Journal of the International Neuropsychological Society (2017), 23, 719–731.

Copyright © INS. Published by Cambridge University Press, 2017.

doi:10.1017/S1355617717000844

Emotions Are Rising: The Growing Field of Affect INS is approved by the American
Psychological Association to sponsor
Continuing Education for psychologists.

Neuropsychology INS maintains responsibility for this

program and its content.

Skye McDonald
School of Psychology, University of New South Wales, Sydney
(RECEIVED February 14, 2017; FINAL REVISION July 12, 2017; ACCEPTED July 17, 2017)

Abstract

Thirty years ago, the neuropsychology of emotion started to emerge as a mainstream topic. Careful examination of
individual patients showed that emotion, like memory, language, and so on, could be differentially affected by brain
disorders, especially in the right hemisphere. Since then, there has been accelerating interest in uncovering the neural
architecture of emotion, and the major steps in this process of discovery over the past 3 decades are detailed in this
review. In the 1990s, magnetic resonance imaging (MRI) scans provided precise delineation of lesions in the amygdala,
medial prefrontal cortex, insula and somatosensory cortex as underpinning emotion disorders. At the same time,
functional MRI revealed activation that was bilateral and also lateralized according to task demands. In the 2000s,
converging evidence suggested at least two routes to emotional responses: subcortical, automatic and autonomic
responses and slower, cortical responses mediating cognitive processing. The discovery of mirror neurons in the 1990s
reinvigorated older views that simulation was the means to recognize emotions and empathize with others. More recently,
psychophysiological research, revisiting older Russian paradigms, has contributed new insights into how autonomic and
other physiological indices contribute to decision making (the somatic marker theory), emotional simulation, and social
cognition. Finally, this review considers the extent to which these seismic changes in understanding emotional processes
in clinical disorders have been reflected in neuropsychological practice. (JINS, 2017, 23, 719–731)
Keywords: Emotion, Affect, Social cognition, Arousal, Decision making, Social cognition

The neuropsychological assessment of emotion is typically
overshadowed by assessment of language, executive pro-
cesses, learning, and so on, as affect is difficult to assess using
traditional approaches. Despite the challenges, emotion is an
aspect of brain function that is a critical determinant of
human behavior and so fundamental to neuropsychology.
The past 3 decades has seen growing momentum in under-
standing its neural underpinnings and clinical implications.
In 1872, Darwin described emotions as behavioral patterns
that are important for the species’ survival (Darwin, 1872).
Supporting this, seminal cross-cultural research (Ekman and
Friesen, 1971; Izard, 1971) revealed that people of different
cultures are highly consistent in their expression of anger,
fear, happiness, surprise, disgust, and sadness, suggesting
these are innate and integral to communication. This set the
stage for a generation of research that almost exclusively
focused on the perception, expression, and experience of
these six basic emotions. Increasingly, the social nature of
emotions is coming into focus and other emotions (trust,
Correspondence and reprint requests to: Skye McDonald, School of
Psychology, University of New South Wales, Sydney, 2052. E-mail:
s.mcdonald@unsw.edu.au
719
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envy, flirtation, etc.) are being examined (Adolphs, Tranel, &
Damasio, 1998; Reynders, Broks, Dickson, Lee, & Turpin,
2005; Rosenberg, McDonald, Rosenberg, & Westbrook,
2016). These are more subject to learning and cultural var-
iation but, none-the-less, critical when considering how
emotion disorders disrupt social competence. The following
overview (see Table 1 for summary) considers major mile-
stones in research of the basic emotions in the past 30 years
THE 1980s: THE RIGHT HEMISPHERE IN
EMOTION PROCESSING
In 1975, Heilman and colleagues reported several patients
with right hemisphere lesions who could not comprehend
emotional prosody of speech (Heilman, Scholes, & Watson,
1975). In 1979, Ross and Mesulam described two cases with
right hemisphere lesions who lost their capacity to impart
affect in speech. Thus, the right hemisphere was attributed a
role in affective speech processing, potentially mirroring the
role of the left hemisphere in propositional speech (Ross,
1981). The 1980s onward saw sustained research extending
the role of the right hemisphere in emotion to include
expressivity and perception of face Borod, Koff, Lorch, &
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Table 1. Major milestones in emotion research over the past 30 years
Time Method
1971 Cross-cultural studies of emotion
1975–1980 Observation/testing of normal adults and adults with
lateralised lesions on CT scans
1980s Testing children with autism
1990s MRI scans of people with disorders of emotion
fMRI scans of normal adults engaged with emotional materials
Single cell recording of neurons in the macaque monkey
Skin conductance recording in adults with brain lesions
Iowa Gambling Task given to adults with frontal/amygdala
lesions
2000s Convergence of MRI, fMRI, and animal research
fMRI scans of normal adults performing/ experiencing actions,
touch and pain and observing others doing the same
2010s Facial mimicry, skin conductance, etc., in adults with brain
lesions
Convergence and expansion of ToM and emotion research in
patients with neurological, psychiatric and developmental
disorders
Note. “Patients” refer to adults with brain lesions.
RH = right hemisphere; LH = left hemisphere; CT = computed tomography; MRI = magnetic resonance imaging; fMRI = functional MRI; ToM = Theory of Mind.
720
Findings
Reporting that basic categories of emotion are invariant across cultures, consistent with the view that they are
innate and mediated by specific neural structures.
First reporting of RH patients with disorders of emotional prosody.
Evidence that RH is dominant for emotions and/or specialised for negative emotions.
First suggestion that social dysfunction in autism reflects a lack of ToM.
Specific structures found to be associated with emotions: amygdala, prefrontal cortex, anterior cingulate gyrus,
insula, and somatosensory cortex; RH often but not always implicated.
Bilateral activation of same structures as above; differential activation of LH vs. RH dependent on task demands.
Discovery of mirror neurons in F5, that fire when an action is executed and when observing someone else
performing that action.
Evidence that patients with ventromedial frontal lesions lack an orienting response to emotional material.
Evidence of impaired task performance and lack of skin conductance used to propose somatic marker theory,
i.e., that people use somatic cues to guide complex decision making.
Theoretical models of neural pathways for implicit (ventral) vs. explicit (dorsal) emotion processing.
Evidence of a mirror neuron system in human inferior frontal/parietal areas; proposal that we simulate actions
and experiences of others and, therefore, understand the intentions behind them.
Increasing evidence (some from decades earlier) for the role of simulation in emotional understanding and
empathy; evidence for a specific loss of response to negative materials in some clinical disorders.
Development of a broad construct of social cognition, a specialized system for understanding others that entails
both affective and cognitive aspects. Rapid expansion of interest in the field as indicated by numerous new
journals emerging with specialized focus on social and affective neuroscience.
S. McDonald
 The growing field of affect neuropsychology
Nicholas, 1985, 1986) and gestures (e.g., crying and laugh-
ing) (Ross & Mesulam, 1979). During the 1980s, for the first
time, it was demonstrated that people with right hemisphere
damage had broader problems extracting emotional content
from pictures (Cicone, Wapner, & Gardner, 1980) and words
(Brownell, Michel, Powelson, & Gardner, 1983; Wapner,
Hamby, & Gardner, 1981), leading to the view that the right
hemisphere is dominant for emotional processing generally
(Heilman, Bowers, & Valenstien, 1985). Research in healthy
adults supported this, finding a right hemisphere advantage for
emotion perception via tachistoscopic viewing (Heller & Levy,
1981) and dichotic listening (Bryden, Ley, & Sugarman, 1982)
and for facial expressivity (Borod & Caron, 1980).
A contemporaneous, alternative view was the “valence
hypothesis,” that is, that the left hemisphere is specialized for
positive and the right hemisphere specialized for negative
emotions (Silberman & Weingartner, 1986) or the related
“approach (left) - withdrawal (right) hypothesis” (Davidson,
1984). Rapid presentation of facial expressions to one
hemisphere in normal adults (Ley & Bryden, 1979;
Reuter-Lorenz & Davidson, 1981) demonstrated a hemi-
spheric bias for processing positive (left) and negative (right)
emotions (Silberman & Weingartner, 1986). Patients with
right hemisphere damage were reportedly indifferent or
euphoric while those with left hemisphere damage commonly
experienced depression (Gainotti, 1972; Sackeim et al.,
1982). These responses were thought to reflect the disable-
ment of normal positive, approach related responses follow-
ing left hemisphere lesions (thus a swing to depression) and
conversely the disablement of negative, withdrawal respon-
ses following right hemisphere lesions (thus the swing to
euphoria) (Davidson, Pizzagalli, Nitschke, & Kalin, 2003).
Research into emotion perception has also suggested a
valence effect with the right hemisphere dominant for
negative emotions while both hemispheres played a role in
positive (Adolphs, Jansari, & Tranel, 2001).
THE 1990s: MRI IDENTIFIES SPECIFIC
STRUCTURES UNDERPINNING EMOTION
Lesion-based research in the 1980s was hampered by two
issues. First, most work focused on patients with middle
cerebral artery stroke who were heterogeneous with respect
to intra-hemispheric pathology. At the same time, computed
tomography (CT) produced low-resolution images. In the
1990s, magnetic resonance imaging (MRI) provided dramatic
improvements in the visualization of brain lesions and identifi-
cation of specific structures associated with emotion processing.
The amygdala, interconnected with the hypothalamus,
thalamus, basal forebrain, and brainstem, as well as neo-
cortex, reciprocally interacts with the autonomic nervous
system (Emery & Amaral, 2000) making it integral to emo-
tional behavior. Using MRI, rare patients with focal amyg-
dala damage were identified who had impairments in
recognizing fear and other negative emotions in faces
(Adolphs, Tranel, Damasio, & Damasio, 1994) and voices
(Scott et al., 1997) and loss of the autonomic fear response to
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721
aversive stimuli (Bechara et al., 1995). Lesions were usually
bilateral, although in some studies right amygdala lesions
produced poorer performance than left (Adolphs & Tranel,
2004; Adolphs, Tranel, & Damasio, 2001).
The prefrontal lobes also represented an important candi-
date for mediating emotions. It was long known that frontal
lobe injury led to changes to socio-emotional behavior
(Benton, 1968; Stuss & Benson, 1986; Weinstein & Kahn,
1955). In the 1990s, circumscribed lesions in the orbital/
medial prefrontal cortex and ventral, anterior cingulate cortex
were identified as specific to emotional behavior, associated
with poor emotion perception, lowered self-reported emo-
tional experience, especially for negative emotions, and
apathy, disinhibition, lability, aggression, and personality
change (Barrash, Tranel, & Anderson, 2000; Grafman et al.,
1996; Hornak, Rolls, & Wade, 1996). This pattern led to
views that the medial prefrontal system (especially the right)
has a role in regulating “high autonomic arousal” emotions
such as anger and fear (Adolphs, 2002a). Lesions to the (left)
anterior insula cortex along with the basal ganglia were also
implicated, specifically perception of disgust in patients with
focal brain lesions (Calder, Keane, Manes, Antoun, &
Young, 2000) and in Huntington’s disease (Sprengelmeyer
et al., 1996). Selective impairment in fear (amygdala) and
disgust (insula) were regarded as evidence for a double
dissociation, demonstrating that specific emotions were
associated with specific structures (Adolphs, 2002b).
A major stepping stone in current emotion theories came
from evidence that emotion perception could be disrupted by
lesions in somatosensory and motor cortex (especially in the
right hemisphere: Adolphs, Damasio, & Tranel, 2002;
Adolphs, Damsio, Tranel, & Damsio, 1996). These studies
suggested that processing visual or auditory affective stimuli,
“as if” it were one’s own, might play a role in its identification.
Dissociations were also reported suggesting that prosody and
facial affect engaged overlapping but discrete cerebral systems
(Adolphs et al., 2002) as did moving versus static emotional
stimuli (Adolphs, Tranel, & Damasio, 2003).
THE 1990s: FUNCTIONAL IMAGING
REVEALS NEURAL ACTIVATION
In parallel to MRI lesion research, functional imaging rapidly
emerged as a powerful adjunct, providing opportunities to
observe localized brain activity in normal adults when
viewing emotional materials. Using positron emission
tomography (PET) normal adults showed left amygdala
activation to angry and fearful faces even when their attention
was diverted from the expression (Morris et al., 1996). This
was even found in a patient with unilateral brain damage and
no conscious awareness of an image transmitted to his
blinded right hemi-field (Morris, DeGelder, Weiskrantz, &
Dolan, 2001). Functional magnetic resonance imaging
(fMRI; Belliveau et al., 1991), a cheaper, less-invasive
technique than PET, led to an explosion of interest in emo-
tion. There have been literally hundreds of fMRI studies of
normal adults exposed to emotional stimuli.
 722
Meta-analyses of these generally suggest bilateral activation
of specific structures in response to emotional stimuli.
Amygdala activation was found when participants passively
observe facial expressions. Despite earlier reports, there was
little evidence of greater activation to negative expressions
(Baas, Aleman, & Kahn, 2004; Costafreda, Brammer, David,
& Fu, 2008; Sergerie, Chocol, & Armony, 2008). Left and
right amygdala activation varied due to task. Language-based
tasks activate the left amygdala, whereas masked emotions are
more likely to activate the right amygdala briefly with rapid
habituation (Costafreda et al., 2008; Sergerie et al., 2008).
Using fMRI meta-analysis, Lindquist, Wager, Kober, Bliss-
Moreau, and Barrett (2012) also challenged traditional views
that certain types of emotion (such as fear) were mediated by
specific structures (such as the amygdala). Their results sug-
gested key structures are not activated by specific emotions but,
rather, play a role that is important for specific emotions. Thus,
the amygdalae are engaged in orienting responses to novel and
arousing events rather than fear specifically, the insula is
engaged in self-awareness of body sensations rather than dis-
gust in particular, and the ventromedial frontal lobes appears to
integrate external and internal high arousal sensations rather
than simply mediating anger. It has also been shown that early
sensory cortices are activated by affective (vs. neutral) sensory
input, suggesting a role in emotional experience beyond simply
processing sensory inputs (Satpute et al., 2015).
2000s: TWO NEURAL MODELS OF EMOTION
PROCESSES
The explosion of MRI, fMRI, animal, and experimental
research during the 1990s provided the impetus to develop
two complementary models of neural systems of emotion that
emerged in the 2000s.
Explicit Versus Implicit (Autonomic) Processing
Animal research by LeDoux and colleagues suggested that
the “flight or fight” response is mediated by very rapid, coarse
evaluation of potential sources of danger in the environment
processed mainly by subcortical routes (LeDoux, 1995). In
humans, a ventral system was identified that entails the
amygdalae, insula, ventral striatum, and anterior cingulate
and prefrontal cortex. This system identifies emotionally
significant stimuli; produces affective, autonomic responses;
and provides automatic regulation (Lieberman, 2007;
Phillips, Drevets, Rauch, & Lane, 2003).
In contrast, complex emotional judgements occur more
slowly, engaging the dorsal lateral and medial prefrontal
cortex and anterior cingulate gyrus as well as hippocampus
and temporo-parietal regions (Lieberman, 2007; Phillips
et al., 2003). This system mediates effortful processing of
emotional stimuli and engagement of relevant cognitive
processes (e.g., language). The two systems are intimately
and reciprocally associated. Emotion tasks that require verbal
mediation, for example, labeling, increase activation of
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S. McDonald
dorsolateral prefrontal cortex (Hariri, Bookheimer, &
Mazziotta, 2000; Keightly et al., 2003) and reduce activation
in both amygdalae (Hariri et al., 2000).
Shared Neural Representations for Self
Versus Other
In 1992, a major breakthrough occurred with the discovery of
mirror neurons in the F5 area of the macaque’s frontal cortex
(approximating the human Broca’s area), which activated when
the subject both undertook a meaningful action and observed
that same action in others (di Pellegrino, Fadiga, Fogassi,
Gallese, & Rizzolatti, 1992). It has since been revealed that, in
humans also, overlapping areas in the inferior frontal lobe,
including the premotor area, and inferior and superior parietal
lobes activate when both observing and performing actions
(Grèzes & Decety, 2001; Molenberghs, Cunnington, &
Mattingley, 2012) or even hearing sounds associated with
actions (Gazzola, Aziz-Zadeh, & Keysers, 2006).
Such “mirroring” only occurs to meaningful actions and is
thought to provide a mental representation of an action and its
goal, allowing the observer to anticipate and understand the
intention behind it (Rizzolatti & Sinigaglia, 2010). Emotional
stimuli lead to similar patterns of activation extending to the
insula, amygdalae, and the superior temporal sulcus (Carr,
Iacoboni, Dubeau, Maxzziotta, & Lenzi, 2003; Pfeifer,
Iacoboni, Mazziotta, & Dapretto, 2008), suggesting a role for
action simulation in emotion understanding (Iacoboni, 2009).
Whether this co-activation reflects mirror neurons in
humans remains controversial. Unlike single cell recordings
in monkeys (Rizzolatti, Fadiga, Gallese, & Fogassi, 1996),
most evidence in humans is indirect arising from voxel-based
patterns of activations, although single-cell recordings in
humans support their existence (Mukamel, Ekstrom, Kaplan,
Iacoboni, & Fried, 2010). Even so, the notion that over-
lapping areas mediate both direct emotional experience and
observed experience has gained momentum. Furthermore,
simulation is not limited to observing actions. Both simple
touch to the hand and observation of touch activate
the somatosensory cortex (Kuehn, Mueller, Turner, &
Schutz-Bosbach, 2014; Schaefer, Heinze, & Rotte, 2012).
The anterior cingulate gyrus, thalamus, somatosensory
cortices, and insula are activated when experiencing painful
stimuli in oneself with overlapping but not identical struc-
tures involved when observing others in pain (Jackson,
Rainville, & Decety, 2006).
PHYSIOLOGICAL EVIDENCE FOR MODELS
OF EMOTION PROCESSES
fMRI and other techniques, such as electroencephalography
(Fox et al., 2016), provide unprecedented opportunity to
observe brain activation. However, as they are correlational
in nature, they give only indirect evidence of the functional
significance and, on occasion, this may be erroneous. For
example, Feinstein et al. (2016) reported a rare patient with
 The growing field of affect neuropsychology
bilateral lesions of the “pain matrix,” that is, the insula,
anterior cingulate, and amygdala, who still experienced pain,
sometimes excessively. They argued that the common inter-
pretation that the pain matrix mediates the emotional
significance of pain may be misdirected, and it may have
another role, for example, regulation.
Psychophysiological measurements provide a complementary
approach to understanding emotional processing. Although such
measures had a long tradition in Russian neuropsychology from
the 1960s, much of this literature was never published in English
(e.g., see Luria, 1973). Western psychophysiological research,
which has accelerated since the 2000s, has converged with the-
orizing from structural and functional imaging to refine under-
standing of emotion processes.
EVIDENCE FOR AUTONOMIC RESPONSES
TO EMOTIONAL STIMULI
In normal adults, skin conductance responses (SCR, indi-
cating the orientation reflex) occur in response to fearful
stimuli even when participants are not overtly aware of them
(Esteves, Dimberg, & Ohman, 1994; Ohman & Soares,
1994). Damasio, Tranel, and Damasio (1990) reported that
five patients with ventromedial frontal lesions lacked this
orienting response to emotionally charged pictures. Further-
more, people with traumatic brain injuries (TBIs), many of
whom experience ventromedial frontal pathology, have
abnormally low arousal (skin conductance level) at baseline
(Fisher, Rushby, McDonald, Parks, & Piguet, 2015;
McDonald, Rushby, et al., 2011) and habituate unusually
rapidly to angry faces (McDonald, Rushby, et al., 2011).
Their startle response is also abnormally unresponsive to negative
images (Saunders, McDonald, & Richardson, 2006; Williams &
Wood, 2012). A similar lack of startle response was reported in
people with amygdala lesions (Angrilli et al., 1996; Buchanan,
Tranel, & Adolphs, 2004; Funayama, Grillon, Davis, & Phelps,
2001) supporting the notion that the amygdalae, in concert with
the ventromedial frontal lobes, mediate autonomic responses to
emotional events with or without conscious awareness.
Evidence for Simulation
Psychophysiological techniques have also shed light on the
role of simulation in emotion. Studies of normal adults in the
1990s demonstrated that observers experience activation of
their own cheek (zygomaticus major) and brow (corrugator
supercilii) muscles when observing another person expres-
sing happy or angry emotions, respectively. Mimicry occurs
spontaneously and rapidly, even without conscious aware-
ness (Dimberg & Thunberg, 1998; Dimberg, Thunberg, &
Elmehed, 2000), suggesting an automatic process. This
observation re-invigorated a view initially proposed by Lipps
(1907, cited in Hoffman, 1984) that facial feedback engen-
ders a shared emotional experience (emotional contagion)
that helps identify the emotion being observed. This view
clearly dovetails into implications of the mirror neuron sys-
tem. Furthermore, deficits in facial mimicry have been
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723
reported in people with low empathic ability (Sonnby-
Borgström, Jönsson, & Svensson, 2003) as well as clinical
conditions associated with low empathy, such as schizo-
phrenia (Park, Mathews, & Gibson, 2008).
Clinical evidence based on people with lesions to ventro-
medial frontal cortex or as a result of TBI suggests that
loss of emotion simulation extends beyond facial mimicry.
While there can be loss of facial expressivity (Dethier,
Blairy, Rosenberg, & McDonald, 2012) and spontaneous
facial mimicry (Angrilli, Palomba, Cantagallo, Maietti, &
Stegagno, 1999; McDonald, Li, et al., 2011), there is also
lowered autonomic arousal to facial expressions (Blair &
Cipolotti, 2000; de Sousa et al., 2011; Hopkins, Dywan, &
Segalowitz, 2002) and reduced subjective appraisal of emo-
tional material (Hornak et al., 1996; Saunders et al., 2006)
and the effects of postural feedback (Dethier, Blairy,
Rosenberg, & McDonald, 2013).
Thus, disruption of emotional contagion can occur at
numerous points in a complex system from motor mimicry
through to arousal and the subjective evaluation of the emo-
tional experience. Of interest, when emotional contagion is
impaired, this is usually limited to negative emotions (Blair &
Cipolotti, 2000; McDonald, Rushby, et al., 2011). This
valence specific effect suggests that disruption occurs at a
different stage to mirroring which, otherwise, should affect
all emotions equally. It does, however, fit with the notion that
autonomic responses are mediated by the ventral system
(Phillips et al., 2003) that has evolved to detect potential
danger and elicit an immediate arousal reponse.
While both emotion perception and emotional contagion
can be disrupted following brain lesions, evidence for a
causal link is far from established. On the one hand, accu-
mulating behavioral evidence suggests that loss of mimicry
impedes emotion recognition. Disrupting the (left) premotor
cortex using transient magnetic stimulation decreases emo-
tion recognition accuracy and increases reaction time
(Balconi & Bortolotti, 2013). Botulin toxin that impairs facial
movement also reduces emotional experience and emotion
recognition (Davis, Senghas, Brandt, & Ochsner, 2010).
People with locked in syndrome and facial paralysis are less
efficient than normal when recognizing (negative) emotions
(Pistoia et al., 2010) as are normal adults prevented from
mimicry (Niedenthal, Brauer, Halberstadt, & Innes-Ker,
2001).
However, there is also evidence to the contrary. While loss
of contagion and poor emotion recognition do co-occur in
individual patients (Blair & Cipolotti, 2000), they are not
correlated in people with brain injury (McDonald, Li, et al.,
2011; McDonald, Rushby, et al., 2011) nor in adults with a
complete disorder of peripheral autonomic function (Heims,
Critchley, Dolan, Mathias, & Cipolotti, 2004). A similar lack
of relation is seen in normal adults (Blairy, Herrera, & Hess,
1999; Hess & Blairy, 2001). Thus, while mimicry may
facilitate emotion perception, there is insufficient evidence
that it is essential. It may have other functions, for example,
to communicate empathic understanding (Bavelas, Black,
Chovil, Lemery, & Mullett, 1988).
 724
ATTRIBUTING EMOTIONS WITH A ROLE
IN COGNITION
A major development in contemporary neuropsychology has
been the recognition that emotion has a role in cognition.
Two important theoretical developments have been the
somatic marker theory (1990s) and the construct of social
cognition (2000s).
Somatic Marker Theory
The influential “somatic marker” hypothesis arose in the 1990s
(Damasio, Tranel, & Damsio, 1991), suggesting that emo-
tional responses can guide understanding of complex response
contingencies even before conscious awareness (Bechara,
Damasio, Tranel, & Damasio, 1997). Most work used the Iowa
Gambling Task (IGT) in which people learn reward con-
tingencies given feedback. Both normal adults and those with
ventromedial frontal lobe lesions have a SCR following feed-
back about their choices. Normal adults reportedly demon-
strate these changes in anticipation of their choice, even before
they can verbalize the rules. People with ventromedial damage
do not (Bechara et al., 1997; Bechara, Tranel, Damasio, &
Damasio, 1996; Naccache et al., 2005). Similar results were
found with people with specific amygdala damage, except, in
these cases, there was no SCR at all, even after feedback
(Bechara, Damasio, Damsio, & Lee, 1999).
As a result of this work, it was argued that somatic
responses assist with decision making, especially in personal
and social situations, where precise calculations of the out-
come of a course of action is not possible (Bechara, 2004).
Although interest in the somatic marker theory has been high,
poor performance on the IGT is not limited to those with
frontal lesions (Levine et al., 2005). Other cognitive abilities,
such as working memory (Hinson, Jameson, & Whitney,
2002), intelligence (Toplak, Sorge, Benoit, West, &
Stanovich, 2010), and reversal learning (Fellows & Farah,
2005) influence IGT performance.
Whether physiological responses occur before conscious
awareness also remains controversial. Densely amnesic patients
who cannot learn the IGT do not display anticipatory SCRs
(despite having intact SCRs to punishment), and healthy adults
have demonstrated differential anticipatory SCRs only after
explicit knowledge of IGT contingencies was attained (Fernie &
Tunney, 2013; Gutbrod et al., 2006). In all, it appears that
somatic markers are involved in decision making on the IGT, as
is conscious processing (Guillaume et al., 2009), but are not
necessarily critical to successful performance.
Social Cognition
Since the 2000s, there has been a groundswell of interest in the
role of emotional processes in social performance.
This was heralded by the 1980s research describing how
emotional and humorous materials were poorly processed
following right hemisphere lesions. In 1985, Baron Cohen,
Leslie, and Frith proposed that children with autism lack
the ability to impute mental states, that is, lack Theory of Mind
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S. McDonald
(ToM; Baron Cohen, Leslie, and Frith, 1985). More recently,
these attributes have been subsumed under the construct of
social cognition, that is, the ability to understand the minds of
other people in relation to ourselves (Amodio & Frith, 2006),
including judgments about what they are thinking, feeling, and
intending by their behavior.
Social cognition also includes empathy, social connected-
ness, and making broader social judgments, such as attitudes
about social groups and morality. Not all social cognition is
related to emotion. Cognitive ToM tasks simply require
understanding what another person might think and believe.
On the other hand, affective ToM refers to understanding
what another person feels (Mitchell & Phillips, 2015). fMRI
research has demonstrated activation of the anterior dorsal
medial prefrontal cortex and bilateral temporo-parietal junc-
tions when performing any mental judgment but with addi-
tional activation of the orbitofrontal cortex, temporal poles,
and bilateral premotor cortex for affective judgements
(Molenberghs, Johnson, Henry, & Mattingley, 2016). Lesion
studies suggest that ventromedial (especially right) lesions
are associated with impaired affective ToM judgments, such
as understanding irony and faux pas (Shamay-Tsoory,
Tomer, Berger, Goldsher, & Aharon-Peretz, 2005).
IMPLICATIONS FOR CONTEMPORARY
CLINICAL PRACTICE
Since the late 1990s, it has been recognized that impairments
in emotion processing are pivotal to understanding neuro-
psychiatric disorders (Borod et al., 1990), including schizo-
phrenia (Kohler, Walker, Martin, Healey, & Moberg, 2010;
Phillips, 2003), bipolar and other mood disorders (Cusi,
Nazarov, Holshausen, MacQueen, & McKinnon, 2012;
Green, Cahill, & Mahli, 2007), and intellectual and genetic
developmental disabilities (Roelofs, Wingbermühle, Egger,
& Kessels, 2017), as well as people with acquired brain
injury. Characterization or socio-emotional impairments has
greatly aided diagnosis and understanding of these disorders.
For example, psychosocial changes following severe TBI
are common (Brooks, Campsie, Symington, Beattie, &
McKinlay, 1986) but were poorly understood before systematic
research into emotional impairments.
Recently it has been estimated that up to 39% of adults
with moderate-severe TBI suffer problems of emotion per-
ception (Babbage et al., 2011). They also self-report dis-
proportionately low levels of empathy (Williams & Wood,
2010; Wood & Williams, 2008), blunted emotional experi-
ence (Croker & McDonald, 2005), and low self-awareness of
their own emotions (i.e., alexithymia; Williams & Wood,
2010). Up to 70% of adults with TBI demonstrate apathy
(Kant, Duffy, & Pivovarnik, 1998), and irritability is one of
the most common behavioral complaints (Demark &
Gemeinhardt, 2002) along with impulsivity and aggression
(Kinsella, Packer, & Olver, 1991). Emotion disorders are not
necessarily correlated to standard neuropsychological tests
(Spikman, Timmerman, Milders, Veenstra, & van der Naalt,
2012), but do predict social behavioral problems in adults
 The growing field of affect neuropsychology
(McDonald, Flanagan, Martin, & Saunders, 2004; Spikman
et al., 2013) and children (Yeates et al., 2004).
In frontotemporal dementia, different constellations of
emotion impairment characterize sub-types. Semantic
dementia, arising from initial asymmetric deterioration of the
temporal lobes (primarily left), causes problems, not only
with language and semantic comprehension, but restricted
food interests; changed eating behavior; increased apathy;
impaired emotion perception, insight, and empathy; poor
mental state judgements; and poor emotional memories
(Landin-Romero, Tan, Hodges, & Kumfor, 2016). Patients
can also present with asymmetric deterioration of the right
temporal lobe, resulting in even more severe emotion per-
ception and behavioral problems, which suggests that it is the
right temporal lobe that mediates these deficits in both groups
(Kumfor et al., 2016).
Behavioral variant frontotemporal dementia is similarly
characterized by early behavior disturbance, disinhibition,
poor emotion perception, and low empathy; although, in this
case, these difficulties appear to arise from bilateral orbito-
frontal and left temporal deterioration (Kamminga et al.,
2015). Impaired empathy and emotional perception predict
carer distress in the frontotemporal dementias (Hazelton,
Irish, Hodges, Piguet, & Kumfor, 2016).
Schizophrenia is defined by changes in socioemotional
processes (Penn, Corrigan, Bentall, Racenstein, & Newman,
1997), including emotional flattening, anhedonia and per-
secutory delusions (Phillips, 2003), disorders of social cog-
nition broadly (Savla, Vella, Armstrong, Penn, & Twamley,
2013), and emotion process specifically (Irani, Seligman,
Kamath, Kohler, & Gur, 2012). Poor social cognitive abilities
in schizophrenia more accurately predict community func-
tion than traditional cognitive measures (Fett et al., 2011).
Assessment
Given the relevance of emotional processes to interpersonal
function and outcome, they should be assessed routinely.
However, while some clinical measures have been available
for decades (Borod, Tabert, Santschi, & Strauss, 2000), this is
one area where change has been slow. Despite 84% of clin-
icians working in brain injury reporting that at least half of
their clients had problems in social cognition (including
multiple facets of emotion), less than 22% reported using any
kind of formal assessment (Kelly, McDonald, & Frith, in
press). Furthermore, professions differ in terms of who they
believe to be responsible, with psychologists, neuropsycho-
logists, occupational therapists, and speech pathologists each
of the view that the responsibility lies with the other (Kelly,
McDonald, & Frith, 2017).
Current, consensus-based recommendations about outcome
measures in brain injury include self- and proxy questionnaires
to assess emotional behaviors (such as aggression and irrit-
ability), psychological status (such as negative and positive
mood states), and arousal (apathy, disinhibition) (Wilde et al.,
2010), and only recently has emotion perception and social
cognition been added (Honan et al., in press). In contrast, in the
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725
field of schizophrenia, emotion perception has been recog-
nized as a core cognitive ability and included in the National
Institute of Mental Health (USA) MATRICS cognition battery
(Kern et al., 2008; Nuechterlein et al., 2008).
Although clinicians do not typically assess emotion, there
are tests available with normative data. The Florida Affect
Battery (Bowers, Blonder, & Heilman, 1991) and the Diag-
nostic Analysis of Non-Verbal Accuracy (Nowicki, 2010)
assess emotion perception as does the social perception
subtests in the Advanced Clinical Solutions battery (Wechsler,
2009). The Awareness of Social Inference Test (TASIT)
(McDonald, Flanagan, & Rollins, 2011; McDonald, Flanagan,
Rollins, & Kinch, 2003) uses audiovisual vignettes of actors to
assess emotion, mental judgments, and conversational infer-
ence (McDonald, 2012) in adults and also adolescents
(McDonald et al., 2015), and a brief version has recently been
developed (Honan, McDonald, Sufani, Hine, & Kumfor,
2016). The NEPSY-II (Korkman, Kirk, & Kemp, 2007)
assesses both emotion and ToM in children from 3 to 16 years
while the Social Language Development Test (Bowers,
Huisingh, & LoGiudice, 2010) and the Clinical Evaluation
of Language Fundamentals (Wiig & Secord, 2014) assess
conversational and pragmatic inference from child to early
adulthood.
Rehabilitation For Emotional Disorders
Research into remediation for emotional and social perception
deficits started to emerge in the 2000s for people with autism
spectrum disorders (Bölte, Feineis-Matthews, & Poustka,
2008), schizophrenia (Combs et al., 2007; Horan, Kern, Green,
& Penn, 2008), and acquired brain injury (Bornhofen &
McDonald, 2008a, 2008b). Accruing evidence, especially in
schizophrenia, suggests that training of emotion perception,
via direct instruction, repetitive practice, and role plays, can be
effective (Cassel, McDonald, Kelly, & Togher, 2016; Kurtz &
Richardson, 2012; Roelofs et al., 2017).
Training of emotion regulation such as anger management
has traditionally followed cognitive-behavioral principles
(Demark & Gemeinhardt, 2002; Golden & Consorte, 1982).
The use of autonomic measures to monitor deficits in arousal
and regulation opens the horizons to investigate other tech-
niques, such as biofeedback, to improve heart rate variability
and consequently emotional balance (Francis, Fisher,
Rushby, & McDonald, 2016). There is also potential in using
direct cortical stimulation to improve depression, psycho-
motor speed (Boggio et al., 2008; Loo et al., 2012), and
inhibitory control (Jacobson, Javitt, & Lavidor, 2011).
CONCLUSION
The past 30 years has witnessed a seismic shift in under-
standing the neural and functional nature of human emotion.
From broad sweep notions of right hemisphere dominance,
new methodologies have specified brain structures and net-
works. Breakthroughs have arisen from a convergence of
methodologies to identify damaged structures, observe
 726
normal neural activation, and measure psychophysiological
responses at different stages in emotional processing. Emotion
research has expanded neuropsychology to consider the role of
emotions in cognitive processes such as decision making
(Bechara, Tranel, & Damasio, 2000) and memory and learning
(Rolls, 2000). The construct of social cognition has emerged
that addresses how emotional processes affect social judge-
ments more broadly.
Despite this, many questions remain. One conundrum is
the contrast between apparent bilateral activation for emotion
perception and social cognition as revealed by fMRI and yet
specific right hemisphere involvement suggested by lesion
research. This parallels language research where fMRI acti-
vation consistently implicates bilateral activation in language
tasks in contrast to lesion work that consistently implicates
the left hemisphere (see Price, 2012). So what exactly is the
contribution of right hemisphere processes? Possibly the
right hemisphere plays the larger role in emotion processing
simply because the left hemisphere has re-organized to
accommodate other functions such as language (De Winter
et al., 2015). Alternatively, the right hemisphere may mediate
arousal and attention to emotional significant events
(Langner & Eickhoff, 2013).
While simulation has captured the research community’s
imagination, its neural and functional nature is yet to be
articulated. Observation of another’s emotional state causes
resonance throughout the brain, from early sensory cortices,
through to association and motor cortex, frontal, amygdala,
and subcortical processing. This suggests that emotional
experience develops continuously, reflecting the fluctuating
and dynamic interaction of multiple sources (Raz et al., 2013).
However, exactly how feed-forward and feedback interactions
occur and their functional significance remains underspecified.
Ongoing research focusing on the temporal dynamics of
emotion systems should provide new insights. In the mean-
time, emotion appears to influences almost every perceptual,
mnemonic, cognitive, and executive process in the brain.
The past 15 years has seen a groundswell of interest in the
emotional sequelae of various clinical disorders, useful not
only diagnostically but because they add to the capacity of
neuropsychological testing to predict everyday difficulties
(Cattran, Oddy, Wood, & Moir, 2011; Fett et al., 2011;
Shimokawa et al., 2001). Emotion is also the target for a new
era in remediation research. Despite this, neuropsychological
practice has changed little. Assessment of emotion perception,
emotional experience (other than mood disorders), and/or
emotion regulation using available tests/questionnaires is not the
norm. Hopefully, this will change as clinical training embraces
the latest evidence of the role of emotions and a new generation
of clinicians step forward to take up the mantle of assessors and
remediators in the complex and vital field of emotion.
ACKNOWLEDGMENTS
The Awareness of Social Inference Test (TASIT), mentioned in this
manuscript, is sold commercially by Pearson Assessment, and the
author receives royalties for this.
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https://www.cambridge.org/core/terms. https://doi.org/10.1017/S1355617717000844
S. McDonald
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