
Similar to the correlation pattern analysis, this method avoids multiple testing and thus
avoids the inflation of type-I error. In contrast to the correlation pattern analysis, however,
the GLM employs the F-statistic, which usually has a higher test power than the chi-square
statistic (Cohen, 1988). Two different versions of the GLM may be considered.
The most commonly applied method is the ANOVA approach. The continuous affect
dimensions are reduced to categorical between-subjects variables (e.g. by a median split in
high and low scorers), and—together with factors for hemisphere and region—introduced
into the analysis as independent variables (see Kirk, 1995, for a full treatment). For example
a typical ANOVA setup may be a hemisphere × region × affect group analysis of alpha
power at single sites. In case of significant effects, standard follow-up tests facilitate the
decomposition of the omnibus effects (Kirk, 1995). Unfortunately, this approach has two
serious disadvantages (see Aiken and West, 1991, for a discussion). First, the loss of infor-
mation that will occur when a continuous dimension is reduced to a categorical variable
with only few classes may impair statistical precision and test power (Cohen and Cohen,
1983). Second, split operations may yield statistical artifacts, in particular if applied to small
samples (Bissonnette et al., 1990).
However, this disadvantage may be overcome by the multiple regression approach. Like
in an ANOVA, the topography may be introduced into the analysis with categorical factors
(by effect coding), but the affect dimensions are now introduced as continuous independent
variables. For the example given above, a typical setup may be a hemisphere×region×affect
dimension analysis of alpha power density at single sites. Significant main and interaction
effects might be followed up with simple regression analyses (see Aiken and West, 1991, for
procedures). For the example given above, a significant three-way interaction would indi-
cate that the slopes of the simple regressions of alpha activity on depression are significantly
different for different electrode sites along the saggital and lateral direction, or stated differ-
ently, that associations between asymmetry and affect differ between regions. This omnibus
result may be decomposed with separate hemisphere × affect analyses for each region. Now
a significant interaction effect would indicate that the slopes of the simple regressions of
alpha activity on depression are different between both hemispheres, i.e. that there is an
association between asymmetry and affect for that region. To aid the interpretation of this
interaction one may plot the two simple regressions. This nested analysis procedure has
several advantages. First, it minimizes the number of tests, and thus, counteracts a type-I
error inflation (Hays, 1994). Second, it makes use of the repeated measurements and em-
ploys the F-statistic, which increases the statistical power, and thus, minimizes the type-II
error rate (Cohen and Cohen, 1983; Cohen, 1988). Third, this approach avoids the hazard
of statistical artifacts (Bissonnette et al., 1990).
To sum up, the associations between asymmetry and affect may be analyzed with a
correlation or GLM approach. If the former were used, uncorrected tests for each correlation
would result in an inflated type-I error rate and a classical Bonferroni approach would result
in increased type-II error rate, thus, these methods cannot be recommended. However,
more sophisticated procedures like the sequentially rejective Bonferroni procedure or the
correlation pattern analysis may effectively overcome these drawbacks. Within the GLM
approach, the number of comparisons are kept low with hierarchical testing, which keeps
the familywise type-I error low. However, the use of percentile splits in order to reduce
continuous affect variables to categorical between-subjects factor for classical ANOVAs
cannot be recommended because of statistical shortcomings such as increased type-II error
rate and statistical artifacts. In contrast, a multiple regression approach allows the inclusion
of continuous independent variables, and thus, circumvents this problem effectively. At
the present time, no systematic comparisons of the three endorsed methods exist (rejective
Bonferroni procedure, correlation pattern analysis, multiple regression), thus, the researcher
will be wise to consider all of them and select the approach that best fits his or her needs.
Nonetheless, it appears that the GLM/regression approach has the advantage of a greater
statistical test power, and additionally allows to treat different reference schemes as an
independent factor (see above). Thus, this method may be recommended.
7. How to deal with methodological issues in practice?
The measurement of individual differences in anterior EEG asymmetry is associated with

a multitude of methodological problems, some of which are rather easy to resolve but others
are more challenging. A rather undemanding issue is the assurance of good reliability, which
can be easily archived with a sufficient length of EEG recording. Because a recording period
of 8 min would ensure excellent reliability of asymmetry measures and since handling and
storage of large data files is easily handled by modern computers, this may be considered as
an advantageous procedure. Another manageable issue is to secure statistical validity, which
might be threatened by an inflated type-I error due to multiple testing. Several methods
to counteract this problem are available such as the rejective Bonferroni procedure, the
correlation pattern analysis, and multiple regression approaches. Each of these methods
will work effectively and are easy to use, thus, the researcher may pick the method that best
matches his or her question.
In a similar manner, the treatment of ocular artifacts poses no serious difficulty. Although
the artifact rejection approach has the theoretical limitation that the specification of rejection
criteria is associated with difficulties, empirical evidence suggests that even great variations
of these criteria do not substantially affect individual differences in measures of anterior EEG
asymmetry. Thus, this method appears to serve the purpose. It should be noted, however, that
the frontopolar sites show an exceptional susceptibility for ocular artifacts. If these sites are
included into the data processing and analysis, a rather conservative rejection criterion might
be considered. The regression approach has the disadvantage that it removes anterior brain
activity from the data, but this method appears to have no distorting effects on frontal EEG
asymmetry. Thus, as long as used for the study of individual differences, this approach might
be recommended as an alternative to the rejection procedure. Finally, the MSEC approach
may have its specific merits, but it has also limitations for the measurement of anterior EEG
asymmetry and its robustness for this purpose is empirically not established yet.
A more demanding issue is the reduction of unwanted state-like fluctuations of anterior
EEG asymmetry, which requires the collection of data in multiple sessions, and thus, is
expensive. The easiest way to handle this problem is maybe the collection of data in two
occasions and the aggregation of the asymmetry measures across both sessions; some evi-
dence suggests that the resulting measures may have at least acceptable trait specificity. An
aggregation across three occasions would be more favorable, because it may produce mea-
sures with even good trait specificity but it also increases the cost of a study. The inclusion
of four or more sessions, however, has no obvious advantage. Other approaches that aim to
reduce the state-like fluctuations by selecting subjects with “stable” asymmetries appear to
have grave limitations and may not be recommended.
Another thorny issue is the EEG reference problem, which has presently no definite
solution. In practice, the methodological strategy will depend on the research goal of the
study. If the aim of a study is the search for a biological marker of emotional and mo-
tivational traits, then the psychological/behavioral construct validity of the measure is of
importance. For this research, different reference schemes may be used and those schemes
will be selected that yield the most robust associations between asymmetry and the behav-
ioral traits. If the aim of the research is a test of a theory that operates with the construct
“asymmetry of cortical activity”, however, then good neurophysiological construct validity
is paramount. Since each reference scheme has apparent limitations, the task is to choose
the lesser of evils. At the present time, some empirical and theoretical arguments point
to the (mathematically) linked ears/mastoids as a working solution as long as potential
data are the basis for the asymmetry measures. Nonetheless, it must be observed that the
ears/mastoids are not electrically inactive reference sites, thus, some distortion of anterior
alpha asymmetry must be expected. A viable alternative to this approach may be the use of
CSD data as a basis for asymmetry measures. These quantities are reference-free, but this
advantage comes for the price of greater expenditure during data recording (more electrodes
are needed for CSD estimation) and greater complexity of data processing. Ideally, a study
might combine the linked ears/mastoids reference and the CSD approach. Other reference
montages such as the common vertex or the average reference may have less favorable
signal-to-noise ratios for anterior alpha activity, and may be less appropriate. No matter
whether the psychological/behavioral or neurophysiological construct validity is of prior
importance, the systematic comparison of reference schemes may be facilitated by a GLM
analysis that includes a repeated measures factor for the EEG method. If the association
between asymmetry and behavior is not dependent upon a particular method, this might
indicate that—within the limits of the implemented measurement procedures—the findings
can be interpreted with some confidence.
There is no doubt that research on individual differences in brain asymmetry and emotion
is a fascinating topic. On a first glance, the empirical investigation of this association seems
to be an easy venture—all one has to do is measure anterior resting asymmetry and affect
dispositions and correlate them. In a close up view, however, this task becomes challenging,
and to pursue a better understand of how the brain organizes emotion may lead to another
insight: there is no pleasure without pain.
Acknowledgements
I thank John Allen, Jim Coan, and Eddie Harmon-Jones for helpful comments on this
article.
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Methodology
Issues and assumptions on the road from raw signals
to metrics of frontal EEG asymmetry in emotion
John J.B. Allen∗ , James A. Coan, Maria Nazarian
Department of Psychology, University of Arizona, P.O. Box 210068, Tucson, AZ 85721-0068, USA
Abstract
There exists a substantial literature examining frontal electroencephalographic asymmetries in

emotion, motivation, and psychopathology. Research in this area uses a specialized set of approaches
for reducing raw EEG signals to metrics that provide the basis for making inferences about the role
of frontal brain activity in emotion. The present review details some of the common data processing
routines used in this field of research, with a focus on statistical and methodological issues that have
captured, and should capture, the attention of researchers in this field.
© 2004 Published by Elsevier B.V.
Keywords: Frontal electroencephalographic asymmetry; EEG; Emotion; Methods; State and trait
The field of research examining frontal electroencephalographic (EEG) asymmetries in

emotion and psychopathology is now over two decades old, with over 80 published studies
documenting relationships between asymmetries in frontal EEG power and emotion-related
traits and states (see Coan and Allen, 2004, this issue, for review). Although data reduction
and analytic techniques have varied across studies, there are many common approaches that
have become quite popular for transforming raw EEG signals to metrics that provide the basis
for making inferences about the role of frontal brain activity in emotion. These approaches
involve many transformations of the data, and in that process involve assumptions that can
impact the interpretations scientists can levy from a given pattern of results.
The aim of this paper, therefore, is to provide a general overview of some of the common
steps involved in data processing in this field, highlighting the assumptions and the impact of
violations of these assumptions for interpreting findings. It is important to note that none of
the issues raised in this paper call to question the now well-replicated relationships between
∗ Corresponding author. Tel.: +1-520-621-4992.

E-mail address: jallen@u.arizona.edu (J.J.B. Allen).
0301-0511/$ – see front matter © 2004 Published by Elsevier B.V.

doi:10.1016/j.biopsycho.2004.03.007
184 J.J.B. Allen et al. / Biological Psychology 67 (2004) 183–218
the metrics of EEG asymmetry and emotional constructs. The issues will, however, have
implications for how the findings best be interpreted.
1. From raw signals to handy metrics
Investigators who examine frontal EEG asymmetry use a set of relatively specialized
signal processing routines, which will be reviewed anon. This review is not intended so
serve as a primer for basic signal processing, but rather is designed to highlight the data
reduction trail typically followed in this specific research domain. For a basic primer, many
sources are available, including easily accessible chapters by Gratton (2000) and by Reilly
(1987), and a more in depth treatment by Glaser and Ruchkin (1976).
Fig. 1 depicts the many steps typically involved in transforming electroencephalographic
signals into metrics that putatively are related to how active various brain regions may be.
This process involves taking a signal collected in the time-domain (Panel A, left side), and
converting it to a frequency-domain representation, usually in the form of a power spectrum
(Panel A, right side). This spectrum, which collapses data across time, summarizes which
frequencies are present to greater or lesser degrees in the time-domain signal. Whether data
are collected from an extended resting period involving several minutes, or from discrete and
relatively short emotion-related segments, this spectral analysis approach always involves
examining the frequency composition of short epochs (Panel B), on the order of 1 or 2 s
each, and averaging power spectra across many such epochs. In the case of resting data,
this involves epoching a large data segment into many smaller epochs. In the case of EEG
acquired in the context of fleeting emotional expression or experience, the data segment
might still require being epoched into a few smaller epochs, and data from several such
expressions or experiences would then be aggregated.
By using epochs that are only 1 or 2 s-long, one more closely approximates an assumption
underlying the Fourier transform, the method used to derive power spectra from raw signals.
Fourier analyses assume a periodic signal (the stationarity assumption), and moreover that
any periodic signal can be decomposed into a series of sine and cosine functions of various
frequencies, with the function for each frequency beginning at its own particular phase.
A periodic signal is one that repeats, and does so at uniformly spaced intervals of time.
Although strictly speaking EEG signals are not periodic, as the repetition of features is
not precisely spaced at uniform intervals, by selecting short epochs one can analyze small
segments of data that will have features that repeat in a highly similar fashion at other points
in the waveform.
Epoching typically involves the construction of overlapping epochs (Panel B), as weight-
ing functions applied in the process of “windowing” (described below) prior to frequency
analysis result in the central portion of the epoch receiving the most weight, and distal
portions receiving negligible weight (Panel C). By overlapping the epochs, all data points
receive maximum weighting in some epoch.
Windowing is used to avoid creating artifactual frequencies in the resultant power spec-
tra. Because Fourier transforms assume a periodic signal, it is assumed that the signal in
the epoch repeats infinitely both forwards and backwards in time, and without the win-
dowing function to reduce the ends of the epoch to near-zero values, discontinuities would
J.J.B. Allen et al. / Biological Psychology 67 (2004) 183–218
Fig. 1. Depiction of the various data reduction steps typically used in frontal EEG asymmetry research. Panel A depicts a 10-s segment of raw data from a single channel
on the left, and the spectral representation of this epoch on the right. Panel B illustrates the process of epoching the longer segment into shorter overlapping 2-s epochs.
Panel C depicts the impact of the Hamming window (dotted bell curve) on a single epoch, with the gray line representing the raw signal and the black line representing
the signal after the application of the window. Note that a discontinuity would result if a copy of the raw (gray) signal were concatenated following this signal, but no
such discontinuity would result for a similarly concatenated windowed (black) signal. Panel D displays the net weighting (black line, scaled to fit graph) of overlapping
hamming windows (gray lines) for 2-s epochs. Panel E illustrates the impact of averaging power spectra. The top nine gray lines are the spectral representation of nine
2-s epochs, and the lower black line is the average spectrum. Note that alpha power (8–13 Hz) is somewhat variable from epoch to epoch, but that the average spectrum
reveals a distinct alpha peak. Vertical axis in Panel E is power in ␮V2 .
185
result if one were to place a copy of the epoch immediately before or after itself. Fourier
methods would introduce a variety of spurious frequencies to reconstruct a signal with such
discontinuity. By windowing, the discontinuity is avoided (Panel C), but at the expense of
preventing the data near the end of the epoch from being fully represented in the resultant
power spectrum. The overlapping of epochs (Panel D) provides a solution to this latter
problem, as data minimally weighted at the end of epoch x will be weighted more heavily
in epoch x + 1.
Most computer signal processing packages use a fast Fourier transform (FFT), which as
the name implies is considerably faster and computationally less complex than the more
general case discrete Fourier transform (DFT). The FFT requires that the epochs to be
analyzed have 2n data points. Data are often sampled at a rate that is a power of two, thus
allowing epochs of 1 or 2 s, but in other cases of sample rates that deviate from a power of
two (e.g., 250 Hz), epoch length will need to be tailored accordingly (e.g., 2.048 s). For a
data segment of 1024 data points, the DFT will take about 10 times longer to arrive at the
same result as the FFT.1
The result of the FFT is two spectra, a power spectrum and a phase spectrum. The power
spectrum reflects the power in the signal at each frequency from dc to the Nyquist frequency,2
with a spectral value every 1/T points, where T is the length of the epoch analyzed. The
phase spectrum presents the phase of the waveform at each interval 1/T. These two spectra
can jointly be used to reconstruct the original time-domain waveform. Psychophysiologists,
however, typically discard the phase spectrum and focus their analyses only on the power
spectrum.
As an FFT is applied to each epoch, many power spectra result, and the average of these
power spectra is ultimately taken as the basis for analysis (Panel E). The data in this resultant
spectrum might entail between 20 and 200 data points (the precise number being T × (f/2),
dependent on the epoch length T and the sample rate f), a substantial reduction from the
raw data signal that will likely have hundreds of data points per second for several minutes.
The spectra represent, therefore, a relatively economical representation of the original sig-
nal, with higher sampling frequencies and longer epochs resulting in more spectral points.
Further reduction is accomplished by summarizing data within conventionally-defined fre-
quency bands. Alpha power, either total (␮V2 ) or density (␮V2 /Hz), is most often examined,
and is typically operationalized as power between 8 and 13 Hz in adults, although lower
frequencies have been examined in children (for review see Coan and Allen, 2003b), as
these lower frequencies in the developing brain are assumed to be equivalent to adult alpha
1 The DFT transform is a general case instantiation of the Fourier transform for discretely sampled signals, but
it is computationally intensive, with the time taken to compute the spectral representation being proportional to
the square of the number on points in the series. The comparable computation time using the FFT, by contrast, is
proportional to N(log2 (N)). For an epoch of 1024 points (N = 1024), the DFT will take 102.4 times longer than
the FFT to compute the spectral representation of the signal.
2 The Nyquist frequency, named after Henry Nyquist, is the fastest frequency that can be represented for a given
sampling rate, and is equal to 1/2 the sampling rate. Nyquist, whose entire career was at AT&T Bell Laboratories,
published a 1928 paper (Nyquist, 1928) in which he proposed a theorem that a sample rate twice as fast as the
highest signal frequency will capture that signal perfectly. Stated differently, the highest frequency which can be
accurately represented is one-half of the sampling rate, and this frequency has come to be known as the Nyquist
frequency.
J.J.B. Allen et al. / Biological Psychology 67 (2004) 183–218 187
3 Skewness
2.5
2
Raw
1.5
0.5
0
-1.5 -1 -0.5 0
Ln-Transformed
Kurtosis
9
8
7
6
5
Raw
4
3
2
1
0
-1 0 1 2 3
Ln-Transformed
Fig. 2. Skewness statistic (top panel) and Kurtosis statistic (lower panel) for natural log transformed (X-axis) and
raw (Y-axis) power values. Statistics were calculated on 34 subjects with complete resting EEG data reported in
Coan and Allen (2003a) for each of 18 scalp sites (FP1, FP2, F3, F4, F7, F8, FTC1, FTC2, C3, C4, T3, T4, T5, T6,
TCP1, TCP2, P3, P4) using the average reference. The solid line in each plot represents the demarcation between
improvement towards normality (above the line) from greater deviation from normality (below the line) as a result
of the natural-log transformation.
(e.g., Fox and Davidson, 1987). Alpha power is then taken as an index of the inverse of
cortical activity (Davidson, 1988), an assumption that will be explored further below.
Alpha power at any given site then is typically natural log transformed, as untransformed
power values tend to be positively skewed, as depicted in Fig. 2. The top panel of Fig. 2
depicts the Skewness Statistic for the raw power values (Y-axis) and the natural-log trans-
formed values (X-axis) at each of 18 scalp sites. The lower panel similarly depicts the
Kurtosis statistic for the same data set. The solid line in each plot represents the demarca-
tion between improvement towards normality (above the line) and greater deviation from
normality (below the line) as a result of the natural-log transformation. As can be seen
from the figure, the transformation improves the skewness for 89% of the scalp sites, and
improves kurtosis for 83% of the scalp sites. In absolute terms, using the 95% confidence
intervals, prior to natural-log transformation, 94% of sites deviated significantly from nor-
mality in terms of skewness, and 83% deviated significantly in terms of kurtosis. Following
transformation, only 33 and 39% of sites still deviated significantly from normality in terms
of skewness and kurtosis, respectively. Thus although some sites still exhibit distributions of
natural-log transformed scores that deviate from normality, the natural-log transformation
substantially improves the distributional characteristics of the data.
2. Comparing left and right activity
Because asymmetrical activity is of interest, investigators often use a difference score

(ln(Right) − ln(Left) alpha power) to conveniently summarize the relative activity at ho-
mologous right and left leads.3 The difference score thus provides a simple unidimensional
scale representing the relative activity of the right and left hemispheres, with higher scores
putatively indicative of relatively greater left frontal activity (assuming that alpha is in-
versely related to activity). An additional benefit of this difference score metric is that it
provides some degree of correction for overall alpha power, as large individual differences
in overall alpha power could be confounded with the magnitude of the asymmetry. The
correction for overall power stems from the fact that the natural log difference score metric
is not a simple difference score, but a difference of natural log transformed scores. Rules
of logarithmic subtraction state that the difference of two natural-log transformed scores is
equivalent to the natural log transform of the ratio of these scores:

R
ln(R) − ln(L) = ln (1)
L
Thus this difference metric is actually the natural log transform of the ratio of right to left
alpha power, which provides some degree of correction for overall power expressing each
subject’s asymmetry in terms of a ratio. The extent of the correction is confirmed by com-
paring the values of the natural log difference score metric to another sometimes-utilized
metric, a “normalized” difference score computed as (R − L)/(R + L). This normal-
ized difference score metric correlates over 0.99 with the natural log asymmetry metric
(ln(Right) − ln(Left); Allen et al., 2004). There is in fact a nonlinear function relating these
two metrics over a broad range of scores, because when either R or L gets very small, the
normalized metric is bounded by the values 1 and −1 and the natural-log asymmetry metric
will not have such bounds. Over the range of values encountered in asymmetry research,
however, the function is almost perfectly linear, as illustrated in Fig. 3.
The difference metric is rather handy in several respects, notably that it mitigates the
impact of individual differences in skull thickness that would have sizeable influences on
recorded signal amplitude (Eshel et al., 1995; Leissner et al., 1970; Pfefferbaum, 1990), and
the difference scores can simplify analyses, such as those involving correlations between
frontal asymmetry (as a difference score) and an individual difference measure (e.g., Be-
3 Similar distributional improvements as a result of natural log transformation are seen for the asymmetry
scores based on these log transformed values. Comparing asymmetry scores based on the difference of natural-log
transformed and untransformed values, the transformation improves the skewness of the asymmetry score for 67%
of the scalp sites, and improves kurtosis for 89% of the scalp sites. In absolute terms, using the 95% confidence
intervals, prior to natural-log transformation, 67% of the differences scores deviated significantly from normality
in terms of skewness, and also kurtosis, but following transformation, only 22 and 33% of asymmetry scores still
deviated significantly from normality in terms of skewness and kurtosis, respectively.
Fig. 3. The relationship of the asymmetry metric (ln(Right) − ln(Left)) and a metric normalized for overall power
((R−L)/(R+L)), over a large range of possible alpha power values. In asymmetry research, the ln(Right)−ln(Left)
metric produces scores that typically are in the range of ±0.5, the range demarcated by the two lines, where the
relationship is linear. From Allen et al. (2004), reprinted with permission from Blackwell Publishing. © 2004,
Society for Psychophysiological Research.
havioral Activation Scale; Coan and Allen, 2003a; Harmon-Jones and Allen, 1997; Sutton
and Davidson, 1997).
Difference scores have been criticized for their potential unreliability, as errors of mea-
surement with each of the constituent scores are compounded when the difference score is
calculated. The reliability of change scores is of greatest concern, however, when the con-
stituent scores have modest reliability. Alpha power at a given lead, however, demonstrates
extremely high reliability, with coefficient alpha values typically over 0.90 based on 8 min
of data. Moreover, the reliability of the difference score for frontal regions has been calcu-
lated in several studies and routinely is high, excepting frontal pole sites (e.g., coefficient
alphas for frontal asymmetry (difference) scores ranging from 0.85 to 0.90 at baseline in
Allen, Urry, Hitt, and Coan (2004); from 0.76 to 0.91 in Coan and Allen (2003a); a median
of 0.83 in Coan et al. (2001); from 0.80 to 0.93 in Reid et al. (1998); and from 0.81 to 0.92
in Tomarken et al. (1992)).4
4 A separate issue concerns the power of statistical tests that employ difference scores. The power of significance
tests using difference scores is only indirectly influenced by the reliability of these scores. Significance tests of
differences can be powerful even if the reliability of the difference scores is near zero (Overall and Woodward,
1975; Zimmerman et al., 1993). The paradox pointed out by Overall and Woodward (1975) is that difference scores
with zero reliability can in fact give rise to high power to detect a significant difference. The paradox is resolved
when one considers that reliability of the difference scores depends on the existence of variance in the difference
score that can reliably rank-order individuals in terms of the magnitude of their difference scores, but that the
power to detect a difference involves assessing a mean difference between the two scores relative to the variance in
Despite the simplicity of the difference score, the contribution of activity in each hemi-
sphere is ultimately of interest, which will require analyses involving the examination of
data from each hemisphere as a difference metric is uninformative with respect to the con-
tribution of each constituent hemisphere (Davidson et al., 2000a). The most straightforward
approach involves analyzing (ln-transformed) power at left and right sites in an analysis of
variance (ANOVA) or the more general linear model (GLM), with not only region (anterior
to posterior) as a factor, but hemisphere (left versus right) as well. In these models, indi-
vidual differences in overall power are removed, and region specific variations in power
(e.g., occipital alpha is greater than frontal alpha) are partitioned as region main effects. In
such a model, with EEG power as the dependent variable, the interaction of an independent
variable with hemisphere will yield the same information as a main effect of this inde-
pendent variable when using asymmetry scores as the dependent variable. The follow-up
tests to decompose the interaction can then examine the contribution of each hemisphere
individually.
The standard ANOVA approach provides a straightforward method of examining the
power from each hemisphere’s lead or leads when the independent variable of interest is
amenable to the ANOVA approach, such as when comparing depressed and nondepressed
subjects, or when comparing two or more emotion elicitation conditions. This approach
is limited, however, as the standard ANOVA with a between subjects or within subjects
factor fails to allow for an examination of the power at a given lead or leads with a contin-
uously varying independent variable such as ratings of emotional valence or intensity, or
an individual difference variable such as behavioral activation. There exist a few published
approaches that have included a continuous predictor in the model, the whole-head and
homologous-lead residualized power approach first reported by Wheeler et al. (1993), and
the hierarchical general linear model strategy (e.g., Coan and Allen, 2003a) or mixed model
strategy (e.g., Kline et al., 2002).
2.1. Residualized power approach
Wheeler et al. (1993) adopted a two-stage analytic approach, examining first the corre-
lation between the asymmetry difference score and continuous measures of self-reported
this difference score. Thus if one constituent score (e.g. Left activity) were for every subject a constant k less than
the other constituent score (e.g. Right activity), then there would be no variability in the difference scores, and no
reliability. On the other hand, the mean difference score would be k, with no variance around that mean, allowing
for a powerful statistical test that the mean difference is significantly different than zero, and that a statistically
significant difference has been found. The pragmatic implications are that the reliability of difference scores if are
of little consequence if one wishes to test the significance of such a difference (e.g. to test that Right activity is
greater than Left activity for the group as a whole), but the reliability of the difference score will be highly relevant
when one is using the difference score to examine how individual differences in that difference score relate to
other variables of interest (e.g. how individual differences in the asymmetry score relate to individual differences
in BAS scores). In the latter case, the reliability of the difference score will impose constraints on the magnitude
of the correlation that can be observed, as the maximum correlation that can be observed between two variables
will be the square root of the product of the reliability of the two variables. Thus, because a sizable portion of the
research examining frontal EEG asymmetry is concerned with the relationship of individual differences in frontal
EEG asymmetry to other individual difference measures, the reliability of the asymmetry metric assumes great
importance.
Table 1
Correlations between natural-log transformed alpha power at homologous leads collected for 8 min under resting
conditions
Sites Reference
AR LM
FP1–FP2 0.997 0.998

F7–F8 0.983 0.971
F3–F4 0.990 0.992
FTC1–FTC2 0.975 0.943
C3–C4 0.977 0.981
T3–T4 0.918 0.891
TCP1–TCP2 0.944 0.948
P3–P4 0.965 0.982
T5–T6 0.907 0.932
Note. AR: average reference, LM: computer linked mastoid reference; data from 34 subjects reported in Coan
et al. (2001).
affect. Upon finding significant correlations, the second stage was to investigate the contri-
bution of each hemisphere, but unconfounded by the large individual differences in power
due to irrelevant factors such as scalp thickness. Power at a given electrode (e.g., F3) was
residualized, using a hierarchical regression, first entering the average power across avail-
able scalp sites, and as the second step entering power from the homologous lead (e.g., F4).
The resultant residualized values were then correlated with the variable of interest (e.g.,
self-reported affect).
The first step of this procedure preserves individual patterns of activity across scalp sites,
adjusted for overall power. The second step of this procedure was introduced by Wheeler
et al. (1993) ostensibly to statistically account for volume-conducted activity from the ho-
mologous electrode. It is unclear why one would be more concerned with volume conduction
from a lead over the opposite hemisphere, which in many instances is considerably further
away from the site of interest than ipsilateral leads adjacent to the site. On the other hand,
the activity between homologous leads is often highly correlated, with alpha power values
being correlated on the order of 0.95 or even higher (see Table 1),5 and could in part reflect
the dense contralateral cortico-cortical connections between some homologous regions as
well as volume conduction effects. As seen in Table 1, correlations are uniformly high, but
higher yet between closely spaced homologous leads (e.g., FP1 and FP2) as compared to
more widely spaced homologous leads (e.g., T5 and T6). Whether volume conducted, or
the result of interconnectivity, the second step of the regression approach of Wheeler et al.
then statistically controlled for shared variance between left and right homologous leads,
which is likely to be substantial.
5 The fact that the difference between these highly correlated sites is nonetheless predictive of state affect
and individual differences merits a brief comment. The asymmetry score reflects the difference between the
contribution of the activity of the left and right leads within subjects, whereas the correlations between sites reflect
the similarities of activity at each lead across subjects. It is thus the case that between-person differences in alpha
power at a given site are substantially larger than the within person differences between sites, but that the latter
nonetheless have some degree of predictive validity.
Fig. 4. Correlations between Behavioral Activation Scale (BAS) scores and EEG asymmetry (left panels) and resid-
ualized power at constituent sites (right panels), for data under an averaged reference (AR) and computer-averaged
mastoids (CAM) reference. Data from subjects presented in Coan and Allen (2003a).
The results of this procedure produce what has become a fairly typical pattern: for each
significant correlation between the R − L difference score and a criterion, two significant
correlations emerge, approximately equal in magnitude to the original correlation, but op-
posite in sign to one another, at the constituent leads. Correlations at the right lead maintain
the sign of the R − L difference score, and correlations at the left lead reverse direction. For
example, Wheeler et al. (1993) found that the F4–F3 (ln-transformed) asymmetry score cor-
related with positive affect 0.45, and that residualized ln-transformed power at F4 correlated
0.44 and at F3 correlated −0.49 with positive affect. Similarly, Harmon-Jones and Allen
(1998) found that the F4–F3 (ln-transformed) asymmetry score correlated 0.48 with trait
anger, and that residualized ln-transformed power at F4 and F3 correlated 0.45 and −0.46,
respectively, with trait anger. To illustrate more generally this pattern, Fig. 4 presents corre-
lations between BAS scores and asymmetry scores (left panels) and residualized power at
constituent sites (right panels). Treating these correlations themselves data points, the ob-
tained values from residualized power at right leads correlated 0.94 with the values obtained
using the difference score, and the values from residualized power at left leads correlated
−0.88 with those obtained using the difference score. Additionally, the values obtained
using residualized left values correlated −0.87 with those obtained using residualized right
values.
Thus, the procedure that was originally devised to examine the independent contributions
of each hemisphere would appear to distribute the variance relatively equally and in opposite
directions across the two hemispheres, which would be expected if activity at homologous
leads is extremely highly correlated, as is the case with homologous left and right lead power
(Table 1). To demonstrate why such a pattern would be expected with such highly correlated
data, consider the impact on residualizing left hemisphere power on right hemisphere power.
The residualized score (Lresid ) for a left hemisphere lead (L) is given by
Lresid = L − L̂ (2)
where L̂ is the predicted power at the left hemisphere lead given power at the right hemi-
sphere lead, determined by the raw score regression (prediction) formula:
L̂ = a + b(R) (3)
where a is the intercept and b is the unstandardized regression coefficient. In the case where
L and R are nearly perfectly positively correlated (see Table 1), with the distribution of each
having virtually identical means and standard deviations, the intercept a will approach 0,
and the regression coefficient b will approach one,6 reducing Eq. (3) to:
L̂ ≈ 0 + 1(R) = R (4)
Substituting the results of Eq. (4) for L̂ in Eq. (2), it is revealed that, when L and R are
nearly perfectly correlated:
Lresid = L − L̂ ≈ L − R (5)
Thus this residualization procedure produces residual values for left hemisphere leads that
will approach the value L − R as the correlation between left and right leads approaches
1.0, provided that the unstandardized regression coefficient approaches 1 and the intercept
approaches 0. Similarly, by implementing Eqs. (2)–(5) for right hemisphere residualized
(Rresid ) and predicted (R̂) scores, it will be the case that residual values for right hemisphere
leads will approach the value R−L as the correlation between left and right leads approaches
1.0. Therefore, this procedure will make it appear that right hemisphere leads correlate with a
criterion variable in the same direction and approximate magnitude as the R − L difference
score, and that left hemisphere leads correlate with a criterion variable in the opposite
direction but same approximate magnitude as the R − L difference score.
6 Empirically, it appears to be the case that the unstandardized regression weight is very close to one and
the intercept is very close to zero. Resting data for 34 subjects (from Coan et al., 2001) were used to predict
left hemisphere frontal activity from the homologous right hemisphere frontal activity. For the prediction of four
frontal sites (FP1, F7, F3, and FTC1), each from its homologous right hemisphere site (FP2, F8, F4, and FTC2),
across both LM and AR reference schemes (for a total of eight separate regressions), the median unstandardized
regression coefficient was 1.028 (range: 1.012–1.071) and the median intercept was −0.039 (range: −0.098 to
0.031).
2.2. Revised residualized power approach
More recently, Davidson et al. (2000a) have proposed an improved variant on the method
of Wheeler et al. (1993), one that does not include homologous lead power in the resid-
ualization calculations. This approach first residualizes the criterion variable on whole
head power, and then calculates correlations between the residualized criterion variable
and power at each individual site (Davidson et al., 2000a, p. 41; Davidson, 2002, personal
communication). This method obviates the problem detailed above using the homologous
lead to residualize power at each site, but will produce a large set of correlations (one for
each scalp site) that are not tested formally in a model that can control for experiment-wise
alpha slippage. Such correlations are quite informative, but ultimately must be regarded as
descriptive. To adequately test the relationship between power at each site and the criterion
variable, an omnibus model is required. Although the precise model will depend on the
nature of the investigation, and the theory being tested, an alternative approach might be
for investigators to specify a hierarchical general linear model in testing the relationship
of left and right sites to criterion variables, as highlighted below. Such an approach might
limit the undesirable probabilistic artifacts involved in multiple statistical tests, optimizing
risk for both type 1 and type 2 errors in estimating both the impact of whole head power
and effects of interest. Further, such single model approaches may economize data analytic
effort and reporting.
2.3. Hierarchical general linear models
Hierarchical general linear models can simultaneously account for the multiple sources
of variance contributing to the relationship between cortical asymmetry and criterion vari-
ables. Such models can include both categorical and continuous predictors, and can be
constructed to test a variety of specific hypotheses of interest, including those related to
overall power, hemisphere, and even reference scheme, all in a single model. In fact, in-
teractions with reference scheme can be entered into such a model in order to determine
whether relationships between asymmetry and the criterion variable are dependent upon
reference scheme.
In constructing the model, some general principles may guide the investigator. First, the
model should be explicitly specified, and whenever possible should be an omnibus model
that can test all effects of interest at once. Second, the investigator should use theory to
guide the ordering of the main effects followed by the interactions of these main effects. In
most cases, main effects per se will not be of interest (e.g., they may reflect the contribution
of overall power to the prediction of the criterion variable, or differences in overall power
between anterior and posterior regions), but the interactions will be of interest. Interactions
of hemisphere and region in predicting the criterion variable, for example, would be found
if there are frontally-specific hemispheric differences in the contribution of left and right
leads to the prediction of the criterion variable. A higher-order interaction with reference
scheme would further indicate that the pattern of findings is reference-scheme dependent.
Of course, the use of theory and careful sensitivity to the possibility of spurious interaction
effects is particularly important as the complexity of interactions increases. As interaction
effects reach beyond third order, the probability of overfitting the observed data—essentially
modeling meaningless residual variance—increases. While testing for most or all effects
of interest in an omnibus model is highly desirable, it is not advisable if doing so requires
the modeling of very complex (e.g., greater than fourth order) interactions. Thus a third
principle might be to reduce the potential for spurious findings and complex interactions
in the hierarchical linear model designed to test for specific contribution of hemisphere
by first running a simpler but conceptually related model using the asymmetry scores.
Then, following this simpler model, natural-log transformed power at constituent sites can
be entered for the relevant regions where the asymmetry score identified a relationship
between asymmetry and the criterion variable.
As an illustration, data from Coan and Allen (2003a) are presented, the same data that were
used in Fig. 4 to illustrate the residualization approach. First, an omnibus hierarchical linear
model using asymmetry scores from eight regions across the scalp under both averaged
reference and computer averaged mastoids reference schemes were used to construct a
model predicting BAS scores. To code reference scheme, data from each reference scheme
were concatenated, and a contrast-coded variable was used to code for reference scheme
(cf. Aiken and West, 1991). The model first entered the main effect of reference scheme,
followed by the main effects of regions ordered according to theoretical interest and results
of previous studies. Sites entered first were frontal and anterior temporal sites, followed
by sites from central to parietal: F4–F3, F8–F7, FTC2–FTC1, T4–T3, C4–C3, T6–T5,
TCP2–TCP1, and P4–P3. Finally, interactions of each region with reference scheme were
entered to test for the reference-specific effects. In this model, only the main effect of
F4–F3 was significant in predicting BAS scores (F(1, 46) = 8.5, P < 0.01), with trends
for contributions from the main effects of F8–F7 (F(1, 46) = 3.6, P < 0.10) and C4–C3
(F(1, 46) = 3.6, P < 0.10). Reference scheme did not interact with any effects in this
model.
Thus the focus of the subsequent analysis was to examine the contribution of left and
right hemisphere in the significant midfrontal region. In this hierarchical general linear
model, BAS scores were the dependent variable to be predicted by (1) whole head power;
(2) reference scheme and (3) natural log-transformed alpha power in the left (F3) and right
(F4) hemispheres. This model, with whole head power entered first, is akin to the procedure
described by Davidson et al. (2000a) to statistically partial out the effect of overall power in
predicting BAS score. In this model, main effects of each site were of interest. Interactions
with reference scheme were entered into the model in order to determine whether any
relationships between site and BAS scores were dependent upon reference scheme.7
The overall model was approached statistical significance (F(9, 54) = 1.94, P =
0.07, adjusted-R2 = 0.12). Results indicated a main effect of the right hemisphere at
F4 (F(1, 54) = 9.61, P < 0.01, η2 = 0.15) but not of the left hemisphere at F3 (F(1, 54) =
2.49, P = 0.12, η2 = 0.04). No interactions with reference scheme were significant, in-
dicating that individual differences in right frontal activity were related to differences in
BAS scores, and that this main effect of the right hemisphere was not dependent upon
reference scheme. Fig. 5 depicts specific left/right relationships with BAS scores for F4
and F3. To estimate regression lines for both F3 and F4 separately, two hierarchical gen-
7 Had the first model included additional regions of significance, such a model could also include the interaction
between hemisphere (left, right) and region (e.g. mid-frontal and lateral-frontal).
BAS
55 right
50
45
40
35
30
left
25
20
-2 -1 0 1 2 3
ln(Alpha Power)
Fig. 5. Regression lines for left and right midfrontal (F3 and F4) ln-transformed alpha power predicting BAS scores.
The regression equations depicted are: BAS = (5.12) × (Left) + 37.41; BAS = (−1.98) × (Right) + 36.658.
eral linear models were run, one each for F3 and F4. For these models, reference scheme,
whole head alpha power, and each site were entered such that (1) the effects of reference
scheme and whole head alpha power were each removed before the b-coefficient for each
site was estimated, and (2) dependence upon both reference scheme and whole head power
could be estimated. Notably, neither model is, by itself, statistically significant, but it is
nevertheless useful to estimate such curves in the service of understanding the significant
effects reported above. Apparent using this method, but not the residualization approach,
is that the relationships between BAS and each hemisphere are not a mirror opposites, but
in fact BAS is robustly related to right hemisphere activity, and largely not related to left
hemisphere activity, a surprising result given the theoretical notions concerning the left
hemisphere and approach-related motivation (Coan and Allen, 2003a,b; Davidson, 1992,
1998; Harmon-Jones and Allen, 1997).
3. Data acquisition
3.1. How much raw data should be acquired?
Sufficient data are required to ensure that reliable estimates of EEG activity are derived.
Although the power spectrum derived from any single epoch via the FFT will reflect both
frequencies that are common across epochs as well as those idiosyncratic to any given
epoch, averaging together multiple spectra can allow those frequencies to emerge that are
present in a reasonably large proportion of epochs (see Fig. 1, Panel E), while mitigating the
influence of infrequent or irregular signals (Nunez, 1981), which might often be considered
noise. Thus an investigator, by averaging across epochs, makes the implicit assumption
that the frequencies that appear commonly across epochs are of interest, and epoch-specific
variations are of little interest. In the case of estimating trait asymmetry with the goal of
predicting psychological traits or psychopathology, this is clearly a reasonable assumption.
On the other hand, a recent investigation found that variability from epoch to epoch was
itself an important correlate of neuroticism (Minnix and Kline, 2004).
To reliably estimate EEG asymmetry at any given assessment session, investigators and
reviewers often suggest that 8 min of resting EEG asymmetry are necessary to obtain ade-
quate internal consistency reliability, as this was the number reported in the first psychome-
tric investigation of resting EEG alpha asymmetry (Tomarken et al., 1992). Substantially
fewer 1-min samples, however, also can produce acceptable estimates of internal consis-
tency (Tomarken et al., 1992), and estimates based on even shorter time frames of 2 min
have proven similarly reliable (Coan et al., 2001).
Tomarken et al. (1992) assessed the reliability of fewer than 8 min of data in a way
that confounded the length of recording with the number of discrete items included in the
calculation of coefficient alpha; i.e., they used the Spearman–Brown prophecy formula to
estimate the reliability for shorter recording periods, estimating alpha based on six asymme-
try values for 6 min of data, seven values for 7 min, and eight values for 8 min. To adequately
test whether fewer minutes of recording would produce estimates of internal consistency
comparable to those obtained with more minutes of recording, it would be required to keep
the number of values constant despite changes in the length of recorded data, as Cronbach’s
alpha will be higher given more minutes (items) for analysis (Lord and Novick, 1968).
In a recent study (Allen et al., 2004), reliability estimates from 2, 4, 6, and 8 min of data
were compared. Specifically, the first 2, 4, and 6 min as well as all 8 min of recorded data
were divided into eight blocks each. Each block contained 2-s overlapping epochs that were
subjected to Fourier analysis as reviewed above. In each case, eight asymmetry values were
obtained, reflecting the asymmetry score averaged across 1/8 of the total time of recording
(15 s for the 2-min data, 30 s for 4-min data, 45 s for the 6-min data, and 60 s for the 8-min
data). These eight values were then treated as items on an eight-item scale to assess internal
consistency reliability.
Fig. 6 shows the results for frontal regions as a function of reference scheme. As can
be seen in the figure, the number of minutes of recording exerts relatively little influ-
ence on the estimate of internal consistency compared to the number of blocks included
in creating the estimate. Whether 2, 4, 6, or 8 min of data are utilized, very small dif-
ferences are apparent when all eight data segments are used as items for the purpose of
estimating internal consistency reliability. Reliability estimates begin to diverge, however,
when fewer segments are utilized to estimate reliability. Thus highly internally consistent
measures of asymmetry can be obtained with considerably fewer than the conventionally
accepted 8 min of recorded data, provided that internal consistency is estimated with a
sufficient number of constituent blocks. To highlight this point, consider a comparison
of two comparable data points from Fig. 6: four 60-s blocks or eight 30-s blocks, which
correspond to identical timepoints from the EEG record. In all nine cases (3 regions × 3
reference schemes), the internal consistency of the latter is higher than the former, by
an average of 0.06 reliability units. It also appears to be the case that when fewer than
four blocks are used to estimate the reliability, the expected rank ordering of reliabilities
becomes less orderly, in some cases with longer recording blocks demonstrating lower
reliability than shorter blocks. Thus, regardless of the total length of data collected, at-
tempting to estimate reliability with insufficient blocks will lead to misleading estimates
of internal-consistency reliability. If investigators have fewer than 8 min of data available,
reliable estimates of asymmetry can likely be derived, but it is recommended that inves-
tigators report the internal consistency reliability of asymmetry scores based on the data
198
J.J.B. Allen et al. / Biological Psychology 67 (2004) 183–218
Fig. 6. Cronbach’s alpha internal consistency estimates for resting alpha asymmetry as a function of region, reference scheme, length of data recording, and number of
blocks (items) used to calculate alpha. The number of subjects ranges from 19 to 28, reflecting that some subjects did not have enough artifact-free 2-s epochs to compute
power spectra for the for shorter recording intervals, or that a recording site was bad for a given subject. Midfrontal: F4–F3, lateral frontal: F8–F7, and Fro-Tem-Cen:
fronto-tempo-central. From Allen et al. (2004), reprinted with permission from Blackwell Publishing. © 2004, Society for Psychophysiological Research.
available, detailing how many epochs were treated as items in the calculation of Cronbach’s
alpha.
3.2. What reference montage is preferred?
The choice of reference has been referred to as “perhaps the most divisive issue among
current EEG researchers” (Davidson et al., 2000a, p. 33). Although rational arguments have
been levied in favor of one or another reference scheme (e.g., Hagemann et al., 2001; Reid
et al., 1998), it remains an empirical question which reference scheme has the greatest
predictive validity with respect to motivation, emotion, and psychopathology. Investigators
would ideally like measures of spectral power at a given site to reflect the activity at that
site, and not at the reference lead. For this purpose, investigators often search for a relatively
inactive reference, and have used linked ears or mastoids, averaged ears or mastoids, or an
average reference comprised of the average of activity at all recorded EEG sites. The average
reference, given a sufficiently large array of electrodes in a spherical arrangement around
the head, will nicely approximate an inactive reference, as activity generated from dipoles
will be revealed as positivity at one site and negativity at a site 180◦ opposite this site,
with the sum across sites thus approaching zero with a sufficiently representative sample
of the sphere. Smaller montages, and those that do not provide coverage approximating the
sphere, however, will have more residual activity in the average reference.
Especially troubling is the Cz reference, which has been utilized more often in the EEG
asymmetry literature than other reference montages (see Coan and Allen, 2003b for review).
The Cz reference has been criticized as potentially under- or over-estimating activity at the
target site (Hagemann et al., 2001). Moreover, empirical comparisons of data from different
reference schemes have found Cz to be the least related to other reference schemes (e.g.,
Hagemann et al., 2001; Reid et al., 1998). The fact that many studies have successfully
identified predicted relationships using the Cz reference suggests at least two non-mutually
exclusive possibilities: (1) significant results using the Cz reference reflect, in part, not only
the relationship of constructs with frontal asymmetry, but also with sources of variance
unique to the Cz reference (e.g., overall alpha power); and/or, (2) asymmetry scores us-
ing the Cz reference may have more irrelevant variance (error or systematic) with respect
to asymmetry, and may therefore result—across studies—in inconsistencies in the pattern
of empirical relationships with motivation, emotion, and psychopathology. Distinguishing
between these possibilities will be facilitated if investigators report results from multiple
reference montages. Moreover, various reference schemes can be conceptualized as con-
tributing unique sources of error variance to any given analysis, providing the researcher
with semi-independent measures of EEG activity, with findings that are statistically inde-
pendent of reference scheme being considered the most generalizable, being less likely to
reflect only the reference-specific “method” variance (cf. Campbell and Fiske, 1959).
3.3. Impedances in asymmetry research
It has been customary in EEG asymmetry research to strive to obtain low and symmetrical
impedances during subject preparation. Intuitively, this seems desirable, as one would wish
to have a strong noise-free signal by lowering impedance, and would like to guarantee that
any observed alpha power asymmetries reflect an underlying asymmetry in activity, rather
than an asymmetry in impendence to recording the underlying signal. As pointed out by
Ferree et al. (2001), however, contemporary high impedance amplifiers mitigate the impact
of scalp impedances on the recorded signal, as the loss in the observed signal due to scalp
impedances is directly related to the average impedance of the measurement and the refer-
ence electrode, and inversely related to the amplifier input impedance. Because amplifier
input impedances are typically on the order of tens (or even hundreds) of megaohms, and
scalp impedances on the order of a few kilohms, small changes in scalp impedance do not
appreciably impact the observed signal, as the magnitude of the amplifier input impedance
is at least 1000 times greater than the scalp impedance.
The observed voltage for a given electrode E with a given reference electrode R is the
measured voltage difference between these electrodes, or VE −VR . This difference, VE −VR ,
is influenced by electrode impedance ZE and reference impedance ZR and input impedance
Zin as follows (Ferree et al., 2001, p. 538):
2
Z E + ZR ZE − Z R 1
VE − VR = VD 2− + VC +O (6)
Zin Zin Zin
where VD is the actual differential-mode signal (VE true −VR true )/2, and VC is the common-
mode signal (VE true − VR true )/2. The latter term VC results primarily 60 cycle (US)
or 50 cycle (Europe) ambient noise, and the extent to which it emerges is a function of
impedance mismatch. The former term VD is primarily the signal of interest, resulting
from voltage potential differences between the two sites, but attenuated by the ratio of
the scalp impedances to the amplifier input impedance. Since the scalp impedances are
a tiny fraction of the size of the input impedance, even appreciable differences in scalp
site impedance will not measurably attenuate the voltage potential difference observed be-
tween the two sites. The final term in the equation is a residual term to account for other
sources in the differential amplifier circuit that influence the observed voltage potential
difference, the sum of which are negligible (Ferree, 2002, personal communication). The
mathematical notation O is standard for “order” in Taylor series, and simplifies the expres-
sion without appreciably altering the result obtained with the simplified equation involving
only the first two terms. In the full equation there are a series of higher order terms in-
volving powers of 1/Zin , which the term O(1/Zin )2 denotes. With a high input impedance
Zin , the impact of (1/Zin )2 will be negligible, and the impact of higher powers approaches
zero.
Fig. 7 depicts the impact of mismatched impedances under conditions likely to be encoun-
tered in a psychophysiological laboratory. The data depicted in Fig. 7 show the observed
asymmetry score (ln(Right) − ln(Left)) as a function of amplifier input impedance, and
impedance at left (zleft ) and right (zright ) leads. Data in the left panel depict the impact of
mismatched left and right lead impedances with an input impedance of 10 m (that of the
Neuroscan Synamps system, Neuroscan a Compumedics Company, El Paso, TX), and data
in the right panel depict the same with an input impedance of 20 m (that of the Grass
Model 12 Neurodata system, Grass Telefactor an Astro-Med Inc. Product Group, West
Warwick, RI). Data were obtained by solving Eq. (5) independently for left and right leads,
for impedances ranging from 0.2 to 10 k, assuming a reference electrode impedance of
Fig. 7. Asymmetry score (difference of natural log scores) as a function of amplifier input impedance, and
impedance at left (zleft ) and right (zright ) leads. For both plots, reference electrode impedance is set to 1 k.
The computed voltage at both left and right leads was squared to produce power units, and the difference of the
natural log transformed power values (ln(Right) − ln(Left)) was plotted on the vertical axis. Top two panels depict
the observed asymmetry score when the right lead’s true signal was 5 ␮V larger than the left, and the lower two
panels depict the asymmetry score when the right lead’s true signal was 0.5 ␮V larger than the left. Note that the
top two panels are on the same scale, and the bottom two panels share a different scale.
1 k.8 The resultant values for left and right leads were then used to compute the asymmetry
score (ln(Right) − ln(Left)) for all combinations of left and right impedances.
Two aspects of Fig. 7 warrant comment. First, the overall impact of impedance mismatch
ranging from 0 to 10 k between left and right leads is negligible, and apparent only in the
sixth decimal place of the asymmetry score. Differences between hemispheres and between
groups of subjects, on the other hand, are readily apparent in the first decimal place (cf.
Henriques and Davidson, 1990, 1991; Reid et al., 1998). Differences in left and right lead
8 Results remain essentially unchanged if reference impedance is higher than 1 k, as the reference impedance
appears similarly in the equation for calculating observed left lead and observed right lead voltage.
impedances are thus unlikely to spuriously create or mask veritable differences in left and
right alpha power. Second, the impact of the mismatch is further attenuated as a function
of the higher input impedance amplifier. Asymmetry scores vary by 7.7 × 10−6 with the
10 M input impedance, and by 3.9 × 10−6 with the 20 M input impedance, when true
voltage differences are 0.5 ␮V. Variation would be even less with higher input impedances
(such as the 200 M input impedance of the Net Amps, Electrical Geodesics Inc., Eugene,
OR).
3.4. Dealing with ocular and muscular artifacts
EEG recordings may contain not only brain electrical activity, but non-cerebral contri-
butions to the observed signal, including artifactual contributions of the scalp muscles and
potentials generated by eye movements and blinks (Gratton, 1998; Picton et al., 2000).
Although careful screening and rejection of data segments contaminated by the artifacts is
likely to remove many of the artifacts, it may be desirable to obtain an estimate of the extent
to which such artifacts may be influencing the results of an investigation.
3.4.1. Electrooculographic (EOG) influences

The eyes, being ion-filled imperfect spheres, carry a positive charge at the relatively
leptokurtotic cornea, and a negative charge at the relatively platykurtotic retina. Being
mobile, these charged spheres create electrical fields that are observed as signal in the case
of EOG recordings, or artifact in the case of EEG recordings. Moreover, the conductive
eyelid acts as a variable resistor as it slides across the cornea, momentarily distributing
the ocular potential across the scalp. Thus ocular movements and blinks can be observed
in scalp-recorded EEG, with the magnitude of the EOG signal decreasing as a function
of the distance from the eyes. Although a majority of the signal of ocular origin is in the
delta and theta range (Gasser et al., 1985; Hagemann and Naumann, 2001), slower than
the 8–13 Hz alpha range of interest in EEG asymmetry research, some activity in the alpha
band will inevitably be present, some potentially of neural origin (cf. Iacono and Lykken,
1981). The concern that activity of ocular origin may contaminate scalp-recorded EEG has
prompted investigators utilizing EEG asymmetry to often reject epochs containing blinks
or other ocular artifact. Moreover, the concern that the EOG signal may contain alpha-band
activity of neural origin has discouraged investigators from employing a simple correction
procedure that subtracts a portion of the time-domain EOG signal from the time-domain
EEG signal, for doing so might also subtract alpha activity of neural origin.
Hagemann and Naumann (2001) carefully examined the contribution of ocular sig-
nals to scalp-recorded EEG asymmetry scores. Reviewing the literature, Hagemann and
Naumann (2001) suggested that ocular artifacts are not likely to artifactually create or miti-
gate alpha-band asymmetries from homologous scalp leads, because: (1) power in the alpha
band that is observed in EOG recordings is predominantly neural in origin, thus making
it unlikely that ocular movements and blinks will appreciably alter scalp-recorded alpha
activity, and (2) eye-movements and blinks are propagated relatively symmetrically. The
symmetric propagation of vertical eye movements and blinks is apparent in the raw signal,
but even lateral eye movements will be reflected similarly in the power spectra of left and
right sites due to such movements creating similar magnitude but phase reversed deflec-
tions; the FFT will produce similar power spectra but different phase spectra, with only the
power spectra of interest in EEG asymmetry research.
Assessing the contribution empirically, Hagemann and Naumann (2001) found that alpha
asymmetry scores (ln(Right)−ln(Left)) derived from 8 min of resting EEG were highly sim-
ilar when computed with versus without epochs containing ocular artifacts. The correlations
between asymmetry scores from a dataset that included all epochs free of non-ocular artifacts
and the same dataset with ocular-contaminated epochs were greater than 0.82 for all re-
gions except the frontal pole, which was substantially lower. Effects of ocular-contaminated
epochs, however, were larger for single sites than for corresponding asymmetry scores, fur-
ther supporting the notion that ocular artifacts propagate symmetrically across most of the
scalp.
Hagemann and Naumann (2001) concluded that the control of ocular artifacts may thus be
unnecessary for correlational analyses involving alpha asymmetry scores, but that analyses
involving mean levels may be influenced by ocular artifacts. Although the data in support
of their conclusion is relatively strong—as the correlations are high between asymmetry
scores from data with versus without artifacts—it is worth noting two issues that were not
considered or assessed fully, and that remain to be investigated empirically. First, no rela-
tionships between alpha asymmetry and a criterion variable (e.g., BAS scores, cf. Coan and
Allen, 2003a; Harmon-Jones and Allen, 1997; Sutton and Davidson, 1997) were investi-
gated. Although the high correlation between asymmetry scores obtained from data with
and without ocular artifacts would suggest that each would demonstrate similar correlations
to a criterion variable, it is possible that the variance that is not shared by the two sets of
asymmetry scores is differentially related to the criterion variable. Because the correlation
between the two sets of asymmetry scores is attenuated the most at frontal leads by the in-
clusion or exclusion of epochs with ocular artifacts, and because it is precisely these regions
that are of greatest interest with respect to the criterion variable, the possibility is amplified
that the two sets of scores may relate differentially to a criterion variable. The second issue
to consider derives from this possibility. Despite the careful analysis of Hagemann and
Naumann (2001), one cannot differentiate between two possibilities: (1) that the true brain
activity is invariant across epochs with and without ocular artifacts, but the presence of the
ocular activity influences the observed EEG recording, or (2) the asymmetry scores differ
because the true EEG activity differs as a function of whether blinks or eye movements are
occurring. Given that eye-blinks show predictable relationships to cognitive processing and
attention (Stern et al., 1984), this latter possibility must be considered in earnest.
3.4.2. Facial electromyographic (EMG) activity

Scalp-recorded EEG alpha activity may artifactually reflect the contribution of EMG
activity (Cacioppo et al., 1990; Friedman and Thayer, 1991). Although the vast majority
of the power in the EMG signal is faster than the alpha band, EMG activity has broad fre-
quency characteristics with some small proportion of activity evident in the alpha band. This
problem is potentially exaggerated by the fact that facial EMG asymmetries—sometimes
similar in direction to reported cortical EEG asymmetries—have been observed (Borod
et al., 1997), although the consistent and robust finding to emerge from this literature is an
asymmetry characterized by greater left side activity in facial expressions in general, across
all specific emotions and elicitation procedures.
Friedman and Thayer (1991) examined the potential magnitude of the EMG contribution
to EEG recordings with the use of a redundancy analysis, which can be used to account for
overlap between cortically derived alpha power and alpha power due to facial muscle activa-
tion. In their analysis, facial EMG accounted for 7% of the variance in cortical EEG activity,
while cortical EEG activity accounted for only 3% of the variance in facial EMG, suggesting
that facial EMG is likely to be responsible for a small but potentially important portion of
the variance in scalp-recorded EEG. This study did not, however, specifically address the
extent to which asymmetries in facial EMG activity were contributing to asymmetries in
scalp EEG.
Coan et al. (2001) assessed the influence of EMG on scalp recorded alpha during a di-
rected facial action task using two strategies. The first, a strategy used also by Davidson
and colleagues (cf. Davidson, 1988; Davidson et al., 2000b), involves assessing EMG fre-
quencies at scalp sites of interest. This approach extracts EMG frequencies (70–80 Hz in
Davidson et al., 2000b or 70–90 Hz in Coan et al., 2001) from the power spectrum at each
site involved in the EEG analysis. Because Coan et al. (2001) were analyzing EEG asym-
metry scores, EMG asymmetry scores (ln(Right) − ln(Left)) were computed on this EMG
frequency band—for all the same regions as were included in the EEG analysis. These
EMG range asymmetries were used as changing covariates in a multivariate repeated mea-
sures analysis of covariance (MANCOVA), which assumes that the EMG covariate changes
within groups with the dependent variable across levels of the independent variable—in this
case the particular facial expression. This changing covariate approach then correlates the
change in the covariate with the change in the dependent variable and subsequently ana-
lyzes the residual variance in a standard MANOVA. Using this strategy, Coan et al. (2001)
found that statistically adjusting for the EMG variance in this way did not change any of
the significant relationships between facial pose and EEG asymmetry.
The second strategy used by Coan et al. (2001) involved an examination of alpha fre-
quencies derived from bipolar EMG leads. This analysis was motivated by noting that
the previous method assumes that all frequencies of the EMG are equally likely to show
asymmetry effects that differ by the manipulation. But it is conceivable that EMG activ-
ity in the 70–90 Hz band may relate differently to a criterion variable than EMG activity
in the 8–13 Hz band, the band of particular interest. Thus whereas the first analysis strat-
egy examined EMG frequencies in EEG leads, the second examined alpha frequencies in
EMG leads. This second approach derived power spectra from bipolar EMG activity in the
frontalis and the temporalis muscle regions. Alpha power asymmetry scores derived from
these EMG leads were thus included as changing covariates the analyses. Because unlike
the first approach, where each region had its own covariate, this approach produced solely a
frontalis alpha asymmetry score and a temporalis asymmetry score, one way repeated mea-
sures MANCOVAs were conducted separately for each region (e.g., one for F4–F3, one for
F8–F7, etc.) since each region could not have its own changing covariate. Analyzing each
region separately, thus increasing the number of analyses conducted, actually provided a
more stringent test of whether the relationships between the manipulation and EEG asym-
metry were influenced by myogenic contributions, because the chances increased of finding
that the covariates rendered a previously significant effect nonsignificant. Statistically con-
trolling for the EMG variance in this way, however, did not change any of the significant
relationships between facial pose and EEG asymmetry.
4. Interpretive issues
4.1. Alpha and activity
A guiding assumption underlying the interpretation of findings involving frontal EEG

alpha asymmetry is that greater alpha power is indicative of less cortical activity in broad
underlying regions (cf. Davidson, 1988). Although there is good evidence to support this
assumption, one might question whether this relationship is ubiquitous.
It has been well documented that sensory input shows modality-specific blocking of alpha
activity at cortical regions involved in processing such input. With visual stimuli, blocking
of alpha over the occipital region occurs about 0.3 s after the presentation of the visual
stimulus (Berger, 1932; Jasper and Cruickshank, 1937; Knott, 1938), but this latency has
been found to vary with intensity and duration of the stimulus (Cruickshank, 1937; Durup
and Fessard, 1936a,b) and to diminish somewhat with a motor response related to the
stimulus (Knott, 1938, 1939; Travis et al., 1937). Recovery time from blocking is generally
about 1 s, but it too varies with stimulus intensity and duration (Cruickshank, 1937; Jasper
and Cruickshank, 1937; Motokawa and Tosiada, 1941).
Similar but less dramatic effects are observed with other sensory modalities. Auditory
stimuli, for example, block occipital alpha less effectively than visual stimuli and with a
somewhat longer latency (Berger, 1930; Gibbs et al., 1935; Travis et al., 1937). Other sensory
stimuli, such as tactile, cutaneous, pain (Berger, 1931, 1932; Jasper and Cruickshank, 1937;
Livanov, 1940; Travis and Barber, 1938) and gustatory (Kitamura, 1939) have been found
to block alpha, at least in their respective cortical areas.
Thus, sensory stimulation that should require active cortical processing leads to modality-
specific alpha blocking, a principle that might lead to the inference that diminished alpha
recorded over any cortical region signifies greater cortical activity. A test of this hypothesis in
regions other than primary sensory regions is hampered by the lack of clearly defined stimuli
to specifically engage those cortical regions in active processing, although several studies
have provided data quite consistent with the notion that greater alpha power is indicative of
less cortical activity in the underlying regions thought to subserve task performance (e.g.,
Davidson et al., 1990).
A consideration of the genesis of the alpha rhythm might prove illuminative for the as-
sumption that diminished alpha recorded over any cortical region signifies greater cortical
activity. A series of studies by Andersen and colleagues (Andersen et al., 1967a,b) sug-
gest that thalamic rhythmicity drives cortical ensembles, the latter which comprise a large
portion of scalp-recorded EEG activity. Andersen et al. (1967b) examined spindles in ani-
mals anesthetized with barbiturates, making the inference that such spontaneous rhythmic
spindle activity is homologous with the human alpha rhythm. Several findings highlight the
basis of their conclusion that thalamic rhythmicity drives cortical rhythmicity, including:
(1) destruction or cooling of cortical regions leaves thalamic spindle activity unchanged
(Andersen et al., 1967b); (2) damage or removal of the thalamus abolished cortical spin-
dle activity (Andersen et al., 1967b); (3) unilateral destruction of thalamic tissue resulted
in the disappearance of ipsilateral cortical spindle activity (Andersen et al., 1967b); (4)
synchronous cortical spindles were not observed in relatively closely spaced cortical re-
gions (those separated by 2 mm or more), but were observed over a much larger distance
between a group of thalamic cells and the cortical area to which they projected (Andersen
et al., 1967a). Thus Andersen and colleagues concluded that spontaneous cortical rhyth-
micity was “generated exclusively by thalamic neurons” (Andersen et al., 1967b, p. 258).
Although cortical systems provide inputs to the thalamus that can disrupt the rhythmicity,
the thalamus, and particularly the reticularis nucleus (Steriade et al., 1985), appears to be
responsible for synchronizing cortical EEG activity.
Recent confirmation of a relationship between thalamic activity and scalp-recorded alpha
activity in humans derives from a positron emission tomography (PET) study (Larson et al.,
1998). During approximately 30 min, EEG and [18 F]-2-fluoro-2-deoxy-d-glucose (FDG)
PET recordings were obtained. Global alpha (8–13 Hz) power was then correlated with
glucose metabolism, and cortical alpha power was strongly and inversely related to glucose
metabolism in the thalamus (Larson et al., 1998). This finding is consistent with the notion
that thalamic activity in response to sensory or cortical input will disrupt alpha rhythmicity.
Thus scalp recorded EEG alpha activity—in a very coarse sense both spatially and
temporally—is inversely related to thalamic activity. Global alpha power across electrodes
and across 30 min relates to thalamic metabolism. Ultimately, however, investigators would
wish to know whether EEG alpha at a given scalp lead is related to cortical activity in the
tissue beneath that lead, a question addressed by Cook et al. (1998). Using H2 15 O PET
imaging allowed them to examine activity in 2 min segments, with a total of eight such
segments per subject. EEG power was calculated for 4 Hz wide bins, starting at 0 Hz and
extending to 40 Hz, at 1 Hz intervals (e.g., 0–4, 1–5, 2–6, etc.). Cerebral perfusion under
each electrode was calculated, and then correlated with each of the EEG spectral bins, re-
sulting in a plot of correlations between EEG power and cerebral perfusion as a function
of frequency. Frequency range played a major role in the relationship of EEG power with
perfusion, such that lower frequencies (those bins with a center frequency below 8 Hz) had
a positive relationship to perfusion, middle frequencies (bins with center frequencies from
8 to 12 Hz) had a negative relationship, and upper frequency ranges (center frequency var-
ied depending on specific operationalization) had a positive relationship (Fig. 8). Apparent
from the figure is that relative power shows a closer correspondence to underlying cortical
activity than does absolute power, which may reflect that the latter is confounded by vari-
ations in scalp thickness much more than the former. Additionally, although alpha power
is inversely related to underlying cortical activity no matter which of the montages was
used, the relationship of beta power (13–30 Hz) to underlying activity varied substantially
as a function of recording montage, exhibiting either a positive or negative relationship
depending on the particular recording montage used.
Thus there is reasonable support for the assumption that greater alpha at a scalp lead
reflects less cortical activity in a broad region(s) contributing to electrical activity recorded
at that lead. Recent data of Cook et al. (1998) suggest, however, that a tighter correspondence
between cortical activity and scalp-recorded EEG is possible with a reattribution technique
these authors have called cordance, although the correspondence in the alpha band is not
vastly improved using this cordance measure (see the lower panel of Fig. 8, taken from
Cook et al., 1998). Whether asymmetry in reattributed power demonstrates relationships
with emotion and individual differences, however, remains an empirical question, but one
worth investigating given the tighter coupling of EEG to brain function that appears possible
using this technique (see also Leuchter et al., 1994, 1999, 2002).
Fig. 8. Correlations between EEG power and PET perfusion values at tissue under the EEG scalp lead. Top panel
depicts absolute power, and lower panel depicts relative power (i.e., power in the 4-Hz wide bin divided by total
power across all spectral frequencies). “Ear reference” is a computer linked ears reference, “source derivation”
is that described by Hjorth (1975) that weights immediate neighboring electrodes in the time domain prior to
frequency-domain transformation, and “reattributed power” is a weighting of power derived from bipolar channels
of nearest neighbors (Cook et al., 1998). Statistical significance is indicated by horizontal lines representing the
magnitude at which a correlation coefficient attains significance: solid line for P = 0.05; large dashed line for
P = 0.01; fine dashed line for P = 0.001. From Cook et al. (1998), reprinted with permission from Elsevier.
Worth noting from Cook et al. (1998), and as apparent in Fig. 8, is that the inverse re-
lationship between cortical perfusion and EEG power is relatively constant throughout the
entire alpha band in these adult subjects. Thus although the 8–13 Hz definition of alpha is
somewhat arbitrary, the correspondence of activity in this range (and perhaps a bit of the
6–8 Hz portion of the upper Theta band) to underlying cortical activity at rest is relatively
uniform in adult subjects. This observation does not suggest a strong functional distinction
between smaller bandwidth divisions, such as upper or lower alpha, at rest in a psychi-
atrically and neurologically healthy population (although some investigators have made an
argument for the utility of subdividing the alpha band for specific tasks and applications,
e.g., Klimesch et al., 1997).
A final issue with respect to interpreting alpha and cortical activity concerns how to
conceptualize resting EEG data. Such resting data necessarily summarizes activity across
several minutes, which will collapse across many variations in brain and psychological state
during the recording period. Although investigators refer to such periods as resting periods,
one might alternatively think of EEG activity during these periods as task-related, with
individual differences in how subjects approach this “task” of resting for several minutes
underlying the observed individual differences in EEG activity. The resting state is rela-
tively uncontrolled, allowing for individual differences in mentation (broadly construed)
during the resting period to influence the measure (cf. Schwartz et al., 1976 for a similar
phenomenon when depressed and nondepressed subjects pondered a typical day while facial
EMG was recorded).
4.2. Robustness or capitalization on chance: the impact of reference schemes, specific

sites, and other variations
Reviewing the literature (see Tables 1–4 in Coan and Allen, 2004, this issue), one is
impressed by the fact that significant relationships involving frontal EEG asymmetry: (1)
derive from data analyzed under a variety of reference schemes, with different studies using
different reference montages; (2) appear to involve different specific frontal regions in dif-
ferent studies; and (3) sometimes involve different frequency cutpoints for operationalizing
alpha band activity. It is premature to know how best to interpret such a pattern of findings,
but these observations suggest at least three non-mutually exclusive possibilities.
First, for those who like to see glasses as half-empty, this could reflect that this research
field suffers—as all do to some degree—from significant inflation of the likelihood of Type
I error, with alpha inflation resulting from the poor control for multiple comparisons, com-
pounded by the many permutations of variables possible when recording from multiple
regions under multiple reference montages, with the possibility of different operationaliza-
tions of alpha-band activity. In the absence of strong theory to suggest that investigators
should find effects at one specific frontal region and not another, or under one reference
scheme and not another, investigators wisely examine multiple sites and reference schemes,
but the incumbent risk of this strategy is that the field as a whole may be inadequately pro-
tected against reporting spurious findings.
Second, for those who like to see glasses as half-full, the fact that relationships with
frontal EEG asymmetry appear with data from different reference schemes at different
times, and at different regions at different times, suggests that these observed variables are
imperfect manifest representations of what should be considered a latent variable, i.e., func-
tional frontal brain asymmetry. This argument would imply that only by recording multiple
regions and under multiple reference schemes can one adequately assess an individual’s
true score on the latent variable. By aggregating over multiple measures, one gains power
and reliability, thus enhancing the ability to find relationships between frontal brain asym-
metry and criterion variables. This argument further implies that the impact of these factors,
such as reference scheme and specific frontal region, should be tested explicitly in a statis-
tical model, such as those detailed previously in the section on hierarchical general linear
models. In the absence of such a model to protect from isolated chance findings appearing
significant, the field may indeed suffer from inflation of Type I statistical error.
The latent trait argument would of course predict that the manifest variables should all
show some modest correlations with the latent trait, and likely with one another. Although
this is true of data recorded under the average reference and the computer averaged mastoids
references, it is less true of data recorded using the Cz reference (Hagemann et al., 1998;
Reid et al., 1998), which shows much lower correspondence with data using the other
reference montages. It is worth noting, moreover, that by far the most common reference
scheme used in frontal EEG asymmetry research is the Cz reference (see Coan and Allen,
2004, this issue), and that most studies do not employ multiple reference montages in their
analysis of the data.
The third possibility is that there exists some systematic relationship between measured or
unmeasured variables and asymmetry at specific sites or under specific reference schemes.
This line of reasoning suggests the differential engagement of various frontal systems as a
function of particular task demands, as a function of factors in the experimental environment,
and as a function of various individual difference variables under study.
At present, it is difficult to assess the likelihood that such effects exist, as most studies do
not assess a range of variables and attempt to relate them to asymmetry at specific regions.
A notable exception comes from a recent study of Miller and Tomarken (2001), in which
manipulations of expected reward or punishment produced changes in mid-frontal EEG
asymmetry (that varied by sex), and manipulation of the required response produced changes
in central asymmetry. These results suggest that there may indeed be task variables that
will impact the specific region in which EEG alpha asymmetry effects are likely to appear.
Nonetheless, there are many other non-task variables that may impact the regional specificity
of EEG asymmetry effects, but such variables may not be known or assessed, thus making
it impossible to discern whether there exists a systematic cause underlying the appearance
of EEG asymmetry effects at some sites in some studies, and other sites in other studies.
4.3. Consistency and variability
Estimates of EEG alpha asymmetry are averages that summarize patterns of brain ac-
tivity across several minutes, either contiguous time segments in the case of resting EEG
asymmetry, or collapsed across numerous discrete but separated time segments in the case
of state-manipulated EEG asymmetry. Although it has been adequately demonstrated that
such estimates possess excellent internal consistency reliability (e.g., Allen et al., 2001;
Coan and Allen, 2003b; Coan et al., 2001; Reid et al., 1998; Tomarken et al., 1992), these
estimates of internal consistency are derived from several segments of data, each of which
is an average reflecting the pattern of brain activity across many seconds of recorded data.
There is a sense in which frontal EEG alpha asymmetry derived from these segments of data
ignores variability on a finer temporal scale. Whether such variability will prove meaningful
is ultimately an empirical question, but the utility of explicitly examining such variability
appears promising. For example, Minnix and Kline (2004) examined the variance estimate
associated with the average FFT from a resting assessment. Subjects who show more second-
to-second variability in frontal EEG alpha asymmetry will have higher variance estimate
across the entire recording epoch. Minnix and Kline (2004) found that increased variability
of this sort was related to higher neuroticism. Thus a trait characterized by greater emotional
lability was found to be associated with more lability in frontal EEG asymmetry as well.
Another way of assessing the stability of frontal EEG asymmetry was first reported by
Baehr et al. (1998), who computed the percentage of time that right alpha is greater than left
alpha at homologous leads. Baehr et al. (1998) found that the percent–time measure bet-
ter discriminated psychometrically-defined depressed subjects from nondepressed subjects
than the traditional asymmetry measure that averaged across the recording period. Allen
et al. (2001) used the percent–time measure as well, finding that it produced comparable
findings to the traditional asymmetry score. Thus although it may be premature to suggest
that this metric has distinct advantages, the extant data suggest its promise and moreover
suggest that it would not result in the elimination of significant findings with the traditional
asymmetry score.
4.4. Keeping straight the states and the traits
Substantial data support the contention that frontal EEG asymmetry can serve as a rel-
atively stable individual difference variable, yet also show predictable state-related fluctu-
ations (see Coan and Allen, 2004, this issue). Evidence in support of the trait-like quality
of frontal EEG asymmetry derives from studies specifically examining stability over time.
Tomarken et al. (1992) assessed the psychometric properties of trait-like frontal EEG asym-
metries, finding that frontal EEG asymmetry demonstrated acceptable test–retest stability
(intra-class correlations ranging from 0.69 to 0.84 across 3 weeks). Similarly, Jones et al.
(1997) found that frontal EEG asymmetry recorded at 3 months of age was highly correlated
with asymmetry at 3 years (r = 0.66, P < 0.01). Similar figures come from Hagemann et al.
(2002), who found that across four different measurement occasions, 60% of the variance
in EEG asymmetry measures was due to individual differences in a temporally stable latent
trait.
To enhance the ability to identify trait-related variance, some studies have specifically
examined subjects who show the greatest cross-session consistency (e.g., Wheeler et al.,
1993), reasoning that the strongest relationships to other traits should be shown by those who
are consistent on the measure of trait EEG asymmetry (cf. Bem and Allen, 1974). Others
have averaged data across multiple sessions to mitigate occasion-specific fluctuations and
presumably derive a better estimate of the trait-related variance in EEG asymmetry (e.g.,
Sutton and Davidson, 1997).
When attempting to account for the nonstable variance in frontal EEG asymmetry, three
sources must be considered: reliable changes from one session to the next, reliable and
systematic changes within session, and unreliability of measurement. Because frontal EEG
asymmetry demonstrates high internal consistency reliability at any given assessment ses-
sion (Cronbach’s alphas typically above 0.95; Reid et al., 1998), it is unlikely that attenuated
test–retest reliability of frontal EEG asymmetry is due to random measurement error. Rather,
a majority of the variance in EEG asymmetry can be accounted for reliable and systematic
sources of variation (Coan and Allen, 2003b) due to:
(1) Stable trait consistency across multiple assessments, which is presumably indicative
of temperamental style and a tendency to respond in a characteristic way when con-
fronted with emotionally evocative situations. An individual’s trait level of frontal EEG
asymmetry represents a quality of that individual—a quality that the individual brings
to a variety of situations and contexts. This trait level is necessarily estimated, by av-
eraging across multiple occasions of measurement (e.g., Sutton and Davidson, 1997;
Wheeler et al., 1993), by modeling it as a latent trait (e.g., Hagemann et al., 2002), or by
accounting for it within the context of a generalizability analysis (as described below).
(2) Occasion-specific variance refers to reliable variations in frontal asymmetry that char-
acterize the variation in resting EEG assessments across multiple sessions of measure-
ment. Such variation may reflect systematic but unmeasured sources such as current
mood, recent life events and/or factors in the testing situation.
(3) State-specific variance refers to changes within a single assessment that characterize the
difference between two experimental conditions or between baseline resting levels and
an experimental condition. State-specific changes as conceptualized here are proximal
effects in response to specific experimental manipulations. Such manipulations should
be reversible and of relatively short duration.
These state-related fluctuations stand in contrast to the occasion-specific fluctuations, which
are assumed to characterize the individual throughout the measurement occasion, reflecting
the high internal consistency reliability estimates such measurement occasions typically
show. Occasion variance is hypothesized to reflect the effects of time- or context-limited
individual difference variables (e.g., mood on the day of assessment, recent or imminent life
events, daily hassles) or alternatively the interaction of the individual with the experimental
milieu in a manner that varies from assessment to assessment (e.g., effects of experimental
milieu or procedures, Blackhart et al. (2002), or experimenter effects, Kline et al. (2002)).
Such effects would not be the result of purposeful state-related experimental manipula-
tions, but would rather represent an interaction of the subject with other experimentally
uncontrolled stimuli.
Most studies of trait frontal asymmetry are not designed to allow for the separation of trait
variance and occasion variance, as most studies entail only a single occasion of measurement
of resting frontal asymmetry. If occasion-specific fluctuations were not sizable, then a single
assessment of trait levels would prove sufficient. Recent evidence (Hagemann et al., 2002),
however, suggests that reliable occasion-specific fluctuations account for approximately
40% of reliable variance in resting frontal asymmetry, while the consistency across multiple
sessions, presumably reflecting a stable trait, accounts for approximately 60%. Further,
there may exist individual differences in the magnitude of occasion-specific fluctuations.
For example, Wheeler et al. (1993) selected a subset of 26 from among 81 women (i.e.,
32% of the sample) who were classified as possessing stable asymmetry, meaning that 68%
of the sample was classified as having unstable asymmetry.
4.4.1. Methods for assessing state, occasion, and trait variance

To reliably delineate sources of variance in frontal EEG asymmetry, an analytic strategy
for decomposing variance components is needed. One such promising general strategy is
generalizability or “G” theory.
Generalizability theory (Cronbach et al., 1972), or “G-theory,” was developed for the pur-
pose of identifying the generalizability and dependability of different independent variables
thought to contribute to a measure’s score (e.g., Di Nocera et al., 2001). The generalizability
of a measure is analogous to more conventional estimates of reliability, such as the intraclass
correlation, while dependability of a measure refers to a measure’s reliability across con-
texts. Generalizability and dependability estimates may be obtained for each independent
variable thought to contribute variance to a measure. In practice, an independent variable
with high dependability is one that contributes variance that is relatively independent of
other independent variables affecting the measure of interest. For example, an estimate of
the dependability of trait variance in frontal EEG asymmetry would allow one to assess
how independent and stable trait variance is from state manipulations and measurement
occasions. In addition to estimates of generalizability and dependability, actual variance
components may be estimated for each independent variable hypothesized to contribute
to an individual’s score at any one time, including variance components attributable to the
interaction of independent variables. G-theory is based fundamentally on an ANOVA model
in the estimation of variance components. A critical difference between G-theory analyses
and classical ANOVA models is that G-theory requires the computation of expected, as
opposed to observed variance components. Expected variance components are estimated
by using specific algorithms employed in very few statistical packages (e.g., SAS PROC
VARCOMP).
As applied to questions of state, occasion and trait variance in frontal EEG asymmetry,
such a model might be defined as follows (cf. Di Nocera et al., 2001):
σy2 = σt2 + σo2 + σs2 + σto

2
+ σts2 + σos
2
+ σtos
2
where σy2 is the total variance for a given variable, in this case frontal EEG asymmetry,
across all occasions and manipulations, σt2 is the variance in frontal EEG asymmetry at-
tributable to individuals (here considered trait variance), σo2 is the variance in frontal EEG
asymmetry attributable to measurement occasion, σs2 is the variance in frontal EEG asym-
metry attributable to experimentally manipulated states, σto 2 is the variance in frontal EEG
asymmetry attributable to the interaction of trait and occasion variance, σts2 is the variance
in frontal EEG asymmetry attributable to the interaction of trait and state variance, σos 2 is
the variance in frontal EEG asymmetry attributable to the interaction of occasion and state
variance, and σtos
2 is the variance in frontal EEG asymmetry attributable to the interaction
of trait, occasion and state variance (confounded with error of measurement).

G-theory thus provides variance component estimates (percent of variance accounted
for by each component), coefficients of generalizability (ρ2 ), as well as coefficients for
dependability (φ or phi), for each independent variable of interest (in this case, trait, occasion
and state components). If, for example, trait variance in frontal EEG asymmetry shows high
dependability in addition to high generalizability, such a finding would bolster the likelihood
that it would prove useful as a liability indicator for risk for psychopathology, or index a
trait-like affective style, as this finding would indicate that trait frontal EEG asymmetry
can be assessed reliably, and that trait frontal EEG asymmetry is independent of state
manipulations and occasion-related fluctuations.
Further, to date no researcher has examined the stability of state manipulations in frontal
EEG asymmetry, over time or otherwise. G-theory provides useful estimates of reliability
that mirror and extend approaches designed to understand intraindividual dynamics, such as
advocated by Mischel and colleagues (e.g., Shoda and Mischel, 1996; Shoda et al., 1994).
Using Shoda and Michel’s approach, such patterns of behavior are represented as if . . .
then . . . probabilities that vary from individual to individual and that presumably reflect
an individual’s underlying personality type (Mendoza-Denton et al., 2001). Effects of this
type are also easily accommodated by a generalizability analysis, as they would be reflected
in σts2 , the trait by state interaction term. Thus, in addition to assessing the dependability of
trait variance across states and occasions, the dependability of state manipulations across
individuals is estimable, as is the dependability of occasion variance across individuals and
states.
Although no investigators have applied the model specified above to data collected across
multiple occasions of measurement, Coan and Allen (2004, this issue) did assess the extent
to which state changes in frontal EEG asymmetry were reliably elicited across subjects,
and the extent to which trait levels of frontal EEG asymmetry were preserved across state
manipulations. The results indicated that trait-specific variance, state-specific variance, as
well as variance attributable to their interaction, each accounted for approximately 10% of
the total explained variance in frontal EEG asymmetry. Trait stability as measured by the g
coefficient (intraclass correlation) was estimated to be moderately high (0.47), whereas state
stability was extremely high (g coefficient = 0.92). Although these results identify stability
and sizable contributions of both trait and state frontal EEG asymmetry, trait variance
as estimated from this single measurement occasion will necessarily include both stable
trait and occasion specific influences. Indeed, while the state variance in response to the
manipulation was highly stable, the trait variance was only moderately so. This may be due
to the influence of unmeasured but relevant occasion specific factors, which future efforts
might profitably explore.
A final note with respect to the G-theory approach concerns its flexibility to assess the
impact of a variety of other factors, such as the effect of reference scheme and specific frontal
region. By including terms to account for variance due to particular reference scheme, or to
the particular frontal region (e.g., F4–F3 versus F8–F7 versus FTC2–FTC1), the magnitude
of these sources of variance and their interactions with trait, occasion, and state variance
can be assessed. Similarly, estimates of the stability of the effects across these factors can
be quantitatively assessed.
5. Synopsis
Research on frontal EEG asymmetry and emotion now represents a substantial body of
literature. There are numerous methodological issues to which the field may have paid in-
sufficient attention, while at the same time paying potentially too much attention to other
factors. The field may have been too concerned with recording at least 8 min of data to ob-
tain reliable estimates of asymmetry, overly concerned about the impact of blink artifacts,
and overly concerned with closely matching impedances at homologous leads. By contrast,
too little concern has generally been given to assessing the impact of reference scheme,
disentangling left from right hemisphere effects using appropriate statistical models, and
discerning whether specific regions are differentially involved in various tasks or as a func-
tion of individual differences. It remains to be determined whether the impact of myogenic
activity substantially influences findings involving EEG alpha asymmetry.
As one reviews the frontal EEG asymmetry and emotion literature (Coan and Allen,
2003a; 2004, this issue), it is apparent that many different data analytic approaches have been
used, resulting in a collection of findings that converge despite rather dramatic differences
in: (1) the conditions under which data were recorded; (2) the manner in which data were
reduced; and (3) the manner in which data were subsequently analyzed. The optimist will
see this as a testament to the robustness of the underlying systems reflected in frontal EEG
asymmetry, and the curmudgeon will see this as representing considerable literature-wide
alpha slippage due to the many permutations of data reduction and analysis. A conservative
intermediate interpretation is that the larger enterprise of interpreting the data and theory
building will benefit from a more solid empirical foundation, one that will require that careful
attention be given to EEG data recording and analysis. The issues highlighted here may best
be regarded as fundamentals that may inform future efforts, to assist in the creation of a
more methodologically consistent and precise data base. Only with such a foundation can
researchers then explore the underlying functional, anatomical and neurochemical systems
that may be tapped by frontal EEG asymmetry.
Acknowledgements
This research was supported, in part, by a grant from the National Alliance for Research
on Schizophrenia and Depression (NARSAD) and an Exploratory/Development Grant from
the National Institutes of Health (1 R21 RR09492) to J.J.B.A., and by a Graduate Research
Fellowship from the National Science Foundation to J.A.C.
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Commentary
What does the prefrontal cortex “do” in affect:
perspectives on frontal EEG asymmetry research
Richard J. Davidson∗
Laboratory for Affective Neuroscience, W.M. Keck Laboratory for Functional Neuroimaging and Behavior,
University of Wisconsin-Madison, 1202 West Johnson Street, Madison, WI 53706, USA
Abstract
This commentary provides reflections on the current state of affairs in research on EEG frontal
asymmetries associated with affect. Although considerable progress has occurred since the first report
on this topic 25 years ago, research on frontal EEG asymmetries associated with affect has largely
evolved in the absence of any serious connection with neuroscience research on the structure and
function of the primate prefrontal cortex (PFC). Such integration is important as this work progresses
since the neuroscience literature can help to understand what the prefrontal cortex is “doing” in
affective processing. Data from the neuroscience literature on the heterogeneity of different sectors
of the PFC are introduced and more specific hypotheses are offered about what different sectors of
the PFC might be doing in affect. A number of methodological issues associated with EEG measures
of functional prefrontal asymmetries are also considered.
Keywords: Frontal EEG asymmetry; Emotion; Prefrontal cortex; Neuroimaging
1. Introduction
It is very gratifying for me personally to be writing this commentary since the publi-
cation of this Special Issue marks the fact that there now exists a substantial corpus of
scientific literature investigating methodological and conceptual issues surrounding the use
of measures of asymmetric prefrontal electrical signals recorded from the scalp surface
to make inferences about emotional processes. With my colleagues and students at the
time, I first reported 25 years ago on the use of asymmetries in scalp-recorded frontal brain
∗ Tel.: +1-608-262-8972; fax: +1-608-265-2875.

E-mail address: rjdavids@wisc.edu (R.J. Davidson).
doi:10.1016/j.biopsycho.2004.03.008
220 R.J. Davidson / Biological Psychology 67 (2004) 219–233
electrical activity to make inferences about emotional processes (Davidson et al., 1979).
At the time, it was a lonely field though there were investigators from other domains of
neuroscience who underscored the important role played by the prefrontal cortex in dif-
ferent aspects of emotional processes (e.g., Nauta, 1971). This Special Issue has brought
together the best of current research using these non-invasive measures to investigate dif-
ferent aspects of the methodology and construct validity of these measures. When I be-
gan to work in this area, research on the central nervous system substrates of emotional
processes was largely restricted to studies in non-human species that focused on the role
of subcortical structures in emotional and motivational processes, leading to a view, still
championed by some (e.g., Panksepp, 2003; but see Davidson, 2003a for a rebuttal), that
the fundamental circuitry for emotion and motivation lies in subcortical zones and that
cortical tissue has little if anything directly to do with emotion. The only exceptions to this
view at the time came from observations of patients with localized cortical brain damage
(e.g., Gainotti, 1972) and from early studies on the role of prefrontal lesions on the socioe-
motional behavior of monkeys (e.g., Myers, 1972). The research featured in this Special
Issue is part of a larger body of work (see e.g., Rolls, 1999 for a modern example) that
forcefully underscores the importance of prefrontal cortex for emotional and motivational
processes.
However, the work represented in this Special Issue has, for the most part, evolved with
little connection to the core neuroscience research on the structure and function of the
prefrontal cortex. I will argue that this state of affairs must change if this work is to become
an accepted part of the influential body of neuroscientific research on the prefrontal cortex.
Just what specific role the primate prefrontal cortex (PFC) might be playing in emotion still
remains elusive and will be one of the several issues I will address in some detail below. The
substantive portions of this commentary will be divided into two parts. The first part will
address some of the fundamental conceptual issues that lie at the core of this work, most of
which were not addressed in the articles in this Special Issue. I will focus on what the PFC
is “doing” in emotion and will draw on other neuroscience literature on PFC from which
insights about its role in emotion might be gleaned. In this section, I will also emphasize
the fact that the PFC is heterogeneous, both anatomically and functionally and any serious
discussion of PFC function must make distinctions among the sub-territories of the PFC.
Also to be emphasized is the fact that the PFC is part of a larger overall circuit and that
other components of the circuitry are crucial for understanding how the brain implements
emotional and motivation processes. It cannot be solely through the prefrontal cortex that
the brain implements emotional and motivational processes. One unwitting consequence
of the work my laboratory began on prefrontal asymmetries and affect is the view that the
prefrontal cortex is the “center” or at least the primary region for all aspects of the emotional
and/or motivational processes in question. It is essential that we remind ourselves that the
prefrontal cortex is part of a larger and more complex circuit and that other components
of this circuitry will undoubtedly be important for many of psychological phenomena of
interest to the readers of this Special Issue. A related issue concerns the nature of the measure
with which we are dealing. It has been easy for those who study EEG frontal asymmetry
to ignore other components of the circuitry because the measure in question here does not
reflect many of the other features of the circuit. In particular, scalp-recorded brain electrical
signals reflect activity primarily from cortex and without more complex source localization
R.J. Davidson / Biological Psychology 67 (2004) 219–233 221
methods which have not been used in any of the articles in this Special Issue, one cannot
make inferences about subcortical signals.
2. Conceptual issues that underlie research on EEG asymmetries associated

with emotion
2.1. Heterogeneity of prefrontal cortex
Many recent reviews have documented the important functional and anatomical divisions
within the prefrontal cortex (e.g., Rolls, 1999). For the purposes of the present discussion,
it is important to simply call attention to this fact and to indicate that the majority of the
neuroscience literature indicates that the prefrontal sector most directly associated with
emotion is the sector that is least likely to be reflected in scalp-recorded brain electrical
signals—namely, orbital frontal cortex (e.g., Hornak et al., 2003). Both the lateral orbital
sectors and the ventromedial sectors have been directly implicated in various aspects of
emotion, with the orbital sectors in particular thought to play an important role in the as-
signment of affective value to stimuli (e.g., Rolls et al., 2003). It is true that there are major
interconnections among the different sectors of the PFC and that the dorsolateral sector
receives input from the orbital sector (Rolls, 1999). However, according to most investi-
gators, the dorsolateral sector of the PFC is primarily associated with various cognitive
processes, particularly with cognitive control (see Miller and Cohen, 2001 for review). It
is the dorsolateral sector which is likely most directly reflected in the scalp signals from
which metrics of functional prefrontal asymmetry are constructed.
Recent neurophysiological data from awake behaving rhesus macaques in whom single
cell recordings were simultaneously acquired from multiple neurons in both dorsolateral
and orbitofrontal sectors of PFC (Wallis and Miller, 2003) provide a new understanding of
what these different regions of PFC may be doing and how they interact. These investiga-
tors recorded single cell activity as well as behavior during a reward preference task. The
monkeys had to choose between pictures associated with different amounts of juice reward.
Neuronal activity in both regions of PFC reflected the reward amount. However, neurons
in the dorsolateral sector encoded both the reward amount and the monkey’s forthcoming
response while neurons in the orbital sector primarily encoded the reward amount alone.
The authors propose that their data are consistent with a model where reward information
enters the PFC via the orbital sector where it is then passed on to the dorsolateral sector and
used to guide behavior. Unfortunately since neurophysiological studies of this kind are so
difficult to perform and since there were only two animals tested, it was not possible for the
authors to compare left- versus right-side recordings. However, one important conclusion to
draw from this work is that tasks that include a response component will be more likely to
show affect-related PFC activation asymmetry in the dorsolateral regions and it is activity
in these regions that are most likely to be reflected in scalp-recorded brain electrical signals.
Recent studies have also identified a ventrolateral region of prefrontal cortex that shows
robust asymmetries during response inhibition tasks. In response to cues that signal the
requirement to inhibit a dominant response, activation of right inferior and middle frontal
gyrus has been found (e.g., Garavan et al., 1999; Konishi et al., 1999). Moreover, patients
with focal damage to the right inferior frontal gyrus show impairments on such tasks (Aron
et al., 2003). Right ventromedial PFC also appears to play a specialized role in the inhibition
of impulsive affective urges. Patients with damage specifically to this PFC sector on the
right side, but not on the left side, have profound abnormalities in emotion-related decision
making (such as on the Iowa Gambling task; Tranel et al., 2002; see also Clark et al., 2003),
making more disadvantageous choices compared with their left-damaged counterparts. It
appears that this sector of right prefrontal cortex may be particularly sensitive to punishment
so that when it is damaged, patients no longer have the usual cues that signal threat and danger
and so tend to act impulsively. It will be important in future research using EEG measures
to utilize tasks that have been well-studied in imaging and lesion studies to determine if
predictable changes in PFC electrical asymmetries occur.
2.2. PFC is part of a complex circuit involving other cortical and subcortical components
Emotion and motivation are instantiated in complex circuitry involving both cortical and
subcortical components. Most major neuroscientists working on these topics have reached
this conclusion (see Rolls, 1999; LeDoux, 1996; Damasio, 1994; Davidson et al., 2000c;
Davidson et al., 2003). For example, we (Davidson et al., 2003) have described a circuit
that primarily involves different sectors of the PFC, the amygdala, hippocampus, insula and
anterior cingulate. Each of these structures plays a different, complementary role in specific
features of emotion. Just as cognitive neuroscience has powerfully demonstrated the utility
of differentiating among specific subcomponents of cognitive processes, so it is essential
that we do the same with emotion. Toward the end of this section, we will explicitly consider
what different sectors of the PFC might be doing in emotion and suggest different functions
for the different sectors. Unfortunately though, little work at the human level has begun to
parse emotion in a fashion that derives from and honors the distinctions that are made at
the neural level. This will be an important task for future research.
With respect to the frontal EEG asymmetry literature, it is imperative that we be mindful
of the fact that PFC, and particularly that sector of PFC likely contributing most to the brain
electrical signals that are the subject of this Special Issue, represents only a small portion of
the critical circuitry of emotion. Thus, for certain types of emotional processes, the presence
of a particular pattern of functional prefrontal asymmetry may be necessary but not sufficient
for the emotional state in question, or may simply be a contributory cause of the emotional
state. For example, as Harmon-Jones (this issue) has demonstrated, certain types of anger
under specific conditions may be associated with relative left prefrontal activation but this
does not mean that the left prefrontal cortex is in any way a “center” for anger in the brain.
We must ask what component of anger might be represented in the left prefrontal cortex and
since left prefrontal activation occurs during other types of emotions, we must further ask
what other brain regions must be recruited for anger to occur. Without additional measures
that reflect other components of the circuitry, it is not possible to effectively address the
question of what the PFC is uniquely doing in emotion.
When the patterns of anatomical connectivity are examined, it is apparent that one major
target of prefrontal neurons from some PFC sectors, is the amygdala. Some researchers
have suggested, based upon this anatomical arrangement, that one function of at least certain
regions of PFC is to modulate or inhibit activity in the amygdala. Davidson (2000, 2002) has
specifically suggested that regions of the left PFC in particular may play an important role in
inhibiting the amygdala. Broadly consistent with this view are new data at the animal level.
For example, Quirk et al. (2003) have shown that stimulation of medial PFC in rodents
decreases the responsiveness of output neurons in the central nucleus of the amygdala.
Caution must be exercised in generalizing from rodent to human PFC but nevertheless, these
data raise the important suggestion that reciprocal relations between at least certain PFC
regions and the amygdala may be important in understanding the functional significance of
this emotion-related circuitry. Using a paradigm to study the voluntary regulation of emotion
modeled after one we developed (Jackson et al., 2000), Ochsner et al. (2002) reported strong
inverse relations between activation in the left ventrolateral PFC and the amygdala when
subjects were requested to voluntarily downregulate their negative affect. These findings
collectively imply that what the PFC is doing in emotion is clearly not mediating emotional
responses but rather moderating patterns of activity in other parts of the circuit that control
the primary emotional response.
2.3. Should measures of emotional experience be used to guide and test theory?
An issue that surfaces in several of the articles in this Special Issue and one that was
noted by Cacioppo (this issue) in his commentary concerns the role of emotional experi-
ence. Most, though certainly not all of the extant research on frontal EEG asymmetry and
emotion is based upon associations with self-report measures of emotional experience or of
emotional traits, our own work included (e.g., Tomarken et al., 1992; Sutton and Davidson,
1997). While there are some important, notable exceptions to this, including some of our
own work examining relations with hormonal and immune measures (e.g., Davidson et al.,
1999; Kalin et al., 1998; Rosenkrantz et al., 2003), much of the literature is based upon
associations with self-report. If we are to uncover what the PFC is doing in emotion, it
will be important that we develop laboratory probes that do not rely solely upon self-report
measures to provide information on aspects of affective processing that may not be directly
reflected in conscious report. A recent example of this is a new study from our lab that
investigated relations between baseline functional prefrontal asymmetry derived from brain
electrical measures and startle responses during and following unpleasant pictures (Jackson
et al., 2003). In this study we specifically hypothesized that functional prefrontal asym-
metry would predict startle measures following the offset of a negative stimulus, rather
than startle magnitude during the stimulus itself. This hypothesis was formulated based
upon our suggestion that the left lateral prefrontal cortex may play an important role in
the inhibition of the amygdala and thus in the downregulation of negative affect. On this
view, the recovery following an unpleasant picture as reflected in the diminution of startle
magnitude post-stimulus offset would reflect the decrease in negative affect following the
negative stimulus and may be modulated by PFC inhibition of the amygdala. Our results
strongly confirmed our hypothesis. Frontal EEG asymmetry did not predict startle magni-
tude during the unpleasant picture; it only predicted startle magnitude following the offset
of the negative picture. It may well be the case that frontal EEG asymmetry measures are
associated with self-report measures of mood, dispositional affect and/or behavioral inhi-
bition and activation. However, these associations are unlikely to be particularly revealing
about mechanism since such associations can arise for a multitude of reasons. Recovering
slowly following the offset of an aversive stimulus may be associated with higher levels
of dispositional negative affect and/or behavioral inhibition but such associations by them-
selves will provide little information to help mechanistically understand what role the PFC
may be playing. Our study with startle measures during and following unpleasant stimuli
is offered as an example of how we can begin to mechanistically dissect the stream of
affective processing to help us better understand the role of the PFC in these processes. On
the other hand, it is important that self-report measures be retained in our future studies
because it is still of great interest to know how conscious mood is associated with prefrontal
function and its correlates. Moreover, conscious mood may be a useful summary index that
integrates and reflects a multitude of processes that are unlikely to be fully captured in any
single process measure, and conscious mood may play an important regulatory function in
behavior.
2.4. Left prefrontal activity and anger—what are the implications?
Harmon-Jones (this issue) reviews a growing corpus of literature that suggests that specific
forms of anger, or anger elicited in particular contexts, is associated with left-sided prefrontal
activation. He argues that these data are consistent with the approach–withdrawal framework
rather than with a valence-based model for frontal EEG asymmetry. More than 20 years
ago, I argued the same point (Reuter-Lorenz and Davidson, 1981) though at that time
had little data to buttress our suggestion. We did publish the first data showing that anger
elicited in infants when it was not accompanied by crying was associated with left-sided
frontal EEG activation (Fox and Davidson, 1988). On the basis of the evidence from his lab,
Harmon-Jones questions whether relatively greater left-sided frontal activity is a positive
trait. There are several issues that are embedded here that should be disentangled. First is the
distinction between baseline levels of asymmetry versus state-related changes. Most, though
not all, of the evidence provided by Harmon-Jones and colleagues is based upon the latter
type of measure, not the former. Secondly, it is important to ask just what the left PFC might
be “doing” in anger-related affective processing. In light of the important data Harmon-Jones
has gathered, it appears reasonable to suggest that one will find activation of the left PFC
in anger-related situations where there are response options that enable the individual to
overcome whatever obstacle is thwarting the goal. As such, in these situations it may indeed
be indeed be the case that “relatively high left frontal brain activity is more psychologically
and physically healthy than relatively less left frontal brain activity” (Harmon-Jones, this
issue), despite suggestions to the contrary, though the requisite evidence to carefully evaluate
this claim has not been gathered. The negative behaviors that frequently accompany anger
may well be subserved by other brain regions that require other methods to detect. And then
there is a growing literature on the peripheral biological correlates of individual differences
in baseline functional prefrontal asymmetry where we have shown that individuals with more
left prefrontal activity have lower levels of the stress hormone cortisol (Kalin et al., 1998),
lower levels of cerebrospinal fluid measures of corticotropic releasing factor (CRF; Kalin
et al., 2000), the central molecule that initiates the cascade of changes in the HPA system
in response to stressful events, higher levels of natural killer activity both at baseline (Kang
et al., 1991) and in response to challenge (Davidson et al., 1999), and higher antibody titers
in response to influenza vaccine (Rosenkrantz et al., 2003). Collectively, these findings
powerfully reveal that individuals with higher levels of left-sided prefrontal activity do
indeed have a more positive profile of peripheral biological indicators. When these findings
are considered in the context of other recent evidence from our lab showing that subjects
with greater relative baseline left-sided prefrontal activity recover more quickly following
a negative event (Jackson et al., 2003) and report higher levels of psychological well-being
(Urry et al., in press), they indicate the left-sided prefrontal activity is associated with a
nomological network that consists of effective coping with negative events and a resilient
profile of peripheral neuroendocrine and immune function. If such individuals are also
more prone to anger in certain situations, it may well be a form of anger that facilitates the
rapid removal of obstacles that are thwarting goals. Of course, this perspective is still very
much in need of additional confirmation and will be informed by studies that investigate
both trait levels of prefrontal asymmetry as well as state variations in anger experience and
expression and state variations in asymmetry. Moreover, the classification of a particular
constellation of biological and/or psychological indicators as “positive” or “beneficial” is
fraught with complexity. It is not my intention here to unpack these complicated issues, but
only to suggest that the compelling new data on anger offered by Harmon-Jones (this issue)
is not at all incompatible with the view that higher levels of left prefrontal activity may be
associated with aspects of resilience.
2.5. What do we know and what must we still learn about what different sectors of the
prefrontal cortex are “doing” in emotion?
Despite the current popularity of frontal EEG asymmetry measures, there is preciously
little research that has systematically manipulated task parameters in a neurally-informed
strategy to test specific hypotheses about the role of the left and right prefrontal cortex in
different aspects of emotional processing. Harmon-Jones (this issue) and Nitschke et al. (this
issue) are notable exceptions. As noted earlier, in light of the limitations of scalp-recorded
brain electrical measures and what they reflect, it is likely that the frontal EEG asymmetry
measures mostly reflect dorsolateral sectors of PFC. On the basis of a large body of both
human and animal studies, we (Davidson et al., 2003) have proposed that greater left-sided
dorsolateral activity may be associated with approach-related, goal-directed action plan-
ning. This would include instances of both pre-goal attainment positive affect as well as
the approach component of anger when response options are available. This analysis im-
plies that these effects will be particularly pronounced during periods of anticipation and
planning. The temporal dynamics of shifting patterns of prefrontal asymmetry during pre
versus post-goal periods is something that still must be systematically examined. We have
been examining a number of tasks that explicitly manipulate reward and isolate periods in
anticipation of reward (e.g., Sobotka et al., 1992; Skolnick and Davidson, 2002; Zinser et al.,
1999; see also Miller and Tomarken, 2001). Though limited, the evidence accumulated to
date indeed suggests that it is particularly during the period in anticipation of reward that
the most pronounced left prefrontal activation is observed.
There is less consensus on what the right lateral sector of PFC might be doing in
withdrawal-related emotion. On the basis of neuroimaging studies of spatial working mem-
ory, we have suggested that activation of right lateral PFC during withdrawal-related emotion
may be associated with threat-related vigilance. In studies with rhesus monkeys conducted
collaboratively with Kalin, we (Kalin et al., 2001) have reported that in response to a manip-
ulation that elicits powerful increases in freezing behavior, there is also a parallel increase
in behavioral signs of vigilance. Moreover, animals who display higher levels of these be-
haviors have greater right-sided baseline levels of lateral prefrontal activity (Kalin et al.,
1998). This line of reasoning leads to a number of testable hypotheses concerning relations
between right-sided PFC activity and the capacity to detect threat-related cues.
Because of the strategic location of PFC, with extensive anatomical connections to poste-
rior cortical regions as well as subcortical regions, this sector of cortex is ideally located to
recruit other processing regions to facilitate adaptive responding. This view of PFC borrows
heavily from that formulated in the cognitive neuroscience literature on the role of PFC in
cognitive control (e.g., Miller and Cohen, 2001).
What of other sectors of PFC that are not directly reflected in frontal EEG? First, we know
that there is extensive intrinsic connectivity among the various subregions of PFC (Rolls,
1999). This pattern of anatomical connectivity can therefore provide the basis for orbital,
ventromedial and ventrolateral sectors of PFC to modulate processing in the dorsolateral
sector. There are also direct roles for these other sectors of PFC in emotion and in fact,
it is precisely these sectors that are not directly reflected in scalp-recorded brain electrical
activity that historically have been most closely associated with emotion. Based largely
upon the work of Rolls in non-human primates and more recently in humans (Rolls, 1999;
Rolls et al., 2003; see also work from our lab by Nitschke et al., 2004), the orbital sector
of PFC can be thought of as cortex that computes affective value. It appears to track the
hedonic response to a stimulus and not the stimulus properties itself. For example, OFC
neurons will fire in response to food in a food-deprived animal. However, once the animal is
fed to satiety, a completely different response in OFC is found to the identical food stimulus
(Scott et al., 1995). In humans, similar effects have been reported. Unfortunately there has
been very little attention paid to possible asymmetries in ventral and orbital sectors of PFC
though there have been some suggestions of asymmetries in these regions OFC consistent
with the general pattern observed in dorsolateral sectors but this needs to carefully studied
(e.g., Kawasaki et al., 2001). And there is increasingly evidence, reviewed earlier, both from
neuroimaging and lesion studies, of asymmetries in the ventrolateral sector of the PFC. It
appears that right-sided ventrolateral PFC is particularly sensitive to cues for punishment
and when damaged, patients display a profound insensitivity to such cues (e.g., Tranel et al.,
2002). In the cognitive domain, this sector of PFC appears to be sensitive to stop cues that
require the inhibition of behavior (Aron et al., 2003; Garavan et al., 1999; Konishi et al.,
1999).
The ventromedial sector has been extensively studied by Damasio and colleagues (e.g.,
Damasio, 1994). They have suggested that ventromedial PFC provides a crucial substrate
for affect-guided decision making. Patients with lesions in this area often have significant
abnormalities in decision making. Based upon recent evidence in rodents, this sector of PFC
may also play a very important role in modulation of the amygdale and extinction learning.
Lesions in this region result in failures to exhibit normal patterns of extinction following the
learning of a classically conditioned aversive association (Morgan et al., 2003). Whether
there are functional asymmetries in this PFC sector and whether they behave in ways that
are similar to those in the dorsolateral sector is something that critically needs study in
future research.
Finally, I wish to end this section by raising the issue of the distal causes of individ-
ual differences in EEG measures of functional prefrontal asymmetry. Tomarken et al. (this
issue) report the striking observation of relations between socioeconomic status (SES) and
prefrontal asymmetry in adolescents. The lower the SES, the greater the relative right-sided
prefrontal activity. Although there are clearly genetic influences on EEG measures of pre-
frontal asymmetry (Coan, 2003), we have suggested that environmental influences, particu-
larly early in development, are likely to be present and to shape aspects of prefrontal function,
including baseline measures of functional prefrontal asymmetry (Davidson et al., 2000a). At
this stage, although the evidence for experience-dependent changes in prefrontal asymme-
try in humans is strictly correlational and does not imply cause, the extant animal data that
explicitly manipulates early environment finds both structural and functional asymmetric
changes in prefrontal cortex (e.g., Lyons et al., 2002), thus clearly implying that important
environmental influences on this circuitry are likely to exist in humans.
This very brief discussion is meant to underscore the importance of functional hetero-
geneity within the PFC and to call attention to the limitations of focusing either explicitly
or in many cases, unwittingly, on just one sector of this massive expanse of cortex.
3. Empirical and methodological issues in the use of frontal EEG asymmetry

measures in studies of emotional processes
3.1. Evidence of progress
The growing literature on methodological issues in the assessment of EEG asymmetry

is leading to important advances that will improve the reliability and validity of these
measures. The evidence presented in this Special Issue clearly establishes prefrontal EEG
asymmetry measures as reflecting, at least in part, trait-like variations in brain function
that appear to predict interesting and important features of affective style. As such, these
measures have much to add to our current armamentarium of methods used to probe links
between the brain and affect. Functional MRI (fMRI) is being used increasingly to study
the neural basis of affect (see Davidson and Irwin, 1999; Murphy et al., 2003; Wager et al.,
2003 for recent reviews). One important limitation of fMRI methods is that they cannot
be used to make inferences about baseline levels of activity though perfusion MR methods
could potentially be used for this purpose (Wang et al., 2003). An important direction for
future research is the use of EEG asymmetry measures to predict individual differences in
fMRI studies of localized neuronal activation patterns in response to affective challenges
(see Shackman et al., 2003, from our lab for recent example). Another critical opportunity
for future research is the use of source localization methods to more precisely describe
the intracerebral sources of the scalp-recorded signals that we measure. Several recent
studies from our lab illustrate the potential utility of these measures and underscore the
differences in information yield when such source localization methods are utilized (e.g.,
Pizzagalli et al., 2002, 2003), although these methods have yet to be compared directly
with functional neuroimaging data as I have suggested above. Also not yet evaluated is
the differential reliability and validity of asymmetry metrics derived from direct surface
recordings versus from source-localized intracerebral signals. And finally perfusion MRI
can be used to obtain baseline data on localized cortical perfusion, and asymmetry can be
computed from these measures and compared to EEG measures obtained from the same
subjects.
3.2. The problem of the reference electrode
As several authors in this Special Issue have illustrated, the different reference electrode
locations used in research on frontal EEG asymmetry continues to be a vexing problem.
While some authors have demonstrated robust and consistent effects across different ref-
erence electrodes, this has not always been the case and it underscores the fact that EEG
recordings reflect the potential difference between two locations and there is no electrically
neutral location anywhere on the body. There still remains much methodological work
to accomplish on this issue including the simultaneous assessment of brain electrical and
hemodynamic or metabolic measures (see e.g., Goldman et al., 2002; Laufs et al., 2003).
By using regional hemodynamic or metabolic measures as a gold standard against which to
compare various EEG metrics, it may be possible to identify a set of procedures that con-
sistently yields the most robust relations between brain electrical signals and more spatially
precise measures of brain function. We have adopted this strategy and have begun to empiri-
cally dissect this complex issue and determine which EEG reference schemes and frequency
bands most directly correlate with direct measures of regional glucose metabolism assessed
with positron emission tomography (Oakes et al., 2004).
One issue of considerable importance to research on EEG measures of functional brain
asymmetry is the use of the linked ears reference, a common choice in studies of frontal
EEG asymmetry (see e.g., Minnix et al., this issue). As Allen et al. (this issue) correctly
show, variations in electrode impedance cannot account for any detectable difference in
signals across electrodes using modern high impedance amplifiers. This is true in all but
one circumstance and that is when electrodes are linked prior to inputting the signal into
the amplifier (Senulis and Davidson, 1989). Thus when a linked ears or mastoid montage
is used, even slight variations in electrode impedance on each side can asymmetrically bias
the signal. It is for this reason that we have suggested that a computer-averaged ears (or
mastoids) reference be used if an investigator wishes to compute a linked ears or linked
mastoid reference (see Davidson et al., 2000b).
3.3. Frequency bands other than alpha
It is striking that none of the articles in this Special Issue that focused on adult subjects
included an analysis of frequency bands other than alpha. In several recent studies we have
examined frequency bands other than alpha including theta, beta and gamma (Pizzagalli
et al., 2001, 2002, 2003). In these studies, we also examined alpha power and in a number of
cases, asymmetrical effects were found in bands other than alpha while effects in the alpha
band were absent. Moreover, in our recent direct simultaneous comparison of EEG and
PET measures of regional glucose metabolism (Oakes et al., 2004), we found that although
alpha shows the predicted inverse relation with metabolism (see also Cook et al., 1998),
the frequency band most consistently and strongly associated with glucose metabolism was
gamma. Thus, although the frontal EEG asymmetry literature has traditionally focused on
alpha power, it is important as we go forward to carefully examine other frequency bands

as these may provide additional information not reflected in alpha power.
3.4. Bilateral variations in PFC are also important
Extant methods of analysis featured in the articles in this Special Issue emphasize, for
the most part, asymmetrical variations in frontal brain activity. The computation of an
asymmetry metric, while serving an important function, also masks the opportunity to
examine bilateral variations in frontal brain activity. The sole exception in this group of
articles is the Nitschke et al. (this issue) report; they illustrate the predictive value of bilateral
variations in alpha power. It is important to underscore the fact that even if condition or
group differences are found in asymmetry, such differences could be superimposed upon
bilateral variations in activity and these bilateral variations in activity may be functionally
significant (see e.g., Schmidt and Trainor, 2001). Future research in this area should include
analysis methods that permit the systematic examination of bilateral variations in activation
and assess the functional significance of such bilateral variations.
3.5. Importance of comparative research
Functional asymmetries are not the sole province of humans. Such asymmetries are found
at many different levels of phylogeny (see Hugdahl and Davidson, 2003 for several reviews).
And given the pervasive presence of affect at virtually all levels of phylogeny where be-
havior itself is observed, functional asymmetries associated with affective processes may
be considerably more ubiquitous across the animal kingdom than asymmetries associated
with language and communication. For example, there is a growing literature in rodents
that is consistent with human data indicating a preferential role for regions of the right
PFC in anxiety and withdrawal (see Berridge et al., 2003). In rhesus monkeys, we have
recorded brain electrical activity from the scalp surface using procedures similar to those
we use in humans and have found differences among animals in baseline levels of asym-
metric prefrontal activity that are reliable over time and show systematic correlations with
behavioral and biological measures that reflect anxiety and stressful responding (e.g., Kalin
et al., 1998, 2000). Such animal models provide a foundation for research where lesions in
particular regions of PFC can be made to establish the differential causal role of left and
right prefrontal regions in specific types of affective behavior.
4. Summary and conclusions
This commentary provides some reflections on the current state of affairs in research
on EEG frontal asymmetries associated with emotion. The first part addresses a series of
conceptual issues and the second part some empirical and methodological issues. Of prime
important for the future of EEG asymmetry research is that it make more meaningful con-
tact with the growing corpus of literature on primate prefrontal function. One of the most
lamentable characteristics of the current work on frontal EEG asymmetry is that it has
evolved largely unconnected with the neuroscience literature on the structure and function
of the PFC. Scalp-recorded measures of prefrontal activity likely reflect primarily dorso-
lateral PFC function, yet the PFC is anatomically and functionally heterogeneous. Careful
consideration of this issue and developing hypotheses based upon findings from the neuro-
science literature should aid future progress. Another critical issue is the fact that the PFC is
embedded in a complex circuit involving other cortical and subcortical structures and these
other structures likely play a very important role in many of the affective processes featured
in the articles in this Special Section. However, because the EEG measures that are utilized
in these studies do not directly reflect activity in other parts of the circuitry, these other
neural components have, for the most part, been ignored by those investigators who study
frontal EEG. Much of the research on frontal EEG asymmetry has examined the correlates
of variations in asymmetry with self-report measures. While these reported associations
have been interesting, they are typically not informative with regard to mechanism because
the specific types of processes affected by prefrontal function are likely to themselves be
opaque to self-report. Thus, while they influence self-report (such as variations in the time
to recovery following a negative event), they are not themselves consciously accessible
and thus such self-report measures will ultimately be uninformative if we hope to build
neurally-inspired theory. The approach-withdrawal model of frontal asymmetry (see e.g.,
Davidson, 1992) receives considerable support from numerous studies in this Special Issue,
most especially from Harmon-Jones, with his findings on anger. The provocative question
of whether or not high levels of baseline left prefrontal activity, in light of the Harmon-Jones
findings, still should be considered to be a positive trait, is addressed, with a tentative affir-
mation, despite the findings on anger. Finally, some discussion of what different sectors of
the PFC might be doing in emotion is introduced.
In the second section of this essay, several methodological issues are considered including
problems with the linked ears or mastoids reference, the importance of examining frequency
bands other than alpha, using analytic methods that permit bilateral variations in frontal
activity to be assessed, and some comments on the importance of comparative research to
address some of the fundamental outstanding questions in this line of research.
The fact of this Special Issue is a testament to the enormous progress that has occurred in
this area of research. It will be exciting to revisit this topic in 5 years since with the advent of
new methods such as functional neuroimaging, particularly when they are combined with
traditional psychophysiological measures (Davidson, 2003b), very rapid and novel progress
can be expected.
Acknowledgements
I wish to thank the many students, trainees and staff members in my laboratory who have
enabled this research program and have been instrumental in it thriving. I particularly wish
to thank Jack Nitschke, Alex Shackman, Carien van Reekum, Jim Coan, Tim Salamons
and Tom Johnstone for their comments on an earlier draft of this manuscript. I also wish to
thank John Allen for his comments on an earlier draft. I also wish to thank the consistent
support of NIMH who has funded most of the research described in this commentary and is
currently providing support through the following grants to RJD: NIMH grants MH43454,
MH40747, P50-MH52354, P50-MH61083 and NIA grant PO1-AG021079.
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Commentary
Feelings and emotions: roles for
electrophysiological markers
John T. Cacioppo
Department of Psychology, University of Chicago, 5848 S. University Avenue, Chicago, IL 60637, USA
Abstract
Asymmetrical electroencephalogram (EEG) alpha activity over anterior regions of the scalp pre-
dicts a variety of outcome measures of interest to emotion researchers. This vast and diverse literature
is examined from three different viewpoints. First, the organization of this vast literature is contrasted
from theoretical and statistical perspectives, and the advantages and disadvantages of each perspective
are considered. Second, the correlates of EEG asymmetry are sometimes treated as criterion (depen-
dent) measures and at other times treated as predictor (independent) measures. Differences in the
interpretation of each are surveyed, and the need for attention to whether EEG asymmetry is a simple
correlate, mediator, or moderator of the associated affective measures is noted. Finally, the studies of
EEG asymmetry and emotion that adopt a psychological perspective are contrasted with those that
adopt a neurophysiological perspective, and the import of each for theory, experimental design, and
analytic strategy is discussed.
Keywords: Electroencephalogram (EEG); Criterion; Predictor
1. Introduction
For centuries scholars regarded feelings (e.g. sadness, fear, anger, disgust, dysphoria)
as the most (if not only) appropriate data for the study of emotion. The reasoning for this
position, on the surface, is straightforward. When one finds oneself teetering dangerously
on the edge of a cliff, positioned in the path of a charging beast, or trapped on the top
floors of a burning skyscraper, the consequences are not subtle: the unmistakable feeling
of fear commands center stage, the expression of terror is etched involuntarily across one’s
face, attention is narrowed to a focal set of stimuli, actions are driven by attempts to avoid
E-mail address: cacioppo@uchicago.edu (J.T. Cacioppo).
doi:10.1016/j.biopsycho.2004.03.009
236 J.T. Cacioppo / Biological Psychology 67 (2004) 235–243
the imminent peril, and metabolic resources are mobilized to support these actions. When
the same set of responses is elicited by normal circumstances, such as when an individual
approaches a podium to deliver a speech, encounters a nonpoisonous snake, or prepares
to board an airplane, normal life is disrupted and individuals complain about the horrific
feelings that hijack their will and their way.
Feelings represent a special class of outcomes that are important to explain in theories
of emotion, to be sure, but it does not follow from their position in center stage that the
most appropriate data for constructing or testing theories of emotion are limited to feelings
or self-reports (cf. Cacioppo et al., 1997, 1999). An important contribution of both the
cognitive revolution in psychology and animal research on emotion is an appreciation that
feelings provide an incomplete glimpse of their underlying information processing struc-
tures and operations. LeDoux (2000), in his recent survey of the field in the Annual Review
of Neuroscience, echoed this point:
It is widely recognized that most cognitive processes occur unconsciously, with only
the end products reaching awareness, and then only sometimes. Emotion researchers,
though, did not make this conceptual leap. They remained focused on subjective emotional
experience. . . . The main lesson to be learned. . . is that emotion researchers need to figure
out how to escape from the shackles of subjectivity if emotion research is to thrive
(LeDoux, 2000, p. 156).
How are we to plumb noninvasively the structures and processes of emotion in humans if
not through self-reports? The work summarized in this special issue suggests that measures
of frontal electroencephalogram (EEG) asymmetry have much to offer in this regard. My
aim in this commentary is to highlight a few themes in this literature that I hope will foster
this effort.
1.1. Theoretical and statistical perspectives
Research on EEG frontal asymmetry and emotion is one of the most promising and fer-
tile in the field. The assortment of variables associated with EEG frontal asymmetry, for
instance, ranges from child temperament (see Fox et al., 2001), the maternal depression of
infants (Jones et al., 2004) and adolescents (Tomarken et al., 2004), self-report measures
of affect and personality (e.g. Tomarken and Davidson, 1994), shyness and social anxi-
ety (Schmidt, 1999), socioeconomic status (Tomarken et al., 2004), basal cortisol levels
(Kalin et al., 1998), and immune function (e.g. Kang et al., 1991) to cognitive dissonance
arousal (Harmon-Jones, 2004), the emotional content of dreams upon awakening (Donzella
et al., 1994), the memory recognition of sad narrative material (Nitschke et al., 2004), and
reassurance seeking (Minnix et al., 2004).
The number of associations between EEG frontal asymmetry and various aspects of emo-
tion is sufficiently large, and the measures that are associated with EEG frontal asymmetry
are sufficiently diverse, that it can be difficult to see beyond these data to underlying or-
ganizations, structures, and processes. One way of dealing with such a complex array of
associations is to rely on a theoretical formulation to guide one’s analysis and interpretation.
The most influential is Davidson’s (e.g. 1993, 2004) model, which specifies that high levels
of relative left frontal activity are associated with the expression and experience of positive,
J.T. Cacioppo / Biological Psychology 67 (2004) 235–243 237
approach-related emotions, and high levels of relative right frontal activity are associated
with the experience and expression of negative, withdrawal-related emotions. Harmon-Jones
(2004) has argued that this model includes both motivational and valence components, which
can be distinguished conceptually and empirically. In doing so, he has identified a valence
model of EEG asymmetry in which high levels of relative left frontal activity are associated
with the expression and experience of positive emotions and high levels of relative right
frontal activity are associated with the experience and expression of negative emotions; and
a motivational direction model in which high levels of relative left frontal activity are associ-
ated with the expression of approach-related emotions and high levels of relative right frontal
activity are associated with the expression of withdrawal-related emotions. Although posi-
tive emotions are typically associated with motivations to approach and negative emotions
are typically associated with motivations to withdraw, there are notable exceptions (e.g.
anger-out). Through the development and tests of competing hypotheses, Harmon-Jones
(2004) and colleagues have pursued the goal of specifying more precisely what the emo-
tional and motivational functions of asymmetrical frontal brain activity might be.
In the pursuit of the simplest single theoretical construct that might account for these
assorted findings, it may be worthwhile to ask whether the various correlates of EEG asym-
metry are themselves sufficiently correlated that they likely result from a unitary underlying
faculty or mechanism. Indeed, philosophers of science have long noted the beneficial effect
of theory testing on scientific progress (see Brazier, 1959), but in the past century there has
been an increasing recognition of the ways in which a theoretical focus can also hinder sci-
entific progress (e.g. by biasing the selection of measurement instruments, Eddington, 1939,
or the construction or interpretation of crucial tests, Greenwald et al., 1986). A multivariate
statistical approach to investigate the structure of the correlates of EEG asymmetry may also
be informative by pointing to possible oversimplifications in existing theoretical formula-
tions and, relatedly, by suggesting new theoretical hypotheses that can be tested empirically.
Consider a thought experiment in which all of the known correlates of EEG asymmetry
(e.g. see Tables 1–4 in Coan and Allen, this issue) were measured in a single study with
a large sample size. Would one expect EEG asymmetry to predict each of these outcome
measures? The answer is yes, of course, assuming measurement error was negligible and the
findings reliable. So far, this thought experiment simply constitutes a replication of prior
research. However, because all of the outcome measures in this thought experiment are
obtained from the same individuals, it is possible to use multivariate statistical techniques to
explore the interrelationships among and the statistical coherences among these measures.
It would be possible, for instance, to submit the data from half of the participants to an
exploratory factor analysis using an oblique rotation to examine the statistical structure
of the multivariate dataset. The data from the other half of the participants could then be
subjected to a confirmatory factor analysis to validate this structure.
If the results confirmed these measures were sufficiently coherent and they represented
a single dimension, then not only would this provide additional evidence for their being a
unitary faculty or single mechanism underlying their production, but also the factor load-
ings of the measures should bear on the core features of this unidimensional construct. If,
on the other hand, the results of this thought experiment indicated a single dimension was
insufficient to represent the correlates of EEG asymmetry, the nature of the multidimen-
sional representation and the factor loadings on these dimensions could have considerable
theoretical import, as they would lead to new and testable hypotheses about what precisely
EEG asymmetry is predicting in specific contexts.
The point of this thought experiment is not to prejudge what the outcome might be, but
rather to underscore the complementary role of theoretical and statistical perspectives on a
literature as complex and diverse as that on the associations of anterior EEG asymmetry.
The concept of arousal—once a popular construct in the field of emotion, was undermined
not so much by its lack of empirical support as by its oversimplification of the accumulated
empirical data. Arousal came to stand for such a diverse set of outcomes, many of which
were only so poorly correlated, that the formulation lost its predictive power and, thus, its
scientific import. The same fate need not befall an area of work as fertile as EEG asymmetry
and emotion if both statistical and theoretical approaches are used to complement each other.
1.2. Associations between EEG frontal asymmetry and emotion
Coan and Allen (2004) classified studies of EEG asymmetry and emotion as falling
under one of four categories: (a) research on trait frontal EEG asymmetry and other trait-like
measures, (b) studies of trait frontal asymmetry as a predictor of state dependent changes, (c)
studies of trait frontal EEG asymmetry and measures of psychopathology, and (d) research
on frontal EEG activation asymmetry as a state measure. This categorization leads to several
quick observations. First, EEG asymmetry is not itself a mechanism but rather it is a marker
of some underlying neural processes. Although the first three categories of research concern
trait frontal EEG asymmetry as it relates to traits, state changes, and psychopathology, there
appears to be a paucity of research on the neural structures and processes that are responsible
for these associations (cf. Davidson, 2003). I return to this issue in Section 1.3.
Second, it is judicious to ask for each new association whether EEG asymmetry, or more
specifically the neural mechanism responsible for frontal EEG asymmetry, plays a causal
role in the outcome measure. Although the studies tend to be treated similarly, some studies
of frontal EEG asymmetry are designed to examine behavioral correlates, other studies
treat frontal EEG asymmetry as an independent (blocking) variable and behavioral vari-
ables as the dependent measure, and still others treat one or more behavioral measures as
the independent (blocking) variable and frontal EEG asymmetry as the dependent measure.
These distinctions are significant. Studies of frontal EEG asymmetry designed to examine
behavioral correlates speak only the probability of the co-occurrence of these measures (i.e.
P(EEG asymmetry, behavioral measure)), studies that treat frontal EEG asymmetry as an
independent (blocking) variable and behavioral variables as the dependent measure speak
the probability of the behavioral variable given frontal EEG asymmetry (i.e. P(behavioral
measure/EEG asymmetry)), and studies that treat one or more behavioral measures as the in-
dependent (blocking) variable and frontal EEG asymmetry as the dependent measure speak
the probability of frontal EEG asymmetry given the behavioral variable differs (i.e. P(EEG
asymmetry/behavioral measure)). We have dealt elsewhere with the different implications
for the interpretation of empirical findings for each of these classes of studies (e.g. Cacioppo
and Tassinary, 1990; Sarter et al., 1996). Suffice it to say that statements about the causal
role of frontal EEG asymmetry in producing a particular emotional state or predisposition
are inappropriate in studies that treat frontal EEG asymmetry as the dependent measure and
a behavioral measure (e.g. depression) as the independent (blocking) variable.
Studies that treat frontal EEG asymmetry as a blocking variable and behavioral variables
as the dependent measure are better suited to such interpretations, but alternative interpre-
tations still need to be considered. Allen et al. (2001), for instance, recognized that most
of the extant evidence about the possible role of frontal EEG asymmetry and emotional
responses is based on correlational evidence. To examine the potential causal role of frontal
EEG asymmetry in the production of emotional responses, they used biofeedback training to
increase either relative right or relative left frontal EEG activity. Manipulation checks con-
firmed that 5 consecutive days of biofeedback training produced the expected differences in
EEG asymmetry, and self-reported responses to emotionally evocative film clips indicated
that individuals trained to increase left frontal activity reported more positive affect to a
happy film clip than individuals trained to increase right frontal activity. This is a laudable
effort on a number of fronts, including the attempt to test the causal role played by the neural
processes marked by frontal EEG asymmetry, the extensive biofeedback training provided
to participants over 5 consecutive days in an effort to manipulate frontal activity, and the
treatment of EEG asymmetry as a blocking variable and emotional responses as the depen-
dent variable. It is possible that the biofeedback training operated directly to increase right
or left frontal activity which then in turn led to more positive or negative affective responses
to happy film (see Harmon-Jones, 2004), but the opposite is also possible. For instance, it
is conceivable that participants tried different mental strategies to achieve reinforcement in
the biofeedback training task. If participants discovered during biofeedback training that
thinking happier thoughts led to reinforcement for producing relative right frontal activity
and that thinking less happy thoughts led to the opposite, then the frontal EEG asymmetry
may not have been the cause of the affective responses they observed. Techniques such as
transcranial magnetic stimulation, which would avoid this alternative interpretation, may
prove a valuable additional tool for investigating questions of this form (e.g. see Nahas
et al., 2003).
As Coan and Allen (2004) suggest, experimental designs and statistical tests to deter-
mine whether EEG asymmetry may be serving as a moderator or a mediator of emotional
processes can be especially helpful at this point in time to advance theory and research in
the area. The frontal EEG asymmetry marks some underlying neural process or processes.
Continued efforts are needed to identify the neural processes that underlie the correlation
between resting EEG alpha asymmetry and emotional style and the neural processes that
underlie differential EEG alpha activation in emotionally evocative situations. Neverthe-
less, EEG asymmetry as a marker of these underlying events can be examined using the
procedures outlined by Coan and Allen (2004) to determine whether the processes it marks
are likely to be serving as a mediator, moderator, or simple correlate in a given study. The
frontal EEG asymmetry is conceptualized as a mediator when the neural processes underly-
ing the differential frontal activation is thought to be instrumental in the production of tonic
affective states or state changes (e.g. more or less pleasant or unpleasant feelings about a
stimulus) or approach- or withdrawal-motivational tendencies, whereas frontal EEG asym-
metry is conceptualized as a moderator when the neural processes underlying it are thought
to dampen or augment the processes instrumental in the production of tonic affective states
or state changes. Allen and Coan’s (2004) description of the methodological and statistical
conditions needed to differentiate these possible roles is a valuable contribution to the field
as it may explain some apparent inconsistencies in results (e.g. see Reid et al., 1998).
1.3. Psychological and physiological perspectives
Whether frontal EEG asymmetry is treated as an individual difference variable or a

state-dependent concomitant, its association to emotion and emotion-related constructs
has generally reflected a search for functional relationships to other behavioral constructs
rather than a search for underlying neural mechanisms. The studies comprising this special
issue are a case in point, and they nicely illustrate the theoretical value of this psycholog-
ical approach to the study of frontal EEG asymmetry and emotion. Indeed, Coles et al.
(1987) noted in their discussion of event-related brain potentials (ERPs) that knowledge
of the neural substrates of ERPs is logically neither necessary nor sufficient to ascribe
psychological meaning to ERP components, and this is true for frontal EEG asymmetry,
as well. The ascription of psychological meaning to the ERP components, frontal EEG
asymmetry measures, or any other such marker ultimately resides in the quality of the
experimental design and the psychometric properties of the measurements. Although nu-
merous aspects of the physiological bases of ERPs remain uncertain, for instance, func-
tional relationships within specific paradigms have been established between elementary
cognitive operations and components of these potentials by systematically varying one
or more of the former and monitoring changes in the latter (e.g. Coles et al., 1986).
This literature has also revealed that the psychological interpretation of an ERP measure
may differ across paradigms—a finding that should serve as a cautionary note to those
who wish to interpret EEG asymmetry measures as necessarily reflecting the same sub-
strates, predispositions, or information processing operations across different paradigms
or methods of measuring frontal asymmetries (cf. Hagemann et al., 1998; Reid et al.,
1998).
Continued efforts are also needed, however, to further specify the neural processes or
processes that are responsible for the pattern of resting EEG alpha asymmetry associated
with specific facets of emotional style and those that are responsible for differential EEG
alpha activation in emotionally evocative situations (cf. Davidson, 2003, 2004). Among the
major evolutionary advances in humans is the striking development of the human cerebral
cortex, especially the frontal region. The cerebral cortex is a mantle of between 2.6 and 16
billion neurons with each neuron receiving 10,000–100,000 synapses in their dendritic trees
(e.g., Pakkenberg, 1966). The frontal lobes constitute approximately 32% of this cerebral
mantle. The vast expansion of the frontal regions in the human brain is largely responsible
for the human capacity for reasoning, planning, and performing mental simulations, and
an intact frontal region contributes to the human ability to reason, remember and work
together. The neocortex in particular is a recent development in evolutionary time, and the
means for guiding behavior through the environment, albeit in a more rigid and stereo-
typed fashion, emerged prior to neocortical expansion. These evolutionarily older systems
likely also play a role in human information processing, emotion, and behavior, and ample
anatomical connections between frontal and limbic regions are documented (Davidson and
Irwin, 1999).
The specification of the neural substrates and processes underlying specific measures of
EEG asymmetry in a given paradigm can constrain and inspire theoretical hypotheses, foster
experimental tests of otherwise indistinguishable theoretical explanations, and increase the
comprehensiveness and relevance of theories of emotion. In addition, the measurement
characteristics and psychometric properties of frontal EEG asymmetry have received careful
attention (e.g. see Allen et al., 2004; Hagemann, 2004), but knowledge of the specific
neural structures and processes underlying tonic and phasic EEG asymmetry measures may
contribute further to the accuracy of its measurement in particular paradigms and in specific
populations.
The point is not that either a neurophysiological or the psychological perspective is pre-
eminent, but rather that both are fundamental to and complementary in studies of EEG
asymmetry and emotion (see also, Hagemann, 2004). Inattention to the logic underlying
psychophysiological inferences simply because one is dealing with observable electrocorti-
cal responses is likely to lead to simple and restricted descriptions of empirical relationships
and/or to erroneous interpretations of relationships involving these responses. An entirely
aphysiological attitude, in contrast, ignores relevant information and therefore increases
the chances of misinterpretations of the empirical relationships that are found between
EEG asymmetry measures and emotional processes or states. It is the joint consideration
of physiological and psychological perspectives that enriches theory and research on hu-
man emotion by reducing errors of operationalization, measurement, and inference. The
field of research on frontal EEG asymmetry appears well positioned for such a multi-level
integrative approach to the study of emotion.
2. Summary
The frontal regions of the neocortex have led to dramatic expansions in emotional, be-
havioral, and social capacities. Perhaps it should not be surprising that research on frontal
EEG asymmetry and emotion has uncovered such a diverse set of associations, therefore.
Rather than reducing this literature to its simplest theme, I have discussed ways investigators
might investigate whether frontal EEG asymmetry bears on separable but ultimately related
facets of affective information processing, expression, and response. Metabolic and elec-
trophysiological images of brain activity hold the promise of examining when and where
affective information processing is unfolding in the brain, from which investigators will
be in a better position to infer the nature of the information processing operation being
performed moment by moment in the brain.
Acknowledgements
Preparation of this paper was supported by National Institute of Mental Health Grant
Number P50MH52384-01A1.
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Biological Psychology 67 (2004) 1–5

Keywords: Frontal EEG Asymmetry; Emotion; Mediators; Moderators

Waisman Center, University of Wisconsin–Madison, Madison, WI 53705, USA. Corresponding author.

2. Moderators, mediators and frontal EEG asymmetry

3. The measurement of frontal EEG asymmetry

J.A. Coan, J.J.B. Allen / Biological Psychology 67 (2004) 7–49

J.A. Coan, J.J.B. Allen / Biological Psychology 67 (2004) 7–49

J.A. Coan, J.J.B. Allen / Biological Psychology 67 (2004) 7–49

J.A. Coan, J.J.B. Allen / Biological Psychology 67 (2004) 7–49

5. Frontal EEG asymmetry as a possible moderator of emotional responding

5.1. Modeling frontal EEG asymmetry as a moderator

Before describing the data analytic identification of a moderator variable, it is important

5.2. Empirical support for frontal EEG asymmetry as a moderator

J.A. Coan, J.J.B. Allen / Biological Psychology 67 (2004) 7–49

based psychological disorders. Indeed, Davidson’s theory of frontal EEG asymmetry as a

6. Frontal EEG asymmetry as a risk factor and possible moderator of

J.A. Coan, J.J.B. Allen / Biological Psychology 67 (2004) 7–49

J.A. Coan, J.J.B. Allen / Biological Psychology 67 (2004) 7–49

J.A. Coan, J.J.B. Allen / Biological Psychology 67 (2004) 7–49

J.A. Coan, J.J.B. Allen / Biological Psychology 67 (2004) 7–49

J.A. Coan, J.J.B. Allen / Biological Psychology 67 (2004) 7–49

J.A. Coan, J.J.B. Allen / Biological Psychology 67 (2004) 7–49

7. Frontal EEG asymmetry as a possible mediator of emotional responding

Systematic alterations in frontal EEG asymmetry in response to specific emotional stimuli

J.A. Coan, J.J.B. Allen / Biological Psychology 67 (2004) 7–49

J.A. Coan, J.J.B. Allen / Biological Psychology 67 (2004) 7–49

J.A. Coan, J.J.B. Allen / Biological Psychology 67 (2004) 7–49

J.A. Coan, J.J.B. Allen / Biological Psychology 67 (2004) 7–49

7.1. Empirical support for frontal EEG asymmetry as a mediator

8. Frontal EEG asymmetry as a trait-like moderator and a state-related mediator

Trait 36 0.003 8.23

Trait 0.002 0.42

9.1. Frontal EEG asymmetry as a moderator of emotion

9.2. Frontal EEG asymmetry as a moderator of psychopathology

9.3. Frontal EEG asymmetry as a mediator

9.4. Future directions

Keywords: Frontal EEG asymmetry; Emotion; Anger; Cognitive dissonance

∗ Tel.: +1-608-265-5504; fax: +1-608-262-4029.

2. Asymmetrical frontal brain activity and emotion

3. Examinations of the relationship between indices of trait affect/motivation and

3.2. Positive and negative affect

3.3. Behavioral activation/behavioral inhibition

4. Examinations of the relationship between resting EEG and responses to

positive affective responses to positive emotion-inducing films (happiness) (Tomarken et al.,

5. Examinations of EEG activity during exposure to emotionally evocative

6. Explanations of the relationship between asymmetrical frontal brain activity and

emotion of anger, we are in a position to answer precisely what the emotional/motivational

7. Anger and approach motivation

7.1. Behavioral evidence

7.2. Subjective evidence

7.3. Hormonal and physiological evidence

Further evidence supporting the conceptualization of anger as involving approach and

7.4. Individual differences evidence

7.5. Summary of section

8. Anger and asymmetrical frontal brain activity

8.1. Asymmetrical frontal activity and trait anger

8.2. Asymmetrical frontal activity and state anger

8.3. Manipulating the intensity of approach motivation in an anger-evoking situation

According to the motivational direction model of asymmetrical frontal activity, approach

8.5. On the reduction of anger-related left frontal activity

9. Dissonance and left frontal activity

10. Discussion of some issues

10.2. Defining emotional valence