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Review
Emotional intelligence:
Lessons from Lesions
J. Hogeveen,1,2,* C. Salvi,3,4 and J. Grafman3,4,5,6,*
Emotional intelligence (EI) is one of the most highly used psychological terms in
popular nomenclature, yet its construct, divergent, and predictive validities are
contentiously debated. Despite this debate, the EI construct is composed of a
set of emotional abilities recognizing emotional states in the self and others,
using emotions to guide thought and behavior, understanding how emotions
shape behavior, and emotion regulation that undoubtedly inuence important
social and personal outcomes. In this review, evidence from human lesion
studies is reviewed in order to provide insight into the necessary brain regions
for each of these core emotional abilities. Critically, we consider how
this neuropsychological evidence might help to guide efforts to dene and
measure EI.
Emotional Intelligence
A long-standing goal in psychology and neuroscience has been to elucidate the mechanisms
that enable individuals to interpret and respond to their environment in an adaptive manner.
Traditionally, this pursuit has focused on critical cognitive abilities verbal comprehension,
perceptual organization, reasoning, problem solving, etc. and their integration into a latent
underlying construct, often referred to as general intelligence or g [1,2]. However, the degree
to which general intelligence alone can predict important personal and social outcomes has
been called into question, with research suggesting that it is an insufcient predictor of upward
social mobility, career success, and creative achievement [35]. Accordingly, applied research
has recently shifted its focus to the study of emotional intelligence (EI; see Glossary),
referring to a set of emotional abilities purported to predict success in the real world above
and beyond general intelligence. Evidence suggests that high EI is associated with improved
mental health [6], better social problem solving [7], superior relationship quality [8], and enhanced
academic and job performance [9,10]. As such, educators and consultants have devoted
signicant efforts to the development of tools to promote EI [11].
EI has been widely adopted in both basic research and applied elds, yet there is a lack of clarity
in the eld with respect to how EI should be dened and measured. Two of the most inuential EI
theories are Bar-On's mixed model and Mayer and Salovey's integrative model. According to
Bar-On's mixed model, EI is dened as an array of noncognitive abilities, which inuence an
individual's adaptive success by shaping his/her interpretation and response to environmental
demands and pressures [12]. However, the use of the term noncognitive to dene EI is
problematic for several reasons, including the fact that emotional abilities must rely upon cold
cognitive systems (e.g., metacognition in emotional awareness, stimulus-driven attention in
emotion recognition). Additionally, many of the noncognitive abilities incorporated into the mixed
model are tangential to the established research literature on emotion and intelligence, resulting
in a heterogeneous set of dimensions that are difcult to integrate into a cohesive EI construct
[13]. Perhaps most concerning, the mixed model's divergent validity is weak, with 62% of the
variance on its companion Emotional Quotient Inventory (EQ-i) being accounted for by
Trends
The validity of emotional intelligence
(EI) has been contentiously debated.
Despite this debate, human lesion studies suggest that several of the emotional abilities that make up EI are
critical to human personal and social
functioning.
Human lesion evidence suggests a
core network of brain regions including
the amygdala, ventromedial prefrontal
cortex, insula, and anterior cingulate
cortex is critical to a range of emotional
abilities.
This evidence should be taken into
consideration when attempting to
dene the factor structure of EI and
develop empirically validated test
materials.
1
MIND [41_TD$IF]Institute, University of
California-Davis, Sacramento, CA,
USA
2
[42_TD$IF]Department [43_TD$IF]of Psychiatry &
Behavioral Sciences, University of
California-Davis, Sacramento, CA,
USA
3
Cognitive Neuroscience Laboratory,
Rehabilitation Institute of Chicago,
Chicago, IL, USA
4
Department of Psychology[3_TD$IF],
Northwestern University, [4_TD$IF]Evanston, IL,
USA
5
Department of Physical Medicine and
Rehabilitation, Feinberg School of
Medicine, Northwestern University,
Chicago, IL, USA
6
Department of Neurology, Feinberg
School of Medicine, Northwestern
University, Chicago, IL, USA
*Correspondence:
hogeveen@ucdavis.edu (J. Hogeveen)
and jgrafman@northwestern.edu
(J. Grafman).
http://dx.doi.org/10.1016/j.tins.2016.08.007
2016 Elsevier Ltd. All rights reserved.
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general intelligence and the big ve personality traits [14]. In the integrative model, Salovey
and Mayer [15] dene EI as the conuence of a set of emotional abilities that enable individuals
to carry out accurate reasoning about emotions and the ability to use emotions and emotional
knowledge to enhance thought [13]. Data from the integrative model's companion measurement tool [45_TD$IF] The MayerSaloveyCaruso Emotional Intelligence Test (MSCEIT)
[16] correlate with general intelligence, but variance explained by other measures is reduced
relative to the EQ-i (14%), suggesting that the integrative model has preferable divergent validity
[14]. Additionally, the MSCEIT is a performance-based measure, whereas mixed models of EI
often deploy self-report measures (e.g., EQ-i). In performance-based methods, the goal is to
measure how well participants perform tasks and solve problems related to emotions, whereas
in self-report methods individuals rate their level of agreement with descriptive statements
about their own emotional abilities [17]. The performance-based approach is typically preferred
in the domain of intelligence research, as it attempts to objectively isolate maximum performance (i.e., ability) in a way that is compatible with the intelligence construct [17]. Thus, for
several reasons, empirical research on EI has typically favored Mayer and Salovey's integrative
or ability-based model of EI, whereas Bar-On's mixed model and related approaches are
more often found in applied elds.
Akin to a lack of consistency in behavioral research on EI, neuroimaging studies have revealed
similarly unclear results. There are six studies that have directly investigated EI on the
Neurosynthi[40_TD$IF] online neuroimaging archive [18], and we conducted a miniature meta-analysis
using these studies to determine whether any particular brain regions have been reliably
associated with EI. Regions-of-interest were manually constructed based on the relevant
neuroimaging tables reported in each paper, and these regions-of-interest were placed on a
glass brain to visualize the degree of overlap between the six papers. The resulting gure
revealed a striking level of inconsistency in brain regions that have been implicated using
traditional measures of EI (Figure 1A[46_TD$IF], Key Figure). Therefore, inconsistencies in both the
behavioral and functional neuroimaging data make it difcult to establish the neurocognitive
factor structure of EI.
Glossary
Alexithymia: a subclinical condition
characterized by diminished
conscious access to one's own
emotional states, and difculty
describing one's emotions to others.
Can be either developmental as in
individuals with comorbid alexithymia
and autism spectrum disorders or
acquired as in patients with
traumatic brain injury.
Emotional awareness: the
conscious experience of discrete
emotional states (also referred to as
feelings).
Emotional intelligence: a set of
core emotional abilities that enable
individuals to interpret and respond
to the emotional states of themselves
and others in order to adaptively
shape thought and behavior.
Emotional Quotient Inventory: a
self-report emotional intelligence (EI)
inventory that accompanies the BarOn mixed model of EI [11]. This test
includes 133 items that yield ve
primary scales with 15 total
subcomponents: (i) intrapersonal
scale (self-regard, emotional selfawareness, assertiveness,
independence, and self-actualization);
(ii) interpersonal scale (empathy,
social responsibility, and interpersonal
relationships); (iii) adaptability (reality
testing, exibility, and problem
solving); (iv) stress management
(stress tolerance and impulse
control); and (v) general mood
(happiness and optimism).
Iowa Gambling Task: a decisionmaking task that is sensitive to
ventromedial prefrontal cortex
(vmPFC) patient decits. Participants
select between four decks of cards,
two of which have a high probability
of losses coupled with a low
probability of large rewards
(disadvantageous net loss decks),
whilst the other two have a high
probability of small rewards and a
low probability of losses
(advantageous net win decks).
Patients with vmPFC damage select
from the disadvantageous decks
more often than controls [96].
MayerSaloveyCaruso Emotional
Intelligence Test (MSCEIT): a
performance-based measure of
emotional intelligence (EI) that is a
companion to the Mayer and Salovey
integrative model of EI [91]. The test
consists of four sections of two tasks
each, designed to assess each of the
capacities of the integrative model
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[4_TD$IF]Key Figure
(B)
Y
Z
Z
X
Z
Y
1.
2.
3.
4.
vmPFC
Amygdala
Insula
Supracallosal ACC
Figure 1. (A) Areas of activation associated with various emotional intelligence scores from previous functional neuroimaging studiesi. (B) Core brain regions implicated in multiple emotional abilities by human lesion studies [97102].[10_TD$IF] Abbreviations: ACC, anterior cingulate cortex; vmPFC, ventromedial prefrontal cortex.
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(A)
(B)
**
***
***
Healthy controls
vmPFC lesions
Healthy controls
Amygdala lesions
2
1
0
1
2
0%
ctrl
<15%
>15%
(C)
(D)
100
Key:
90
Hippocampus paents
80
Healthy controls
2
1
70
60
50
5 V
Learning eect
Amygdala paents
% correct
40
0
MS CT Y Y O Y Y O Y O Y Y Y O O O O Y Y Y Y HT O Y O Y Y O Y Y Y Y Y
(E)
Faux pas
recognion
Parcipants
100 ms
Groups:
Key:
Key:
R vmPFC
PC
P300
L vmPFC
Bi vmPFC
NC
Control
Orbitofrontal paents
Figure 2. [1_TD$IF]Behavioral [12_TD$IF]Consequences [13_TD$IF]of [14_TD$IF]Lesions [15_TD$IF]to [16_TD$IF]Key [17_TD$IF]EI [18_TD$IF]Regions. (A) Anterior insula damage is linked to signicant impairments in emotion recognition in the self
(gure adapted from [25]) and (B) amygdala and vmPFC damages are linked to impaired recognition of others emotions, perhaps due to reduced orienting toward the
eyes (gure reproduced, with permission, from [45,47]). (C) Emotional memory enhancement is diminished in patients with amygdala damage, resulting in an impaired
ability to learn the personality traits of others in amygdala patients. By contrast, this ability is preserved in a patient with medial temporal lobe damage but with an intact
amygdala (gure reproduced, with permission, from [56]). (D) vmPFC patients also have difculty understanding the emotional mental states of others, as evidenced by
reduced faux pas recognition accuracy (gure reproduced, with permission, from [66]). Lastly, (E) patients with medial orbitofrontal cortex (a region within the vmPFC)
damage demonstrate impaired regulation of electrophysiological responses to aversive somatosensory stimulation relative to control participants (gure reproduced, with
permission, from [73]).[19_TD$IF] Abbreviations: NC, normal comparison group; PC, posterior cortex lesion group; L vmPFC, left ventromedial prefrontal cortex [20_TD$IF]lesion [21_TD$IF]group; [2_TD$IF]R
vmPFC, [23_TD$IF]right ventromedial prefrontal cortex[24_TD$IF] lesion group; [25_TD$IF]Bi vmPFC, [26_TD$IF]bilateral ventromedial prefrontal cortex[27_TD$IF] lesion group.
with substantial damage to the anterior insula (AI) had heightened levels of alexithymia relative to
patients with minimal AI damage, patients with no AI damage, and matched control individuals
(Figure 2A) [25]. Further, the extent of damage to the AI signicantly predicted the severity of
acquired alexithymia, after controlling for damage to an adjacent region [anterior cingulate cortex
(ACC)] also thought to play a role in emotional awareness [26]. The ACC also appears to play a
role in emotional awareness, as cingulotomy patients demonstrate signicant reductions in
feelings of tension and anger following removal of supracallosal sectors of the ACC [27]. These
ndings are in agreement with theoretical and neuroimaging work suggesting that the AI
integrates ascending signals about the state of one's own body (i.e., interoceptive signals,
such as heart rate and skin conductance), which are sent to the ACC in order to initiate the
selection and planning of motor and nonmotor (e.g., change in cognitive set or topdown
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regulation of sensory processing) responses to emotional events [28]. The conjoint activity of
these two regions is thought to play a critical role in the generation of subjective emotional
experience [2830]. In addition, two recent case studies suggest that alternative interoceptive
pathways (via the somatosensory cortex and the brain stem) can enable some aspects of
emotional awareness in patients with AI and ACC damage [31,32].
Lastly, the ventromedial prefrontal cortex (vmPFC; including the ventral sector of the medial
orbitofrontal cortex and the perigenual and subgenual ACC) appears to play a role in emotional
awareness as well. Patients with vmPFC lesions show diminished experience of regret following
unfavorable decision outcomes [33] and reduced emotional intensity in day-to-day life [34].
Although vmPFC's role in emotional awareness is a topic of ongoing investigation, based on
what is known about this region's involvement in reward processing (Box 2), it is possible that the
vmPFC computes the reward value of interoceptive states and links them to exteroceptive
events [35].
Emotion Recognition
In addition to emotional awareness, the ability to recognize the emotions of others is essential to
social interaction, and evidence from focal lesion studies has helped to chart the neural bases of
emotion recognition. This work has reliably demonstrated that amygdala lesions disrupt the
ability to recognize emotional facial expressions [3638]. There is controversy surrounding
whether this emotion recognition function of the amygdala generalizes to other modalities such
as prosody. Some groups have found intact emotional prosody recognition in patients with
amygdala damage [39], whereas others have shown signicant impairments [40]. Bilateral
amygdala damage does not seem to impact the execution of emotional facial expressions
or emotional awareness [41,42], suggesting that this structure plays a specic role in processing
emotionally salient exteroceptive stimuli (e.g., observed facial expressions of others). Accordingly, it has been argued that the amygdala acts as an amplier that biases activity at downstream cortical targets to prioritize processing of salient stimuli [43,44].
One downstream target of the amygdala during emotion recognition appears to be the vmPFC.
vmPFC damage negatively impacts the ability to recognize emotional states from both facial
stimuli and prosodic cues [45,46]. Interestingly, a recent eye-tracking study suggests that this
impairment is driven by reduced visual attention to the eyes of others (Figure 2B) [45,47]. This
study suggests that reciprocal interactions between the vmPFC and the amygdala are crucial for
detecting and representing motivationally salient stimulus events [45].
Lesion studies have implicated brain regions involved in interoception and emotional awareness
as also playing a role in emotion recognition. Specically, lesion studies have implicated the
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somatosensory cortex, insula, and ACC in emotion recognition [4850]. A recent voxel-based
lesion-symptom mapping (VLSM) study found that the AI and the ACC play a critical role in
emotion recognition across both pleasant and unpleasant emotion categories [50]. These VLSM
results were replicated by another study of patients with focal resections of the insular cortex,
which demonstrated impaired performance at recognizing facial cues related to fear, happiness,
and surprise [51]. Collectively, the nding that brain regions necessary for rst-person emotional
experience are also necessary for emotion recognition is compatible with the simulation
hypothesis (i.e., that representing the emotional states of others engages the brain networks
involved in representing emotional states in the self, possibly mediated by the activation of the
human mirror neuron system) [52]. However, none of these studies specically looked at
emotional awareness and its relation to recognition [53], and more work is required to provide
stronger evidence for this hypothesis.
Using Emotions to Facilitate Thought and Behavior
Empathy and Prosocial Behavior
Whereas emotion recognition is a critical source of incoming social information, it does not
necessarily drive behaviors in response to that information (e.g., consider a hypothetical
situation in which an individual recognizes unhappiness on the face of a disliked other
recognition in this case will not necessarily provoke a prosocial behavioral response). Beyond
recognition, affective empathy is a catalyst through which another person's emotions can
inuence and mobilize social behavior. Affective empathy refers to the ability to share the
emotional state of another person, and it is a critical source of motivation driving individuals to
perform prosocial behaviors intended to benet the other [54,55]. Diminished affective empathy
following brain injury has consistently been observed in patients with ventrolateral prefrontal
cortex (vlPFC) lesions [56,57] and insular lesions [57,58]. For example, a sample of 192 patients
from the Vietnam Head Injury Study (Box 1) completed the Balanced Emotional Empathy Scale,
a 30-item questionnaire designed to measure affective empathy as a single factor, and a VLSM
analysis demonstrated signicantly reduced emotional empathy in patients with damage to a
network of brain regions, including the vlPFC, insula, and temporoparietal junction [57].
Involvement of this network in affective empathy is compatible with the self to other model
of empathy. According to this model, empathy relies upon both the ability to match others
emotional states in the self (i.e., emotional contagion, implemented by the vlPFC and insula),
and the ability to prioritize processing of self- and other-related representations according to
context demands and individual goals (i.e., selfother control, implemented by temporoparietal
junction) [59].
Emotional Memory
The strong inuence of emotions on memory is critical to the ability to use emotions to shape
thinking and behavior. People have superior memory for emotional events relative to neutral
ones, with emotional memories being signicantly less likely to be forgotten over time [60].
Emotional memory is impaired following lesions to the medial temporal lobes that encompass
the amygdala, hippocampus, and perirhinal cortex [61,62]. Yet, this change in emotional
memory following medial temporal lobe lesions is driven by amygdala damage, as patients
with hippocampal lesions and an intact amygdala either show a normative emotional memory
enhancement [63], or are impaired on memory for both neutral and emotionally salient stimuli
[64]. Emotional enhancement in memory consolidation has important social consequences, and
patients with amygdala damage end up having a difcult time learning the important traits of
others (e.g., trustworthiness, likeability, and competence, Figure 2C) [62]. It has recently been
argued that the amygdala plays a role in coordinating the enhanced consolidation and recall of
emotionally salient information relative to more affectively neutral contextual information [60],
similar to the way it amplies processing of salient information online during emotion recognition
tasks [43].
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Understanding How Emotions Shape One's Own Behavior and the Behavior of Others
Understanding how emotions shape our own behavior and the behavior of others is related to an
ability known as affective theory of mind (ToM), which is a critical milestone in the development
of effective social and emotional abilities [65]. Cognitive ToM refers to the ascription of mental
states to the self and others, commonly measured by having participants observe or read stories
about another individual's behavior, and then asking them to make judgments about their
underlying motivations. Hence, affective ToM is the ability to infer that the thoughts and
behaviors of others are inuenced by underlying feelings, and to interpret those feelings by
relying upon their understanding of how emotions shape their own thoughts and behaviors.
Multiple human lesion studies have found affective ToM to be impaired in patients with vmPFC
lesions [66,67]. For instance, one study found impaired recognition performance on the faux
pas task in 30 patients with vmPFC lesions, relative to both patients with damage to other brain
regions and healthy controls [66]. Faux pas recognition requires the ability to recognize when
someone says something that is inappropriate or insulting in a social context, which requires the
ability to ascribe an emotional response to the listener. The results clearly demonstrated that
vmPFC patients, particularly left vmPFC patients, were signicantly less able to correctly
recognize social faux pas relative to patients with damage to other brain regions and healthy
controls (Figure 2D) [66]. Prefrontal involvement in faux pas recognition appears to be restricted
to medial sectors, as another study replicated the nding that vmPFC damage disrupts faux pas
recognition performance, but this ability was preserved in patients with dorsolateral PFC
damage [68]. Patients with bilateral amygdala lesions are also impaired on faux pas recognition
[69], but the precise role of this region and its network-level interactions with the vmPFC that
might support affective ToM are currently unclear (see Outstanding Questions).
Emotion Regulation
The last emotional ability central to the EI construct is emotion regulation, which refers to the set
of operations involved in modulating ongoing emotional responses in accordance with individual
or social goals. This ability is critical to mental health and social functioning, as emotion regulation
decits have been linked to aggressive behavior, anxiety, and depression [70]. Such affective
psychopathologies are commonly attributed to dysfunctional emotion regulation, including an
overreliance on maladaptive strategies (e.g., avoidance of anxiety-provoking situations or
suppression of emotional facial expressions in such situations), and diminished use of adaptive
strategies (e.g., acceptance of negative feelings or reappraisal of such feelings to give them a
less aversive interpretation) [70]. Signs of dysfunctional emotion regulation have been observed
in individuals with acquired brain injury, particularly patients with vmPFC lesions [71,72]. For
example, patients with vmPFC damage (specically, patients with medial orbitofrontal cortex
damage) demonstrate signicantly greater electrophysiological responses (P3 component) to
emotionally salient stimulus events relative to nonbrain-injured controls, and fail to attenuate
these responses over time (Figure 2E) [73]. This impaired regulation of emotional responses has
signicant social consequences for vmPFC patients: they reject offers to share money with
greater frequency than controls [74], are rated highly on several traits that hinder social rapport
(e.g., irritability, inappropriate affect) [75], and fail to monitor and regulate the emotional states of
others (e.g., reduced frequency of apologies) [76]. Additionally, vlPFC and amygdala lesions
have also been found to disrupt emotion regulation abilities [77,78]. These ndings are compatible with an extensive functional neuroimaging literature suggesting that network-level interactions between the vlPFC, vmPFC, and amygdala are involved in successful emotion regulation
[e.g., 79].
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also impaired in individuals with damage to these regions. In this vein, several recent lesionmapping studies have investigated the neural basis of EI, measured using the MSCEIT [18]. For
example, Krueger and colleagues [80] found that vmPFC damage critically impaired the
strategic factors of the MSCEIT, referring to one's abilities to understand and regulate
emotional responses in the self and others. In addition, Barbey and colleagues [81,82] recently
used a combined latent variable and VLSM approach to rst conrm the hierarchical factor
structure of the MSCEIT, and then to elucidate the network of brain regions involved in EI. This
work found that EI scores on the MSCEIT are reduced following damage to a distributed
network, including the vmPFC, vlPFC, insula, ACC, as well as several other parietal and temporal
brain regions. The fact that lesion-mapping studies of the MSCEIT implicate a network of brain
regions broadly consistent with studies that focus on its constituent emotional abilities provides
preliminary support for the presence of an overarching EI construct.
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including increased anxiety and depression, and disrupted social interaction skills [71,76]. Thus,
emotional abilities appear to play a role in enabling adaptive day-to-day social and personal
functioning, which is compromised in brain-injured patients with impaired emotional abilities.
This suggests that EI, if measured effectively, might be associated with important outcomes in
the real world that could motivate targeted intervention strategies to improve EI.
Outstanding Questions
Concluding Remarks
In this light, the contentious debate surrounding the validity of EI appears to be misguided.
Instead, in our view, research should shift toward empirically validating the hypothesized
component structure of emotional ability outlined in the present review (i.e., perceiving emotions
in self and other, using emotions to guide thinking and behavior, understanding how emotions
inuence our own and others behavior, and regulating emotional responses in self and other).
The data from human lesion studies implicate a consistent network of brain regions, including the
amygdala, vmPFC, insula, and ACC, across multiple component emotional abilities (Figure 1B).
These brain regions are part of an emotion network that is frequently identied in functional
neuroimaging studies of human emotion (see Outstanding Questions) [92]. The involvement of a
core network of brain regions across distinct emotional domains is compatible with the
suggestion of a general overarching EI. However, this hypothesis needs to be evaluated through
careful experimentation. Such work could address two crucial questions to help advance this
eld: Is EI distinct from, or integral to, general cognitive ability? And, to what extent can EI be
summarized by a single underlying factor?
Regarding the rst question, early theories of emotional and social intelligence attempted to
distinguish these abilities from cognitive intelligence [15,93]. Yet, this degree of functional
separation seems untenable. Indeed, recent advances in psychology and neuroscience have
reliably suggested that emotion and cognition are very much integrated in the brain, combining
to shape goal-directed behavior [81,94,95]. For instance, a recent VLSM study suggested that
many of the brain regions involved in EI overlapped with those implicated in general intelligence,
with a strong behavioral association between the two measures [81]. This suggests that the
relationship between emotional and general intelligence may in fact be enmeshed, with EI
measuring individual differences in one's ability to integrate emotions into cognitive operations
(A)
High
emoonal
intelligence
em
i
y, av
o r eh
em l b
m cia
a l so
on ro
o d p
E m y an
th
pa
(B)
Em
o
em o
o nal
on aw
re are
co n
gn ess
i a
on nd
Low
emoonal
intelligence
or
th
on n
o o
Em gula
re
eo Ae
ry c
of ve
m
in
d
Emoonal
ability
Figure 3. Schematic Representations of [28_TD$IF]Scalar and[29_TD$IF] Multidimensional EI Space. (A) A two-dimensional continuum
view of EI and (B) a multidimensional EI space composed of at least four component emotional abilities.
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(e.g., using reward valuations to drive the items held in working memory, using inhibitory control
to regulate aversive emotional reactions).
Regarding the second question, despite agreement that EI is likely made up of several component abilities [12,18], the extent to which these abilities are interdependent or independent needs
to be established. At present, it is unclear whether all of the emotional abilities summarized in the
present review can be integrated into a single underlying EI variable i.e., resembling an EI
continuum across the general population (Figure 3A). Alternatively, such work might instead
reveal that EI is a heterogeneous blend of several contributing variables, in which case
researchers might be better served measuring individual differences in multidimensional EI
space (Figure 3B). These questions of whether cognitive and EI are integrative or dissociable,
and whether EI exists on a continuum or a multidimensional space, would have tremendous
applied value, enabling consultants, educators, and medical practitioners to build EI assessment
tools and training programs with improved convergent, divergent, and predictive validities.
Acknowledgments
The Vietnam Head Injury Study has been supported by the Department of Defense and the National Institute of Neurological
Disorders and Stroke. For further information on the Vietnam Head Injury Study, please contact J.G. at jgrafman@northwestern.edu.
Resources
i
http://neurosynth.org/analyses/custom/a83a4072-85d4-4fd1/
References
1.
Spearman, C. (1904) General intelligence, objectively determined and measured. Am. J. Psychol. 15, 201292
2.
3.
Hunter, J.E. and Hunter, R.F. (1984) Validity and utility of alternative predictors of job performance. Psychol. Bull. 96, 7298
4.
Snarey, J.R. and Vaillant, G.E. (1985) How lower- and workingclass youth become middle-class adults: the association
between ego defense mechanisms and upward social mobility.
Child Dev. 56, 899910
5.
Feist, G.J. and Barron, F.X. (2003) Predicting creativity from early
to late adulthood: intellect, potential, and personality. J. Res.
Pers. 37, 6288
6.
7.
8.
9.
22. Sifneos, P.E. (1973) The prevalence of alexithymic characteristics in psychosomatic patients. Psychother. Psychosom. 22,
255262
23. Henry, J.D. et al. (2006) Cognitive and psychosocial correlates of
alexithymia following traumatic brain injury. Neuropsychologia
44, 6272
24. Williams, C. and Wood, R.L. (2013) The impact of alexithymia on
relationship quality and satisfaction following traumatic brain
injury. J. Head Trauma Rehabil. 28, 1619
25. Hogeveen, J. et al. (2016) Acquired alexithymia following damage
to the anterior insula. Neuropsychologia 82, 142148
26. Lane, R.D. et al. (1998) Neural correlates of levels of emotional
awareness. Evidence of an interaction between emotion and
attention in the anterior cingulate cortex. J. Cogn. Neurosci.
10, 525535
27. Cohen, R.A. et al. (2001) Emotional and personality changes
following cingulotomy. Emotion 1, 3850
28. Medford, N. and Critchley, H.D. (2010) Conjoint activity of anterior insular and anterior cingulate cortex: awareness and
response. Brain Struct. Funct. 214, 535549
10
Downloaded from ClinicalKey.com at Northwestern University - Galter Library September 18, 2016.
For personal use only. No other uses without permission. Copyright 2016. Elsevier Inc. All rights reserved.
30. Craig, A.D. (2009) How do you feel now? The anterior insula
and human awareness. Nat. Rev. Neurosci. 10, 5970
32. Khalsa, S.S. et al. (2009) The pathways of interoceptive awareness. Nat. Neurosci. 12, 14941496
33. Camille, N. et al. (2004) The involvement of the orbitofrontal
cortex in the experience of regret. Science 304, 11671170
59. Bird, G. and Viding, E. (2014) The self to other model of empathy:
providing a new framework for understanding empathy impairments in psychopathy, autism, and alexithymia. Neurosci. Biobehav. Rev. 47, 520532
47. Adolphs, R. (2014) Social attention and the ventromedial prefrontal cortex. Brain 137, 15721574
74. Koenigs, M. and Tranel, D. (2007) Irrational economic decisionmaking after ventromedial prefrontal damage: evidence from the
ultimatum game. J. Neurosci. 27, 951956
75. Barrash, J. et al. (2000) Acquired personality disturbances associated with bilateral damage to the ventromedial prefrontal
region. Dev. Neuropsychol. 18, 355381
76. Beer, J.S. et al. (2003) The regulatory function of self-conscious
emotion: insights from patients with orbitofrontal damage. J.
Pers. Soc. Psychol. 85, 594604
77. Angrilli, A. et al. (1996) Startle reex and emotion modulation
impairment after a right amygdala lesion. Brain 119, 19912000
78. Falquez, R. et al. (2014) Detaching from the negative by reappraisal: the role of right superior frontal gyrus (BA9/32). Front.
Behav. Neurosci. 8, 165
79. Silvers, J.A. et al. (2016) vlPFC-vmPFC-amygdala interactions
underlie age-related differences in cognitive regulation of emotion. Cereb. Cortex (in press)
80. Krueger, F. et al. (2009) The neural bases of key competencies
of emotional intelligence. Proc. Natl. Acad. Sci. U.S.A. 106,
2248622491
Downloaded from ClinicalKey.com at Northwestern University - Galter Library September 18, 2016.
For personal use only. No other uses without permission. Copyright 2016. Elsevier Inc. All rights reserved.
11
81. Barbey, A.K. et al. (2014) Distributed neural system for emotional
intelligence revealed by lesion mapping. Soc. Cogn. Affect. Neurosci. 9, 265272
84. OConnor, R.M. and Little, I.S. (2003) Revisiting the predictive
validity of emotional intelligence: self-report versus ability-based
measures. Pers. Individ. Dif. 35, 18931902
101. Pan, W. et al. (2014) Identifying the core components of emotional intelligence: Evidence from amplitude of low-frequency
uctuations during resting state. PLoS One 9, 18
102. Tan, Y. et al. (2014) The correlation between emotional intelligence and gray matter volume in university students. Brain Cogn.
91, 100107
86. Ct, S. et al. (2010) Emotional intelligence and leadership emergence in small groups. Leadersh. Q. 21, 496508
87. Clarke, N. (2006) Emotional intelligence training: a case of caveat
emptor. Hum. Resour. Dev. Rev. 5, 422441
88. Van Rooy, D.L. and Viswesvaran, C. (2004) Emotional intelligence: a meta-analytic investigation of predictive validity and
nomological net. J. Vocat. Behav. 65, 7195
89. OBoyle, E.H., Jr et al. (2011) The relation between emotional
intelligence and job performance: a meta-analysis. J. Organ.
Behav. 32, 788818
90. Wood, R.L. et al. (2010) Role of alexithymia in suicide ideation
after traumatic brain injury. J. Int. Neuropsychol. Soc. 16,
11081114
91. Wood, R.L. et al. (2014) Anxiety sensitivity and alexithymia as
mediators of postconcussion syndrome following mild traumatic
brain injury. J. Head Trauma Rehabil. 29, E9E17
92. Lindquist, K.A. et al. (2012) The brain basis of emotion: a metaanalytic review. Behav. Brain Sci. 35, 121143
93. Gardner, H. (1983) Frames of Mind, Basic Books
94. Inzlicht, M. et al. (2015) Emotional foundations of cognitive control. Trends Cogn. Sci. 19, 126132
95. Pessoa, L. (2008) On the relationship between emotion and
cognition. Nat. Rev. Neurosci. 9, 148158
96. Bechara, A. et al. (1994) Insensitivity to future consequences
following damage to human prefrontal cortex. Cognition 50,
715
97. Kreifelts, B. et al. (2010) Association of trait emotional intelligence and individual fMRI-activation patterns during the perception of social signals from voice and face. Hum. Brain Mapp.
31, 979991
12
Downloaded from ClinicalKey.com at Northwestern University - Galter Library September 18, 2016.
For personal use only. No other uses without permission. Copyright 2016. Elsevier Inc. All rights reserved.