Biological Psychology 70 (2005) 141–151

www.elsevier.com/locate/biopsycho

Cognitive restructuring and EEG in major depression

Patricia J. Deldin a,*, Pearl Chiu b
a
University of Michigan, Department of Psychology, 2252 East Hall,
Ann Arbor, MI 48109-1109, USA
b
Harvard University, Department of Psychology, William James Hall, Cambridge, MA 02138, USA
Received 30 October 2002; accepted 5 January 2005
Available online 7 March 2005

Abstract

Techniques based on cognitive therapy and electroencephalography (EEG) were used to investigate the predictive utility of EEG alpha power
with regard to mood improvement. Controls and individuals with major depression participated in four EEG recording blocks. Blocks 1 and 4
were resting baselines. During Block 2, Ss were asked to think about their ‘‘most troubling life difficulty.’’ Next, Ss were introduced to cognitive
views of depression and techniques used in cognitive therapy. For Block 3, Ss were asked to use these methods to think again about their life
difficulty. Ss who reported greater post- than pre-intervention happiness (i.e., ‘‘Responders’’) exhibited greater overall cortical activity than Non-
responders. Depressed Responders further exhibited a cortical asymmetry of greater right relative to left activity in frontal areas. The predictive
utility of EEG is discussed with regard to identifying individuals who show mood improvement following cognitive restructuring.
# 2005 Elsevier B.V. All rights reserved.

Keywords: Electroencephalography; Major depression; Cognitive therapy; Treatment predictors

1. Cognitive restructuring and EEG in major
depression
Cognitive theories have been shown to be appropriate for
describing major depression (e.g., Haaga et al., 1991;
Williams et al., 1997), and have led to an efficacious
treatment, cognitive psychotherapy, for the disorder (Elkin
et al., 1989; DeRubeis and Crits-Christoph, 1998). Indeed,
cognitive therapy is considered to be a highly effective
treatment – as effective as pharmacotherapy in many cases –
and potentially more effective when used in conjunction with
medications (Dobson, 1989; Otto et al., 1996). Moreover,
research indicates that depressed individuals who receive
cognitive therapy either alone or with pharmacotherapy may
be less likely to experience a relapse than patients who receive
other forms of treatment (Evans et al., 1992; Thase and
Simons, 1992). However, despite evidence for the efficacy of
cognitive therapy, relatively little is known about the patient
characteristics of those who exhibit a therapeutic response.
* Corresponding author. Tel.: +1 734 647 9863; fax: +1 734 615 0573.
E-mail address: pjdeldin@umich.edu (P.J. Deldin).
The human and fiscal cost of failed treatment motivates the
attempt to refine measures that may discern those who may
benefit from psychotherapy from those who will not.
Potential predictors, mediators, and concomitants of
positive response to cognitive therapy have traditionally
been examined in studies that dismantle components of
psychotherapy (e.g., Jacobson et al., 1996; Jarrett and
Nelson, 1987), that compare pharmacotherapy outcome with
psychotherapy outcome (e.g., Peselow et al., 1990; Fava
et al., 1994), or that attempt to identify predictors of
treatment response using a range of self-report measures or
therapist variables (e.g., Castonguay et al., 1996; Dohr et al.,
1989). Although such studies have provided some insight
into the efficacy and changes associated with various aspects
of cognitive therapy, the results have largely been
inconsistent in yielding a comprehensive system of variables
that may be of clinical utility with regard to therapeutic
response. Investigations of psychosocial factors have also
been inconclusive regarding the utility of any particular
variable, or group of variables, as an outcome predictor of
positive response to cognitive therapy (for reviews, see
Scott, 1996; Whisman, 1993). Indeed, although traditional

0301-0511/$ – see front matter # 2005 Elsevier B.V. All rights reserved.
doi:10.1016/j.biopsycho.2005.01.003
142 P.J. Deldin, P. Chiu / Biological Psychology 70 (2005) 141–151
approaches to identify these predictors have implicated such
assorted variables as therapeutic empathy, perceived help-
fulness of the therapy, homework compliance, degree of life
stress, and symptom severity, as important with regard to the
therapeutic process, none has emerged as a sufficient
predictor of response to cognitive therapy (for review, see
Salkovskis, 1996). Clearly, the patient characteristics that
may be associated with therapeutic response require further
investigation.
There is a growing literature suggesting that examining
brain physiology in addition to psychosocial variables may
be of utility in exploring mechanisms and identifying
predictors of treatment response (Miller and Keller, 2000).
For example, pre-treatment hemispheric advantage on a
dichotic listening task has been found to predict response to
both cognitive–behavioral therapy and fluoxetine therapy
(Bruder et al., 1996, 1997). In addition, abnormal sleep EEG
profiles (based on REM density, REM latency, and sleep
efficiency) have been associated with non-response to both
cognitive–behavioral therapy and interpersonal psychother-
apy in major depression (Thase et al., 1996, 1997). Recent
biofeedback studies also suggest that EEG techniques may
be of utility in exploring mechanisms of therapeutic change
(Baehr et al., 1997; Rosenfeld et al., 1995; Allen et al.,
2001).
As major depression is likely to be an interaction between
psychosocial and biological variables, it seems reasonable to
suggest that therapeutic response may be associated with
cortical physiology. Elucidating this relationship clearly has
significant implications for not only the design and
implementation of effective therapeutic practices but also
for the understanding of the maintenance of major
depression. Thus, the present research investigates the role
and predictive utility of electroencephalographic (EEG)
patterns and changes with regard to positive therapeutic
response.
1.1. EEG alpha
The phenomena of EEG alpha (8–12 Hz) synchronization
during mental relaxation and desynchronization during
mental activity has long been observed (for review, see
Klimesch, 1999), and has led researchers to employ EEG
alpha power as an economical, yet precise, inverse index of
cortical activity (Gevins, 1998). More generally, increased
alpha power during cognitive tasks is thought to reflect a
relative decrease in the proportion of local cortical neurons
that are engaged in a particular task performance (Gevins
and Smith, 2000; Klimesch, 1999).
Research has consistently found a decrease of alpha
power during task solution (e.g., Rugg and Dickens, 1982;
Ramos et al., 1993; McEvoy et al., 2000), as well as task-
specific changes in regional alpha power (e.g., Earle, 1988;
Molle et al., 1999; Bell and Fox, 2003). EEG alpha power
has also received increasing attention as an index of
particular performance and task variables. Specifically,
evidence from studies with tasks varying attentional
requirements suggests that alpha is inversely related to
attentional level and demand during cognitive processes
(e.g., Ray and Cole, 1985; Dujardin et al., 1993). Moreover,
increases in task difficulty have been found to be associated
with a decrease of power in the lower alpha band (8–10 Hz;
Gevins and Smith, 2000). Gevins and Smith (2000) further
noted that a high-ability group of participants (as measured
by scores on the WAIS-R) displayed relatively larger
practice-related increase in alpha power, suggesting that this
group adapted more quickly to task demands, or that they
were able to adopt task performance strategies that took
advantage of processing resources in other cortical regions.
EEG alpha asymmetry has also been used as a measure of
cortical activity in an extensive range of studies investigating
the localization of emotional processing to general cortical
regions. Specifically, it has been suggested that the left and
right frontal regions are specialized, respectively, for the
experiential aspects of positive (i.e., approach-related) and
negative (i.e., withdrawal-related) emotion (e.g., Davidson
et al., 1979; Sackheim et al., 1982; for review, see Davidson,
1998). Evidence further suggests that a frontal asymmetry
(of greater left relative to right pre-frontal alpha power) may
be characteristic of depression and may predispose an
individual to respond with predominantly negative affect
given a negatively valenced stimulus (e.g., Davidson, 1995,
1998; Harmon-Jones, 2003).
Thus, existing research on EEG emphasizes that both
asymmetry and overall levels of cortical activity are likely
to influence an individual’s response, or capacity to
respond, to a particular cognitive or emotional demand.
Indeed, an extensive literature has validated EEG alpha as a
tool for delineating specific cognitive states and processes;
similarly, much literature exists regarding the cortical
asymmetry models of depression and affect. Hence, if
cognitive therapy for depression is considered a task with
high cognitive demand, an individual’s levels and patterns
of cortical activity are likely to moderate the therapeutic
response.
1.2. Cognitive restructuring and EEG
The present study combines the techniques of electro-
encephalography and cognitive restructuring to examine
whether baseline patterns and levels of cortical activity may
be useful indices of mood response to a cognitive therapy
analog. We anticipate that pre-existing levels or patterns of
cortical activity may have predictive utility regarding
whether an individual will exhibit mood improvement
following a brief cognitive intervention. Specifically, we
hypothesize that (1) those who exhibit greater baseline
cortical activity will be at an advantage to report a
therapeutic response to the mood intervention, and/or (2)
that a baseline cortical asymmetry will predispose indivi-
duals to respond more (i.e., those who exhibit greater
relative left frontal activity) or less (i.e., those with relatively
 P.J. Deldin, P. Chiu / Biological Psychology 70 (2005) 141–151
greater right frontal activity) favorably to our cognitive
mood intervention. We will also investigate patterns of
cortical activation concomitant with changes in mood and
cognitive style.
It should be emphasized that though our cognitive
restructuring task is based upon the techniques of cognitive
therapy for depression (Beck et al., 1979; Burns, 1999), it is
a brief, one-time intervention in a laboratory setting, and any
generalization of results to applications of cognitive therapy,
or of our brief intervention to a vehicle of therapeutic
response must be cautious. Nevertheless, our task was based
upon the cognitive restructuring strategies outlined in one of
the most accessible and highly recommended resources for
individuals suffering from depression (Burns, 1999;
Norcross et al., 2003). Thus, the potential of the task to
be an efficient analog to cognitive therapy and to provide a
focused examination of particular components of the
therapeutic process in the laboratory may be considered.
2. Method
2.1. Participants
Thirty-three participants, aged 18–65, were recruited
from the Boston area through advertisements in local
newspapers advertising an ‘‘information processing’’ or
‘‘depression’’ study.
Exclusionary criteria for the depression group included:
major medical illnesses or conditions, cognitive impair-
ments, head injuries resulting in unconsciousness for over
10 min, and any current or past Axis I disorder other than
major depression, except anxiety disorders. Exclusionary
criteria for the control group further comprised all Axis I
disorders. A brief phone interview served as the preliminary
screening for study participation. The Structured Clinical
Interview for DSM-IV, Patient Edition (SCID-I/P; First
et al., 1995) was subsequently administered by a Ph.D. level
clinical psychologist (PJD) or by advanced graduate
students trained in SCID administration.
In order to confirm accuracy of the diagnoses, 25% of the
interview tapes were reviewed by a graduate student trained
in SCID administration. Participants who met criteria for
current major depressive episode (MDE) or normal control,
as determined by the SCID, were invited to take part in the
physiology studies. Because evidence suggests that patterns
of cortical activity in cognitive and affective processes may
differ in left-handed individuals (e.g., Savage, 1993), only
right-handed individuals as assessed with the Edinburgh
Handedness Inventory were included in the present study
(Oldfield, 1971).
The control group included 13 women and 5 men,
ranging in age from 21 to 61 (M = 38.4, S.D. = 13.2), with a
mean education level of 16.1 years (S.D. = 1.9). The
depressed group included 12 women and 3 men, ranging
in age from 18 to 65 (M = 40.6, S.D. = 13.0), with a mean
143
education level of 14.6 years (S.D. = 2.5). The mean
duration of the current depressive episode was 14 months,
and 87% (n = 13) of the depressed individuals had
experienced at least one previous episode of depression.
The groups did not differ in age (F = .801, p > .5), sex
(F = .61, p > .8), or education (F = .707, p > .4). One control
participant and five depressed participants reported having
been in a psychotherapy in which difficulties were discussed
in a manner similar to that employed in our paradigm. Three
individuals were currently taking antidepressant medication.
Preliminary analyses indicate no difference in EEG reactivity
in medicated and unmedicated participants; thus, all subjects
were included in subsequent analyses.
In accord with Harvard University Institutional Review
Board guidelines, informed consent was obtained and it was
emphasized that participants could withdraw from the study
at any time with no adverse consequences. Participants were
compensated US$ 10 for each hour spent in the laboratory.
2.2. Materials
Prior to beginning the physiology recording, individuals
were asked to complete a battery of self-report questionnaires.
The Beck Depression Inventory (BDI) was used to assess
participants’ severity of depression (Beck et al., 1961). The
Beck Hopelessness Scale (BHS) was used to measure
participants’ expectations regarding future events (Beck
and Weissman, 1974). The Spielberger State/Trait Anxiety
Inventory (STAI) was employed as an index of participants’
state and trait anxiety (Spielberger et al., 1970). The
Dysfunctional Attitudes Scale (DAS) provided a measure
of cognitive distortions (Weissman, 1980). Participants also
marked visual analog scales (21 cm) of Happiness (HAP),
ranging from ‘‘the happiest I have ever been’’ to ‘‘not happy at
all,’’ and Sadness (SAD), ranging from ‘‘the saddest I have
ever been’’ to ‘‘not sad at all’’.
As expected, diagnostic groups differed significantly on
all self-report measures (see Table 1).
2.3. Procedure
As outlined below, each individual participated in four
6 min, eyes-closed EEG recording blocks, and engaged in an
introduction to both cognitive views of depression and
Table 1
Participant self-report scores by diagnostic group, mean (S.D.)
Measure Control (n = 18) Major depression (n = 15)
BDI ** 2.2 (.06) 23.8 (8.3)
BHS** 2.1 (2.6) 13.2 (4.2)
STAI-S** 27.5 (4.5) 47.5 (12.7)
STAI-T** 29.3 (5.7) 55.9 (13.7)
DAS** 218 (23.9) 164 (39.6)
HAP (cm)** 13.3 (2.8) 6.6 (4.2)
SAD (cm)** 1.5 (2.7) 11.6 (4.9)
**
p < .01.
144 P.J. Deldin, P. Chiu / Biological Psychology 70 (2005) 141–151
methods used in cognitive psychotherapy to restructure
negative thoughts.
Baseline 1: Subjects were instructed to relax while a
baseline EEG was recorded.
Think 1: For the second recording block, subjects were
asked to think about the ‘‘difficulty in your life that is
troubling you the most’’.
Cognitive restructuring: Prior to the third recording
block, each participant engaged in a two-part introduction to
cognitive restructuring. The information provided was based
upon cognitive theories and therapy of depression (Beck
et al., 1979; Burns, 1999). The first 10–15 min of the session
involved introducing participants to cognitive views of
depression and to types of negative or unrealistic thinking.
Specifically, participants were introduced to the idea that
distorted cognitions can contribute to negative moods, and
that three types of distorted cognition are ‘‘all-or-nothing
thinking,’’ ‘‘magnification,’’ and ‘‘should statements’’. The
latter half of the session included a description of several
methods of identifying and changing negative thinking.
Participants were given strategies to identify unrealistic or
negative thinking and were informed that three ways to
restructure such thinking include: (a) assigning a number
between 0 and 100 to the severity of the difficulty, (b)
examining the facts by making a list of the ways negative
thoughts could be false, and (c) substituting neutral phrases
for emotionally loaded words.
The entire session lasted approximately 30 min, during
which the experimenter was seated next to the participant
with a small table between. To ensure full understanding of
the information, several reality-based examples were
provided with each concept, subjects were given a review
sheet, and prior to the next EEG recording session,
participants were asked to review the material verbally
with the experimenter. If necessary, additional examples
were provided, and if they chose, participants were given the
opportunity to practice identifying and restructuring
negative thoughts. For full text of the cognitive restructuring
protocol, please contact the authors.
Think 2: During the third recording session, participants
were asked to think again about the same life difficulty they
had identified previously in Think 1. They were further
asked to try to use the information provided in the cognitive
restructuring session to identify and restructure specific
negative thoughts about the difficulty.
Baseline 2: Participants were instructed to relax while a
post-task baseline EEG was recorded.
Finally, participants again marked visual scales of
Happiness and Sadness, and also completed a questionnaire
to determine adherence to the task. Participants were then
thanked and fully debriefed.
2.4. Physiological recording
EEG was recorded from F3, F4, P3, and P4 using a lycra
stretchable cap (manufactured by Electro-Cap, International
Inc., Eaton, OH) with electrodes positioned according to the
international 10–20 system. During recording, all sites were
referenced to vertex1 (Cz). Physiological signals were
amplified and filtered through an S.A. Instruments Custom
37/64 Bioamp polygraph. In order to facilitate artifact
scoring, electrooculogram (EOG) data were recorded using
tin electrodes placed lateral to the outer canthi, and above
and below the left supraorbital and suborbital positions.
High- and low-pass analog filter settings were set at 0.01 Hz
and 30 Hz, respectively. Digital sampling occurred at
512 Hz for 6 min during each of the four recording blocks
of the study. All electrode impedances were kept below
10 kV. Participants were instructed to keep their eyes closed
during each recording block.
2.5. Data reduction and analysis
Combined EEG and EOG data were visually inspected to
identify ocular and muscular artifact. When artifact occurred
in a given channel, data from all channels were rejected
(Barlow, 1986).
In order to compute power density of the alpha (8–12 Hz)
band, Fast Fourier Transform (FFT) using James Long
Company Software was applied to all windows of artifact-free
data that were 1 s in duration, with FFT windows overlapping
by 50%. The FFT was performed for each 6 min recording
block. Statistical analyses were conducted on log (ln) tran-
sformed alpha power density for each 6 min recording block.
Asymmetry scores were calculated for frontal and
parietal regions, for each recording block, as the difference
between the log alpha power density in the right hemisphere
lead and log alpha power density in the homologous left
hemisphere lead (e.g., ln F4 alpha power ln F3 alpha
power). Higher asymmetry scores thus indicate greater
relative left hemisphere activity.
2.6. Statistical analyses
In order to examine whether particular patterns of cortical
activity were associated with improved mood in response to
our intervention, scores of pre-intervention happiness were
subtracted from post-intervention happiness, and the
difference was used as a measure of mood response to
the cognitive intervention. This difference score will
subsequently be referred to as the ‘‘happiness response’’
1
The vertex reference was chosen based on its extensive use in studies of
EEG and emotion at the time the study was conducted. Since the study was
implemented, some papers have noted the potentially problematic use of a
sole Cz reference and cited the preferential use of other reference montages
(e.g., averaged mastoids) or concurrent reporting of analysis from several
different montages (e.g., Davidson, 1998; Hagemann et al., 1998, 2001;
Reid et al., 1998). However, our recording montage at the time does not
allow for re-referencing to another montage (i.e., averaged mastoids) for
comparison. Although no reference montage has been definitively found to
be ideal (Coan and Allen, 2003; Hagemann et al., 2001), the potential
impact of the vertex reference is further noted in Section 4.
 P.J. Deldin, P. Chiu / Biological Psychology 70 (2005) 141–151 145

with greater positive values indicating greater self-reported 3. Results

happiness after the intervention than before. In order to
assess the predictive utility of EEG with regard to mood As the happiness response (i.e., change in positive affect;
improvement, those participants who reported greater post- (post-restructuring happiness minus pre-restructuring happi-
than pre-intervention happiness were classified as ‘‘Respon- ness)) reported by controls and depressives was not
ders.’’ Similarly, those who showed negative values of significantly different, F(1, 32) = 1.3, p > .1, participants
happiness response, or who showed no change in happiness for analyses incorporating mood Response status were
response, were classified as ‘‘Non-responders.’’ An inspec- grouped according to response on the Happiness scale. Mood
tion of the range of scores reported on the Sadness scale ‘‘Responders’’ are those who exhibited positive values of
revealed that a majority of control participants reported both happiness response; individuals who reported no-change or
pre- and post-task scores of zero on the Sadness scale, negative happiness response values are classified as ‘‘Non-
indicating that no change in sadness was measurable. Thus, responders’’. Thirty-nine percent of the control participants (7
analyses differentiating Responders and Non-responders of 18) and 60% of the depressed participants (9 of 15) were
using the Sadness scale were conducted only with the thus classified as Responders. As expected, happiness
depressed group. response scores differed significantly between Responders
Separate 2  4  2  2 repeated measures ANOVAs and Non-responders, F(1, 32) = 23.9, p < .0001. See Table 2
were conducted to investigate Response status (Responders, for self-report scores by Response status and diagnostic group.
Non-responders)  Block (Baseline 1, Think 1, Think 2,
Baseline 2)  Region (frontal, parietal)  Laterality (left, 3.1. EEG topography
right) as well as Diagnosis (control, major depression)  -
Block  Region  Laterality. In addition, 2  2 repeated In order to confirm that our physiological data were
measures ANOVAs for Response status  Region and consistent with that reported in the literature, we examined the
Diagnosis  Region were conducted for cortical asymmetry scalp distribution of our EEG recordings. An ANOVA
scores (ln right alpha ln left alpha). investigating Diagnosis  Region  Laterality revealed a
Pearson correlations were computed between degree of
happiness response and total alpha power at each site2 (F3, Table 2
F4, P3, and P4) during each recording block (Baseline 1, Participant self-report scores by diagnostic group and Response status,
Think 1, Think 2, Baseline 2). All correlations were mean (S.D.)
computed both within diagnostic groups and with diagnostic Measure Non-responder Responder
groups combined. All participants
Logistic regression analyses were conducted to assess the BDI+ 8.3 (9.4) 15.6 (14.8)
predictive utility of baseline alpha power with regard to BHS+ 5.3 (4.9) 9.4 (7.5)
STAI-S* 31.9 (11.6) 42.9 (15.2)
identifying those individuals who are likely to exhibit
STAI-T 37.3 (14.0) 47.1 (20.2)
increased happiness after the cognitive intervention task DAS 192 (35.8) 188.6 (47.9)
(i.e., ‘‘Responders’’). In order to account for multi- HAP (cm)* 12.4 (4.6) 8.4 (4.2)
collinearity between activity within cortical regions, new SAD (cm)+ 3.9 (5.5) 8.3 (6.5)
variables ‘‘frontal’’ (ln F3 alpha + ln F4 alpha) and n 17 16
‘‘parietal’’ (ln P3 alpha + ln P4 alpha) were entered as
Control
predictor variables for the categorical dependent variable of BDI 2.4 (2.7) 1.5 (2.8)
happiness Response status (i.e., whether or not an increased BHS 2.3 (1.3) 1.8 (1.1)
happiness score was observed after our intervention). STAI-S+ 26.0 (4.3) 30.3 (3.8)
Finally, a mean split by alpha power was conducted in STAI-T 31.3 (5.2) 27.3 (7.0)
DAS * 206.2 (23.9) 230.5 (17.4)
order to determine the specificity (1 false positive rate,
HAP (cm)+ 14.4 (2.6) 12.1 (2.7)
i.e., rate at which alpha level misidentifies those who exhibit SAD (cm) 1.3 (2.6) 2.1 (3.0)
mood improvement) and sensitivity (true positive rate, i.e.,
n 11 7
rate at which alpha level accurately identifies mood
response) of using alpha power to differentiate Responders Depressed
BDI+ 18.8 (7.3) 27.7 (8.1)
to our intervention. A discriminant function analysis was
BHS* 10.6 (4.6) 16.0 (2.3)
performed to confirm and augment the above analyses to STAI-S 42.6 (13.3) 53.7 (12.5)
assess whether EEG alpha variables would correctly STAI-T+ 48.2 (18.9) 64.1 (6.7)
discriminate those who exhibit mood improvement from DAS+ 161.0 (41.4) 152.7 (32.9)
those who do not. HAP (cm)+ 8.6 (5.3) 5.2 (2.6)
SAD (cm) 8.8 (6.4) 13.6 (2.4)

2 n 6 9
Given the number of sites recorded, we were unable to compute power
*
at individual sites residualized for variance associated with whole-head p  .05.
+
power (Pivik et al., 1993; Wheeler et al., 1993). p  .1.
146 P.J. Deldin, P. Chiu / Biological Psychology 70 (2005) 141–151

between happiness response score and alpha power at all sites

Fig. 1. Log alpha power (uV2) by site and recording block for each
diagnostic group. Note: less alpha indicates greater cortical activity.
main effect of Region, F(1, 32) = 125, p < .0001, indicating
that, as expected, EEG alpha was greater in parietal compared
with frontal regions. No other effects or interactions emerged.
Mean EEG alpha power within the control and depression
groups by task block is provided in Fig. 1.
Groups did not differ according to the number of FFT
windows retained per condition (mean (S.D.), controls:
Baseline 1 = 652.17 (70.64); Think 1 = 623.00 (61.81);
Think 2 = 610.06 (98.83); Baseline 2 = 651.18 (59.95).
Major depression: Baseline 1 = 612.87 (106.54); Think
1 = 633.53 (85.36); Think 2 = 621.00 (119.54); Baseline
2 = 629.33 (84.55)).
3.2. Correlational analyses between happiness response
and alpha power
When the control and depressed participants were
examined together, significant negative correlations emerged
and blocks, indicating that an increased level of overall
cortical activity is associated with greater happiness response
(see Table 3).
The depressed group, as reported in Table 3, demon-
strated significant or marginally significant negative
correlations between happiness response and alpha power
at frontal sites during most recording blocks. Although the
correlations between happiness response and cortical
activity at parietal sites did not achieve traditional levels of
significance, the magnitude of the Pearson correlation
coefficients (ranging from .27 to .49) indicate a medium to
large effect size. Thus with a larger sample size,
significance is likely to be achieved. No correlations
were observed between cortical activity and mood
improvement on the Sadness scale within the depressed
group.
Within the control group, as shown in Table 3, significant
negative correlations were also observed between happiness
response and alpha power at all sites and during each
recording block except Baseline 2.
No significant correlations were observed between
happiness response scores and alpha asymmetry values.
3.3. Absolute alpha power
The 2  4  2  2 repeated measures ANOVAs inves-
tigating Response status  Block  Region  Laterality
revealed a main effect of Response status, indicating that
Responders exhibit decreased alpha power (i.e., increased
cortical activity) at all cortical sites, Response status: F(1,
32) = 5.3, p < .03. Responders’ and Non-responders’ mean
alpha power (with standard deviations in parentheses) were
2.28 (0.2) and 3.14 (0.2), respectively. Although analyses
including the Diagnosis  Response status interaction term
did not reach statistical significance ( p > .2), post hoc
analyses of Responders and Non-responders within each
diagnostic group suggest that the decreased alpha power of
Responders was carried by the depressed Responders
(control Response status: F(1, 17) = 1.2, ns; depressed
Response status: F(1, 14) = 3.6, p < .09).
No significant effects emerged in the ANOVA investigat-
ing Diagnosis  Block  Region  Laterality.

Table 3
Pearson correlations between ln alpha power and happiness response at each recording site and block
Site All participants Depressed participants Control participants
Baseline 1 Think 1 Think 2 Baseline 2 Baseline 1 Think 1 Think 2 Baseline 2 Baseline 1 Think 1 Think 2 Baseline 2
** ** ** ** * + * + * + *
F3 .48 .47 .53 .46 .57 .51 .58 .53 .52 .48 .55 .31
F4 .51 ** .49 ** .56** .49 ** .58 * .55+ .64 * .58 * .54* .45+ .51 * .35
P3 .45 * .40 * .49** .39 * .49 .37 .49 .42 .51* .47+ .54 * .26
P4 .43 * .39 * .47** .35+ .40 .31 .42 .27 .58* .55 * .61 ** .35
*
p  .05.
**
p  .01 (two-tailed).
+
p  .1.
 P.J. Deldin, P. Chiu / Biological Psychology 70 (2005) 141–151
3.4. Asymmetry differences
In order to investigate baseline differences in patterns of
alpha power between Responders and Non-responders, an
ANOVA investigating Response status  Region was
performed for asymmetry scores, F(1, 32) = 4.3, p < .05.
Further breakdown indicated that Responders and Non-
responders exhibited opposite patterns of frontal asymmetry
with the Responders exhibiting negative asymmetry scores
(i.e., ln F4 < ln F3 alpha power) and Non-responders
showing positive asymmetry scores (i.e., ln F4 > ln F3),
F(1, 32) = 5.47, p < .03. Responders’ and Non-responders’
mean alpha asymmetry differences (ln F4 ln F3; standard
deviations in parentheses) were .04 (0.1) and .07 (0.1),
respectively. Although analyses including the Diagno-
sis  Response status interaction term did not reach
statistical significance ( p > .3), post hoc examination of
control and depressed Responders and Non-responders
suggest that the asymmetry effect in Responders was carried
primarily by the asymmetry differences between depressed
Responders and Non-responders (control: F(1, 17) = .55, ns;
depressed: F(1, 14) = 6.2, p < .03).
No further differences emerged in ANOVAs investigating
either Response status  Region or Diagnosis  Region for
baseline cortical asymmetry scores.
3.5. Predictive utility of alpha power
The predictive utility of baseline alpha power for
determining happiness response was first examined through
logistic regression analyses. Analyses indicate that both
frontal and parietal activity are of predictive utility with regard
to identifying those who are likely to respond to the mood
intervention3 (frontal entered first: Step 1 x2 = 9.1, p < .003;
Step 2 x2 = .01, ns; parietal entered first: Step 1 x2 = 7.2,
p < .007; Step 2 x2 = 2.0, ns). Specifically, the odds ratios
indicate that for every unit increase in level of cortical activity,
an individual has between 41% (1 .59; parietal) and 47%
(1 .53; frontal) chance of exhibiting mood improvement in
response to the cognitive intervention.
The potential utility of alpha power for identifying those
likely to exhibit a positive happiness response was further
evaluated using the mean of baseline alpha power as a cutoff
score. This split was successful in differentiating Respon-
ders to our intervention. Though the specificity (1 false-
positive rate, i.e., percentage of ‘‘Responders’’ identified by
alpha power who actually were ‘‘Responders’’) was just
above chance (56%), the sensitivity (true positive rate, i.e.,
percentage of all ‘‘Responders’’ who were accurately
identified by alpha power) was moderately high (81%),
further indicating that examining pre-treatment cortical
activity may be of significant clinical utility.
3
It should be noted that some shrinkage of predictive accuracy is
expected when implementing logistic regression with small sample sizes
(Cohen et al., 2003; Copas, 1997).
147
As the above analyses do not identify a particular cortical
site to be of predictive utility (rather, baseline EEG across all
sites is implicated), baseline alpha at sites F3, F4, P3, and P4
were included in the discriminant function analyses.
Seventy-five percent of the Non-responders, and 87.5% of
the Responders were correctly identified. Overall classifica-
tion was 81.3% (Wilks l = 0.586, x2 = 14.962, p < .01)
indicating that the EEG predictors differentiated between
the two response groups. All four of the variables
contributed significantly to the classification.
4. Discussion
Most striking was the presence and predictive utility of
overall greater cortical activity for identifying those who
reported greater post- than pre-intervention happiness
compared with those who did not report such an
improvement. Several lines of research may provide insight
into this finding. First, a decrease of alpha rhythm (increase
in cortical activity) has consistently been observed during
task solution (i.e., Dolce and Waldeier, 1974; Rugg and
Dickens, 1982; Gutierrez and Corsi-Cabrera, 1988; Ramos
et al., 1993), and it may be argued that those who reported a
mood improvement were merely more engaged in the
restructuring task. However, the Responders showed
decreased alpha power even at pre-task baseline, with no
additional decrease during either unguided or guided
thinking. This specificity suggests that overall cortical
activity is a pre-existing, task-independent factor that may
be associated with, and of predictive utility with regard to,
mood reactivity.
Second, if unilateral relative activity of the right or left
hemisphere is consistent with the preferential experience
and expression of negative and positive emotions (e.g.,
Wheeler et al., 1993; Tomarken et al., 1992), perhaps
bilateral activity, as observed in the present study, is
accompanied by an advantage for the experience and
expression of emotion more generally. If so, such an
advantage may, in part, moderate the mood improvement
reported by this group. Indeed, the anhedonia and
psychomotor retardation characteristic of depressed indivi-
duals may be attributed to a deficit in the ‘‘approach’’ subset
of positive emotion (Davidson et al., 1990). Thus, it may be
that those who exhibited overall greater activity were also
relatively less impaired in processes that lead to the
experience of emotion more generally. Although the small
sample size and preliminary nature of this study hinder the
meaningful analysis of moderator effects of baseline EEG
upon therapeutic response (Baron and Kenny, 1986;
McClelland and Judd, 1993), our data provide intriguing
support for the inclusion of EEG or other biological
measures in addition to the psychosocial client character-
istics that have traditionally been examined as potential
predictors of treatment outcome in cognitive therapy for
depression (Whisman, 1993).
148 P.J. Deldin, P. Chiu / Biological Psychology 70 (2005) 141–151
It is also of interest that the depressed Responders
exhibited a baseline frontal asymmetry of greater right than
left activity compared with depressed Non-responders. As
the Responders reported greater scores on a range of scales
assessing depressogenic symptoms, this pattern of cortical
activity is consistent with evidence that an asymmetry
toward greater right relative to left activity in frontal areas is
both associated with greater negative affect and also
observed in individuals in remission from depression (for
review, see Davidson, 1995, 1998; Henriques and Davidson,
1990). However, the observed mood reactivity in our sample
also seems inconsistent with the literature suggesting that
individuals with such patterns of frontal asymmetry are
predisposed to respond to negative stimuli with greater
negative affect (Davidson, 1995, 1998). Notably, these
studies largely employ passive viewing tasks that use
asymmetry scores to predict the degree of affect elicited by
valenced stimuli. As the current study assesses mood
reactivity in response to a cognitive restructuring task, the
substantial difference between our task and traditional tasks
renders it difficult to draw a direct comparison; indeed, no
investigations to our knowledge have examined the
mechanisms of therapeutic mood response compared with
those of affect elicited by valenced stimuli. Of importance,
in an explicit mood induction procedure, Gotlib et al. (1998)
found that, contrary to expectations, greater pre-induction
right frontal cortical activity did not predict the degree of
induced sadness. They posit that brain systems subsuming
the production of ‘internally generated’ emotion may differ
from those involved with emotion elicited in response to
external stimuli. The asymmetry patterns observed herein
may also be compared with the findings of Bruder et al.
(1996, 1997) that on a dichotic listening task, Responders to
both cognitive therapy and fluoxetine exhibited a right ear
(left hemisphere) advantage and left ear (right hemisphere)
disadvantage, respectively. Bruder et al. (1997) further
posited that dichotic listening paradigms are likely to
involve processes in more posterior temporoparietal regions
which would be consistent with the pattern of parietal
activity in depression proposed by Heller et al. (1995). In the
current study, parietal asymmetry differences between
Responders and Non-responders were not observed.
Together, the present findings suggest that absolute cortical
activity may be integral to mood improvement, and provide
further evidence that frontal patterns of cortical asymmetry
may be an index of depressive state or increased risk for
depression (e.g., Davidson, 1995; Henriques and Davidson,
1990), as evidenced by the greater right frontal activity
exhibited by the participants reporting more severe
depression symptoms.
Finally, no changes in patterns of cortical asymmetry
were observed between any of the four recording blocks.
Several plausible interpretations may be provided for this
observation. First, the task may have not affected pre-
existing patterns of cortical activity. Indeed, the evidence
that EEG patterns shift with mood reactivity is inconsistent
(for review, see Hagemann et al., 1998). Second, the
cognitive restructuring task may have required activation of
other cortical or sub-cortical regions than we measured, or
may have not elicited changes in alpha power. Third, mood
responsivity could be a trait characteristic, one of whose
identifying factors is a relatively greater overall cortical
activity that predisposes an individual to mood reactivity. It
should also be noted that our data indicate no between-group
differences in bilateral baseline cortical activity in controls
and individuals with depression, a finding that at first seems
inconsistent with the bulk of the literature pointing to frontal
hypoactivity in depression (for review, see Pollock and
Schneider, 1990). However, given that our data were
recorded as participants were meeting a new experimenter
and anticipating the beginning of a new task, that depressed
individuals may have been more alert to the testing
conditions, and that anticipatory motivation may decrease
alpha suppression (increase cortical activity; e.g., Zinser
et al., 1999), a direct comparison of our data to this literature
must be tentative.
Although our findings clearly highlight the multi-factorial
nature of depression, the limitations in our protocol provide
motivation for further investigation. First, the use of the active
vertex reference may distort EEG asymmetry calculations
(for discussion, see Hagemann et al., 2001); nevertheless, our
data are consistent with findings of relatively greater right
frontal activity in individuals with greater depression severity.
Unfortunately, our recording montage at the time does not
allow for off-line calculation of an alternate reference (e.g.,
averaged ears) for comparison. Also, the lack of a placebo
group and the use of a single experimenter to conduct the
cognitive restructuring task render it difficult to assess
whether the observed mood response was a consequence of
our cognitive restructuring task, a spontaneous mood
improvement, a result of a pleasant interaction, or an artifact
of the experimental situation. Refining and expanding the
current post-task questionnaires to address more specifically
the nature of mood improvement and of each participant’s
thought process during both the unguided and structured
thinking tasks would facilitate the interpretation of our data.
Further, although our task was based upon the techniques of
cognitive therapy for depression (Beck et al., 1979; Burns,
1999), and a significant increase in happiness was observed in
a majority of the depressed participants subsequent to our
cognitive intervention, it should be emphasized that the task is
a brief, one-time intervention in a laboratory setting. Indeed,
given the importance of interpersonal factors not only in the
maintenance of depressed mood (e.g., Segrin and Abramson,
1994; for review, see Ingram et al., 1996), but also in positive
therapeutic outcome (e.g., Burns and Auerbach, 1996; Arnow
et al., 2003; Klein et al., 2003), greater rapport between the
experimenter and some participants may have, in part,
contributed to positive mood response in these participants.
Thus, any generalization of our brief intervention to cognitive
therapy, or of our results to the therapeutic process, must be
cautious.
 P.J. Deldin, P. Chiu / Biological Psychology 70 (2005) 141–151
4.1. In conclusion
Pre-treatment therapeutic empathy, REM latency, dicho-
tic listening asymmetry, perceived helpfulness of the
therapy, and homework compliance are among the
characteristics that have been implicated as predictors of
response to cognitive therapy for depression (for reviews,
see Scott, 1996; Salkovskis, 1996; Whisman, 1993). The
diversity of findings regarding characteristics that may
predict treatment outcome emphasizes the many interactions
that contribute to major depression and highlights how little
is known about variables that may account for individual
differences in the response to treatment. We suggest that
EEG activity may be of clinical utility with regard to
establish a patient profile for assigning treatment protocols.
We further propose that as an index of general affective
reactivity, global cortical activity has largely, and surpris-
ingly, been overlooked in favor of investigating of
asymmetry metrics that reflect individual differences in
emotional response tendencies.
In sum, it is increasingly evident that a systems approach
toward establishing a patient profile of positive therapeutic
response is necessary. Indeed, it is highly unlikely that
symptom alleviation at a cognitive, emotional, biological, or
other level occurs exclusive of changes in the remaining
systems. Clarifying the interaction among these systems is
critical to the understanding of the maintenance of
depression, and to the refining and development of more
effective and efficient treatments. Our findings add to the
growing literature and provide evidence that baseline levels
and patterns of cortical activity may be of predictive utility
with regard to identifying a subset of depressed individuals
who have an advantage for mood improvement.
Acknowledgements
This research was made possible by NIMH B/START
Grant #1R03M H57694-01 to Patricia J. Deldin, as well as
grants from the Harvard College Research Program and
Harvard Committee on Mind, Brain, and Behavior to Pearl
Chiu. We gratefully acknowledge the technical assistance of
James Long.
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