Social Neuroscience

ISSN: 1747-0919 (Print) 1747-0927 (Online) Journal homepage: http://www.tandfonline.com/loi/psns20

Social neuroscience: undoing the schism between

neurology and psychiatry

Agustín Ibáñez, Adolfo M. García, Sol Esteves, Adrián Yoris, Edinson Muñoz,
Lucila Reynaldo, Marcos Luis Pietto, Federico Adolfi & Facundo Manes

To cite this article: Agustín Ibáñez, Adolfo M. García, Sol Esteves, Adrián Yoris, Edinson
Muñoz, Lucila Reynaldo, Marcos Luis Pietto, Federico Adolfi & Facundo Manes (2016): Social
neuroscience: undoing the schism between neurology and psychiatry, Social Neuroscience,
DOI: 10.1080/17470919.2016.1245214

To link to this article: http://dx.doi.org/10.1080/17470919.2016.1245214

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Oct 2016.
Published online: 27 Oct 2016.

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SOCIAL NEUROSCIENCE, 2016
http://dx.doi.org/10.1080/17470919.2016.1245214

Social neuroscience: undoing the schism between neurology and psychiatry

Agustín Ibáñez a,b,c,d,e*, Adolfo M. Garcíaa,b,f*, Sol Estevesa, Adrián Yorisa,b, Edinson Muñozg, Lucila Reynaldoa,
Marcos Luis Piettoh, Federico Adolfia and Facundo Manesa,b,e,i
a
Laboratory of Experimental Psychology and Neuroscience (LPEN), Institute of Cognitive and Translational Neuroscience (INCyT), INECO
Foundation, Favaloro University, Buenos Aires, Argentina; bNational Scientific and Technical Research Council (CONICET), Buenos Aires,
Argentina; cCenter for Social and Cognitive Neuroscience (CSCN), School of Psychology, Universidad Adolfo Ibáñez, Santiago de Chile, Chile;
d
Universidad Autónoma del Caribe, Barranquilla, Colombia; eCentre of Excellence in Cognition and its Disorders, Australian Research Council
(ACR), Sydney, Australia; fFaculty of Elementary and Special Education (FEEyE), National University of Cuyo (UNCuyo), Mendoza, Argentina;
g
Departamento de Lingüística y Literatura, Facultad de Humanidades, Universidad de Santiago de Chile, Santiago, Chile; hUnit of Applied
Neurobiology (UNA, CEMIC), Buenos Aires, Argentina; iDepartment of Experimental Psychology, University of South Carolina, Columbia, SC, USA

ABSTRACT ARTICLE HISTORY

Multiple disorders once jointly conceived as “nervous diseases” became segregated by the Received 12 May 2016
distinct institutional traditions forged in neurology and psychiatry. As a result, each field specia- Revised 29 July 2016
lized in the study and treatment of a subset of such conditions. Here we propose new avenues for Published online 27 October
interdisciplinary interaction through a triangulation of both fields with social neuroscience. To 2016
this end, we review evidence from five relevant domains (facial emotion recognition, empathy, KEYWORDS
theory of mind, moral cognition, and social context assessment), highlighting their common Social neuroscience;
disturbances across neurological and psychiatric conditions and discussing their multiple patho- neurology; psychiatry;
physiological mechanisms. Our proposal is anchored in multidimensional evidence, including neuropsychiatry
behavioral, neurocognitive, and genetic findings. From a clinical perspective, this work paves the
way for dimensional and transdiagnostic approaches, new pharmacological treatments, and
educational innovations rooted in a combined neuropsychiatric training. Research-wise, it fosters
new models of the social brain and a novel platform to explore the interplay of cognitive and
social functions. Finally, we identify new challenges for this synergistic framework.

On the origins of neurology and psychiatry transdiagnostic approach. In this paper, we delineate a
triangulation among neurology, psychiatry, and social
Currently, neurology and psychiatry represent two dis-
neuroscience. Specifically, we review massive evidence
tinct disciplines with different clinical specializations,
of shared social cognition impairments across neurolo-
research methodologies, and institutional frameworks.
gic and psychiatric diseases, and sketch a prospective
Mr. Gambale loses his memory after a head blow, and
framework to foster more synergistic research and edu-
he is swiftly taken to the neurologist. Instead, if Mr.
cation beyond disciplinary specializations.
Holdsworth believes he is dead, he is referred to a
To understand why this triangulation has not yet
psychiatrist. However, had these patients lived
crystallized, we must trace the historical roots of neu-
200 years ago, both their conditions would have been
rology and psychiatry. In the early and mid-nineteenth
treated as nervous diseases (Price, Adams, & Coyle, 2000;
century, Gall and Spurzheim, followed by Broca and
Reynolds, 1990). Indeed, multiple cognitive and beha-
Wernicke, pioneered the scientific study of complex
vioral domains become similarly compromised in neu-
pathological behaviors in connection to the brain
rological and psychiatric disorders. Social cognition
(Price et al., 2000). Both before and after such contribu-
impairments are prime examples of these commonal-
tions, leading scholars (e.g., Charcot, Freud, Kraepelin,
ities (Ibanez, Kuljis, Matallana, & Manes, 2014).
Bleuler, Alzheimer, Parkinson) favored a joint approach
Nevertheless, while both neurology and psychiatry
to neurological and psychiatric disorders (Martin, 2002).
have established fruitful dialogue with neuroscientific
Admittedly, methodological differences already existed
research, no systematic triangulation with social neu-
between neurologists and psychiatrists. While the for-
roscience has yet been formulated to address social
mer correlated brain syndromes with neuropathological
cognition disturbances from a dimensional,

CONTACT Agustín Ibáñez aibanez@ineco.org.ar Institute of Cognitive and Translational Neuroscience (INCyT), Pacheco de Melo 1860, Buenos Aires,
Argentina
*These authors are the First authors.
© 2016 Informa UK Limited, trading as Taylor & Francis Group
2 A. IBÁÑEZ ET AL.
changes via postmortem and microscopic techniques,
the latter relied on analytical descriptions of behavior
and symptoms. Yet, their analyses pursued the same
goal: characterizing the structure and function of the
nervous system (Cowan, Harter, & Kandel, 2000).
Throughout the twentieth century, however, neurol-
ogists and psychiatrists began to forge different
approaches to disorders of the nervous system, with
separate philosophical rationales, research principles,
and treatment methods (Martin, 2002). In the post-war
Anglo-Saxon and American contexts, the field was
marked by a theoretical and practical divide: neurolo-
gists studied organic brain dysfunctions, searching for
anatomic causes of “neurological diseases”; instead,
psychiatrists, influenced by Freudian theories, were
interested in functional alterations of the mind and
their “psychodynamic causes”. This was particularly
reinforced since the 1930s. Relying on pioneering
brain measurement techniques (such as electroence-
phalography) which offered objective, consistent, and
reproducible findings, neurologists agreed on impor-
tant definitions and criteria (Price et al., 2000).
However, several disorders lacked visible pathological
markers. These became the focus of psychiatrists, who
favored symptom descriptions over laboratory tests.
The opposition between both communities was
reflected in their training requirements and geographi-
cal distributions. The prestigious Archives of Neurology
and Psychiatry, for instance, was quickly dissolved into
two journals with separate agendas: JAMA Neurology
and JAMA Psychiatry.
Such initial separation has had unfortunate conse-
quences. In particular, the consolidation of different
theories, research projects, training methods, and clin-
ical assessment models has hindered the construal of
synergistic neuropsychiatric knowledge (Northoff, 2008;
Price et al., 2000). The complex field of neuropsychiatry
partly bridged such a gap, framing structural and func-
tional aspects as complementary across neurological
and psychiatric diseases (Northoff, 2008). Similarly, neu-
roscientists largely agree on the conceptual futility of
strict separations between both disciplines (Martin,
2002). However, integration efforts so far have been
only partially successful, at best. We propose that this
endeavor could witness major breakthroughs if specific
knowledge from both fields is triangulated with multi-
level insights from social neuroscience.
Despite general positive beliefs about the role of
cognitive neuroscience as a bridge between neurology
and psychiatry (Northoff, 2008; Price et al., 2000), such a
threefold interaction has rarely taken place in the social
neuroscience arena. To a large extent, this is due to the
scarcity of dimensional and transnosological research
and practice within social neuroscience. For instance,
there are virtually no empirical reports of social cogni-
tion domains which directly compare neurological and
psychiatric conditions. Even in some syndromes sec-
ondary to both types of diseases (e.g., Capgrass syn-
drome), direct contrasts of social cognition skills (e.g.,
facial expression recognition) remain unattempted,
which precludes comparisons between different patho-
physiological mechanisms for the same socio-cognitive
domain. Similarly, explanatory models of social cogni-
tion impairments rooted in neurology (e.g., (Dickerson,
2015) or psychiatry (e.g., (Fett, Shergill, & Krabbendam,
2015))) have largely overlooked evidence from the
other discipline. In addition, virtually no academic pro-
grams and funding sources aim to apply the knowledge
of social neuroscience to neurological and psychiatric
disorders featuring similar impairments. Finally, given
that neuroscience has traditionally ignored contribu-
tions from social neuroscience (Nature Neuroscience
Editorial, 2012), the latter’s interaction with neuropsy-
chiatry has been delayed.
A neuropsychiatric approach, moving toward a sys-
tematic triangulation of social neuroscience with neu-
rology and psychiatry, could provide a synergistic arena
for clinical and research developments. Here we focus
on the empirical, methodological, and conceptual con-
tributions that could be derived directly from social
neuroscience in the pursuit of such an aim. An emer-
ging agenda is reframing psychiatric diseases as disor-
ders of social cognition (Schilbach et al., 2013).
Extending these claims, below we sketch a social neu-
roscience approach to various dimensions of neurolo-
gical and psychiatric disorders (Baez, García, & Ibanez,
2016; Ibanez & Manes, 2012).
The paper is organized as follows. First, we character-
ize the tenets of social neuroscience. Second, we
describe behavioral variant frontotemporal dementia
(bvFTD) (Piguet, Hornberger, Mioshi, & Hodges, 2011)
as a prototypical model to map the clinical and biologi-
cal overlaps between several neurological and psychia-
tric disorders. Third, we selectively review key domains of
social neuroscience, highlighting their common distur-
bances in bvFTD and other conditions. We focus on facial
emotion recognition (FER), empathy, theory of mind
(ToM), moral cognition, and ecological assessment of
social context. Fourth, we discuss the prospects of this
triangulation, showing how multilevel network-based
approaches within social neuroscience can open new
opportunities for development. Then, we sketch avenues
of interaction between social neuroscience and neurop-
sychiatry, including theoretical, diagnostic, and pharma-
cological considerations. Finally, we identify novel
challenges for this synergistic framework.
 SOCIAL NEUROSCIENCE 3

Social neuroscience: a tool kit for triangulation presentations of bipolar disorder (BD), major depressive
disorder, attention-deficit hyperactivity disorder
Experimental approaches within cognitive neuroscience
(ADHD), schizophrenia (SZ), and borderline personality
—ranging from animal models to behavioral and ima-
disorder (BPD). Thus, it is often difficult to ascertain
ging studies with humans—shed light on cognitive
bvFTD as the underlying clinical entity (Barutta,
(dys)functions in neurological and psychiatric disorders.
Hodges, Ibanez, Gleichgerrcht, & Manes, 2011; Manes,
Despite the shortcomings mentioned above, this joint
2012). Indeed, in approximately half of bvFTD patients,
approach, in itself, reduces the discontinuity between
behavioral and attitudinal changes are ignored or
constructs in each discipline (Cowan et al., 2000). More
attributed to a primary psychiatric disorder (Woolley,
particularly, the subfield of social neuroscience studies
Khan, Murthy, Miller, & Rankin, 2011). Specifically, social
the biological underpinnings of social processes, as
cognition deficits, typified by contextual inappropriate-
shaped by contextual factors. Psychosocial mechanisms
ness (Baez et al., 2016; Ibanez & Manes, 2012), may be
are conceived as multidimensional phenomena, includ-
overlooked before they become severe, especially
ing social behavior (observable interactions between
because such variable is rarely quantified in structured
people), social cognition (psychological processes
clinical (Gleichgerrcht, Ibanez, Roca, Torralva, & Manes,
underling social behavior), socially driven neural activity
2010) and neuropsychological (Torralva, Roca,
(brain structures and networks subserving social pro-
Gleichgerrcht, Bekinschtein, & Manes, 2009) examina-
cesses), and social functioning (the ability to interact
tion. In sum, as further shown below, bvFTD is a multi-
with others in time and space) (Kennedy & Adolphs,
dimensional condition whose comprehensive study
2012). More generally, social neuroscience addresses
requires integrating socially relevant insights from neu-
the normal and pathological interplay among environ-
rology and psychiatry (Ibanez et al., 2014).
ment, performance, cognition, neural substrates, and
genetics (Ibanez, Kotz, Barrett, Moll, & Ruz, 2014).
The social cognition network is so widespread
(Kennedy & Adolphs, 2012) that it proves vulnerable A dimensional and transnosological
to varied neurological and psychiatric diseases. Given comparison of social cognition domains
the omnidirectional relationship among the above
A key step toward the triangulation we advocate con-
dimensions, a disturbance in any of them could com-
sists in reviewing extant evidence from social neu-
promise relevant neural circuits even in the absence of
roscience with a dimensional and transnosological
primary (neurocognitive) social deficits. Yet, that very
perspective (Association, 2000; Kendler, 1990). A dimen-
feature suggests multiple alternatives to foster recov-
sional approach frames psychopathological processes
ery, capitalizing on spared components of the network.
as continua between normal and pathological
Through its sensitive experimental methods, social neu-
extremes. Similarly, social cognition deficits in a specific
roscience sheds light on the anatomy, function, and
domain (e.g., social decision making) can be present
plasticity of such complex circuitry, regardless of the
not only as a dimensional disturbance across patients,
underlying diagnosis.
but also across subdomains (e.g., regarding fairness,
bargaining, risk, or other relevant variables). Besides, a
transnosological conception acknowledges that specific
Behavioral variant frontotemporal dementia: A key
mental and social faculties can be similarly compro-
model for disciplinary triangulation
mised across disease types (Hyman, 2007; Insel &
The shortcomings of the neurology/psychiatry divide Quirion, 2005; Jablensky, 2005; McGorry & Van Os,
are evident in bvFTD (Ibanez et al., 2014). This neuro- 2013). Although the transnosological approach has
degenerative condition is characterized by frontal, insu- been mostly restricted to the psychiatric field, it can
lar, and temporal atrophy, although such damage may be extended across psychiatric and neurological disor-
not be evident on structural brain imaging early on ders. These dimensional and transnosological view-
(Rahman, Sahakian, Hodges, Rogers, & Robbins, 1999; points concern not only clinical, but also anatomical,
Rascovsky et al., 2011). Initial manifestations involve neurophysiological, molecular, and genetic dimensions.
pervasive changes in personality and social behavior The study of social cognition impairments profitably
(e.g., disinhibition, compulsivity, depression, impulsivity, lends itself to both approaches, since such deficits can
inappropriate conduct), even before cognitive altera- vary in frequency and intensity across a vast array of
tions are observed (Piguet et al., 2011; Santamaría- neurological and psychiatric diseases. Below we deploy
García et al., 2016). Clinical criteria for early bvFTD this framework through a review of five distinguishable
(Manes et al., 2010) are sometimes met by atypical though interrelated domains.
4 A. IBÁÑEZ ET AL.

Facial emotion recognition Huntington’s disease (HD)(Feuerriegel, Churches,

Hofmann, & Keage, 2014; Kumfor & Piguet, 2013;
FER is crucial for social interactions, as it allows people
Novak et al., 2012), multiple sclerosis (MS, Henry et al.,
to infer what others are feeling and act accordingly
2011; Mike et al., 2013), neuromyelitis optica (Cardona
(Adolphs, 2002; Atkinson & Adolphs, 2011; Rutishauser,
et al., 2014), amyotrophic lateral sclerosis (ALS)(Crespi
Mamelak, & Adolphs, 2015). It involves multiple sub-
et al., 2014), mild cognitive impairment (Varjassyova
processes and engages networks distributed along the
et al., 2013), epilepsy (Gomez-Ibanez, Urrestarazu, &
fusiform gyrus, the superior temporal sulcus, the amyg-
Viteri, 2014; Jiang et al., 2014), Cockayne syndrome
dala, the orbitofrontal cortex (OFC), and the basal gang-
(Baez et al., 2013), stroke (Falquez et al., 2014; Yuvaraj,
lia (Adolphs, 2002; Adolphs, Tranel, & Damasio, 2003;
Murugappan, Norlinah, Sundaraj, & Khairiyah, 2013),
Allison, Puce, Spencer, & McCarthy, 1999). Facial, emo-
Rett syndrome (Djukic, Rose, Jankowski, & Feldman,
tional, and contextual integration of information occurs
2014), posterior cortical atrophy (Gonzalez-Gadea,
early in the brain (Ibáñez et al., 2010, Ibáñez, Hurtado,
Ibanez, et al. 2014), and genetic disorders such as
et al. 2011). FER deficits hamper social communication
Prader–Willi syndrome (Key, Jones, & Dykens, 2013)
and induce changes in personality and behavior. They
and Klinefelter syndrome (Van Rijn, Swaab, Aleman, &
are more severe in bvFTD (Kumfor et al., 2011; Kumfor &
Kahn, 2006) (see Table 1).
Piguet, 2013; Lavenu & Pasquier, 2005; Werner et al.,
FER impairments are also present in most psychiatric
2007) (and other subtypes of FTD) than in other demen-
conditions, including BD (Ibanez et al., 2012), BPD (Baez,
tias, even controlling for disease severity (Bertoux, Volle,
Marengo, et al. 2014), major depressive disorder
et al. 2014; Fernandez-Duque & Black, 2005; Kumfor &
(Schepman, Taylor, Collishaw, & Fombonne, 2012),
Piguet, 2013). Crucially, in this condition, they are not
obsessive compulsive disorder (OCD) (Kang,
explained by other cognitive deficits (Kumfor et al.,
Namkoong, Yoo, Jhung, & Kim, 2012), body dysmorphic
2011; L. A. Miller et al., 2012) and seem to impact the
disorder (Buhlmann, McNally, Etcoff, Tuschen-Caffier, &
implicit awareness of its dysfunction (Ibanez, Velasquez,
Wilhelm, 2004), panic disorder (Wang et al., 2013), ado-
Caro, & Manes, 2013).
lescents under social deprivation (Escobar et al., 2013),
FER impairments in bvFTD are associated with atro-
ex-combatants (Tobón et al., 2015), and anorexia
phy in the amygdala, the insula, the OFC, and the
(Fonville, Giampietro, Surguladze, Williams, &
medial prefrontal cortices (Bertoux et al., 2012; Kipps,
Tchanturia, 2014) (see Table 1). In particular, they are
Nestor, Acosta-Cabronero, Arnold, & Hodges, 2009;
pervasive in autism spectrum disorder (ASD) (Aoki,
Omar, Rohrer, Hailstone, & Warren, 2011; Rosen et al.,
Cortese, & Tansella, 2014; Dawson, Webb, &
2002). More particularly, impaired recognition of nega-
McPartland, 2005; Feuerriegel et al., 2014; Sachse
tive emotions, such as disgust and fear, has been asso-
et al., 2014). Electrophysiological evidence shows that
ciated with damage to the left insula and the right
early (decoding) and late (integration) face-processing
amygdala, respectively (Kumfor, Irish, Hodges, Piguet,
disruptions in autistic individuals may occur since age
& Kilner, 2013). Thus, the regions supporting FER over-
three and persist into adulthood (Dawson et al., 2005).
lap with those compromised in bvFTD.
Similar deficits have been reported in SZ (Baez, Herrera,
This skill is disturbed in other neurodegenerative
Villarin, et al. 2013; Fujiwara, Yassin, & Murai, 2014;
conditions. In Alzheimer’s disease (AD), for example,
Kohler et al., 2008; Linden et al., 2010; Ventura, Wood,
FER decreases with the progression of dementia
Jimenez, & Hellemann, 2013), with reduced modulation
(Kumfor & Piguet, 2013; Lavenu & Pasquier, 2005), par-
of face-specific ERPs being evident even in first-degree
ticularly in the domain of negative emotions (Phillips,
relatives (Feuerriegel et al., 2014; Ibanez et al., 2012;
Scott, Henry, Mowat, & Bell, 2010; Rosen et al., 2006).
McCleery et al., 2014; Turetsky et al., 2007). Responses
Such an impairment is only partially influenced by other
to facial emotional stimuli in SZ are also associated with
cognitive deficits (Klein-Koerkamp, Beaudoin, Baciu, &
decreased activation of the fusiform gyrus and the
Hot, 2012). In fact, varied emotional domains are com-
amygdala (Habel et al., 2010; Paradiso et al., 2003).
promised in AD, suggesting a global emotional distur-
The N170 to emotional faces is also impaired in ADHD
bance (Braak & Braak, 1991; Bruen, McGeown, Shanks, &
(Ibáñez, Petroni, et al. 2011). Notably, FER deficits are
Venneri, 2008; Horinek, Varjassyova, & Hort, 2007). FER
marked in Capgras syndrome (the delusion that a friend
deficits are also common in other neurological disor-
or relative has been replaced by an identical-looking
ders, with varying degrees of intensity. These include
impostor), which may be present in neurological and
corticobasal syndrome (Kumfor et al., 2014), prosopag-
psychiatric diseases, such as Lewy body dementia
nosia (De Renzi, 1986; Liu & Behrmann, 2014), progres-
(Fiacconi et al., 2014) and paranoid SZ (Ellis et al.,
sive supranuclear palsy (Kumfor & Piguet, 2013),
1993; Ellis, Young, Quayle, & De Pauw, 1997),
Table 1. FER in neurological and psychiatric conditions.
Study Subjects F Tasks Behavioral findings Biomarker
Bertoux, De AD (CSF profile) (N = 33); bv-FTD N FER test AD performed worse than HC. Bv-FTD impaired compared Not measured.
Souza, et al. (no CSF) (N = 60) and HC to AD and HC for all emotions except happiness and
(2014) (N = 30) neutral. FER in AD was influenced by disease duration
and overall cognitive impairment.
Piguet, Leyton, nfv-PPA (N = 20); lv-PPA (N = 18); N ER Task: (Ekman 60 Faces nfv-PPA group was impaired compared with the other two Predominant left lateralized brain atrophy in PPA groups.
Gleeson, Hoon, HC (N = 21). Test) groups Greater cortical thinning in the left inferior parietal,
& Hodges, posterior cingulate, and inferior temporal regions in lv-
(2015) PPA, and in the insula and right calcarine in nfv-PPA.
All lv-PPA (but not nfv-PPA) had amyloid B deposition
associated w. Alzheimer (Pib-PET imaging).
Kumfor et al. CBS (N = 16); AD (N = 18); HC N FER: Face Perception Task; CBS performed worse than HC on FER. AD: intact High-level ER deficits in CBS associated with atrophy of
(2014) (N = 22). Face Matching; Emotion performance. Ekman 60 and TASIT: CBS and AD the paracentral gyrus/precuneus region and basal
Matching Task; Emotion performed worse than HC. ganglia. In AD ER deficits associated with cortical
selection task; TASIT. thickness in the anterior cingulate and insula, together
MRI scan with the hippocampus, amygdala, and nucleus
accumbens.
Cardona et al. NMO (N = 10) Emotional Morphing Task Reduced accuracy in patients for emotions of disgust, Not measured.
(2014) HC (N = 10) anger
and fear.
Crespi et al. ALS (N = 22) N ER Task (Ekman 60 Faces Global impairment of ER in ALS compared to HC. Significant microstructural white-matter changes
(2014) HC (N = 55) Test) (Diffusion Tensor Imaging) within the motor pathway
in ALS compared to HC.
Liu and CP (N = 8) N Forty front view Caucasian CP: discrimination performance (Holistic Processing) Not measured.
Behrmann HC 1 (N = 32) and HC 2 (N = 8) male faces w. neutral impaired compared to HC.
(2014) expressions
Djukic et al. Rett Syndrome female patients N ER Task of three basic Rett syndrome patients were impaired in ER compared to Not measured.
(2014) (N = 37) emotions (happy, sad HC.
HC (N = 34) and fear)
Gomez-Ibañez Idiopatic generalized epilepsy N FER Task FER impaired in both MTLE and IGE patients. Not measured.
et al. (2014). (IGE) (N = 20) Facial Identity Recognition FIR impaired in MTLE patients.
Mesial temporal lobe epilepsy Task (FIR)
(MTLE) (N = 19)
HC (N = 23)
Fiacconi et al. DLB w Capgras patient (N = 1) N Famous Face Recognition DLB with Capgras showed impairment in FER. Not measured.
(2014)
DLB w/o Capgras patient (N = 1) Fear Expression Rating These deficits were not present in DLB patient w/o
Capgras.
HC (N = 10).

Varjassyova et al. Amnesic MCI (N = 22) N Test of Facial Emotion Deficits in FER but not in FFI in patients compared to HC. Not measured.
(2013) Recognition (FER)
HC (N = 18) Famous Faces
Identification (FFI)
Mike et al. (2013) MS (N = 49) N Faces Test; Eyes Test; Faux Patients performed poorer than HC in the Faces and Eyes Poor Faces test performance correlated with thinning of
Two groups of HC (N = 24 and PasMRI Test (but not left and right fusiform face area of the fusiform gyrus
18) Faux Pas). and an area in the right entorhinal cortex. Performance
on FER and eye gazes tests correlated with T1-lesion
SOCIAL NEUROSCIENCE

load and regional of T1-lesion of association fiber

tracts interconnecting cortical regions related to visual
and emotional processing.
5

(Continued )
 6

Table1. (Continued).
Study Subjects F Tasks Behavioral findings Biomarker
Hot et al. (2013) Mild AD (N = 17) N Emotional Morphing Task Impairment of fear identification in AD patients compared Not measured.
to HC.
Young HC (N = 17) and Older HC
A. IBÁÑEZ ET AL.

(N = 17)
Donix et al. AD (N = 12) N Pictures of: Face/Place— Face recognition was associated to neural networks. Reduced bilateral superior frontal cortical activity among
(2013) HC (N = 12) Familiar/Unfamiliar fMRI AD for familiar versus unfamiliar faces and places.
Also reduced activity in the right middle orbital gyrus.
Group differences in right cerebellum when contrasting
familiar and unfamiliar faces.
Kumfor and Review N Emotion Recognition AD: ER deficits mild on early stages but worse over time. AD: Increased amygdala activity during passive view of
Piguet (2013) AD, FTD (bvFTD; SD; PNFA) Tasks BvFTD: significant ER deficits. (SD & PNFA subtypes also emotional faces (not related to ER nor to specific
PSP and HD present deficits. emotions)
HD: ER deficits for negative emotions (especially disgust). Amnestic MCI: poor FER linked to changes on the left
PSP: Deficits in emotion recognition. uncinate fasciculus on DTI.
FTD: Atrophy in frontal and temporal regions: (amygdala,
insula, orbitofrontal and medial prefrontal cortices)
associated with overall impaired of ER (bv and SD).
Premanifest HD: Ability to detect and process disgust is
related to insula integrity. Happiness and anger
recognition associated with amygdala and striatal
integrity, respectively.
Baez et al. (2013) Genetic Cockayne Syndrome N Emotional Morphing Task Difference in recognizing basic emotions of disgust and Global atrophy in the frontal structures, bilateral
(1) patient (N = 1) anger. cerebellum, basal ganglia, temporal lobe, and
occipitotemporal and occipitoparietal regions.
Klein-Koerkamp Meta-analysis: 24 studies. AD and N Emotional naming task AD patients showed significant impairment in emotional Not measured.
et al. HC Emotional selection task decoding abilities and were significantly impaired in
Emotional matching task decoding emotions regardless of the task used, the
Emotional discrimination stimuli involved, the emotion to be processed or the
task severity of the disease.
Henry et al. MS (N = 64) N FER Test Lower scores for patients in emotion FER. Not measured.
(2011) HC (N = 30)
Bediou et al. MCI (N = 10) N Facial Expression Task Mild AD patients performed worse than HC in facial Not measured.
(2009) Mild dementia (N = 10) expression.
FTD (N = 10) Facial Gender Task FTD performed worse than controls in facial expression
HC (N = 10) and gaze.
Eye Gaze Direction Task FTD and AD differed in expression detection and gaze
discrimination.
MCI showed no impairment.
Werner et al. Frontotemporal Lobar N Emotional Experience and FLD were less likely than HC to recognize that the main Greater accuracy for the fear film associated with greater
(2007) Degeneration (N = 28) Emotion Recognition lobar volumes in the left frontal, right frontal and right
temporal lobes.
Emotional Behavior No group diff. for emotional reactivity (self-reported For the sad film: Accuracy associated w. greater lobar
subjective experience) volumes in the left frontal, left temporal and right
temporal lobes.
(Continued )
Table1. (Continued).
Study Subjects F Tasks Behavioral findings Biomarker
De Renzi, Perani, Review. Prosopagnosia Patients N Matching and age One patient showed impairment in all of the face Right cerebral and occipital lesions. Signal abnormalities
Carlesimo, (N = 27) estimation of unknown recognition tests; one in detected in the temporal mesial regions.
Silveri, & Fazio, faces all but age estimation and one only on memory tests.
(1993)
Famous people (familiar Right hemisphere metabolic reduction in cortical and
or unfamiliar) deep cerebral areas (PET) that were structural
unaffected
27 reported cases of prosopagnosia and RH lesions.

Feuerriegel et al. Review (67 articles): ASD/SZBD/ N/P Facial/emotional N170/ N170 and VPP ERP components associated with FER ability. SZ: smaller amplitudes for the N170 and VPP to
(2014) AD/ADHD/Social M170/VPP emotional and no-emotional tasks. Alcohol
PhobiaDepression/Alcohol dependence, ADHD, AD, MCI, BD, Bulimia and HD
dependenceParkinson/CP/ showed smaller N170 and slower peak latencies to
BulimiaFibromialgia/HD faces. Except SZ and ASD all results using FER tasks
showed impairment in this processing.
Sachse et al. Paranoid SZ (N = 19) P FER No differences for SZ Autism: deficit in the recognition of Not measured.
(2014) High function ASD (N = 22) basic and complex emotions compared to HC and SZ.
HC (N = 20)
Baez, Marengo, et Borderline (N = 15) P Emotion Morphing No group differences for E-Morphing. Not measured.
al. (2014)
HC (N = 15) TASIT Lower scores for TASIT and difficulty w. disgust
categorization (signif. though effect of depression and
anxiety on disgust).

Aoki et al. (2014) Meta-Analysis: 13 studies. ASD P Face recognition Atypical FER in ASD compared to HC. ASD-related hyperactivation in the hypothalamus during
(N = 226) emotional face processing. Most robust finding:
hyperactivation of the left caudate. Abnormalities in
the subcortical structures, such as amygdala,
hypothalamus and basal ganglia associated w. atypical
emotional face processing in ASD. Hypoactivation in
the hypothalamus during emotional-face processing
(2013) Anorexia patients (N = 31) P Implicit facial emotion Both groups showed high accuracy on gender decision on FMRI analysis revealed a greater blood-oxygenation level
HC (N = 35) processing (IFAP) task the implicit FER task but patients with anorexia were dependent (BOLD) response in patients with anorexia
slower on the task than HC. in the right fusiform gyrus to all facial expressions.
Baez, Herrera, SZ (N = 15) P Emotional Morphing Task Poorer accuracy performance in SC for disgust, anger and Not measured.
Villarin, et al. fear.
(2013) (2)
BD (N = 15) TASIT BD performed poorer on fear and sadness recognition.
HC (N = 30) BD slower RT for disgust, surprise and sadness
Both groups performed worse than controls on TASIT but
SC
performed worse than BD
Ibanez et al. Euthymic BP (N = 13) P Dual Valence Task (angry/ No group difference found for DFT. Reduced N170 and facial emotion modulation/N170
(2012) happy—please/ analysis of facial stimuli evidenced fusiform gyrus
unpleasant)
HC (N = 13) Valence effect on accuracy found. activation: Reduced in BD.
SOCIAL NEUROSCIENCE

Schepman et al. Children and adolesc. w. P Face Emotion Task No group differences for ER. Not measured.
(2012) Depression (N = 29)
(Continued )
7
 8

Table1. (Continued).
Study Subjects F Tasks Behavioral findings Biomarker
Depression and conduct disorder Better discrimination of low intensity happy faces by
(N = 23) depressed subjects.
HC (N = 37)
A. IBÁÑEZ ET AL.

Kang et al. (2012) OCD (N = 107) P Emotional Perception Task Impaired Emotional Awareness such as lower perspective Not measured.
HC (N = 130) of face express. taking
and fantasy seeking had a perception bias toward disgust
in response
to ambiguous facial expressions in OCD patients.
Turetsky et al. SZ (N = 16) P Penn Facial Emotion Patients performed poorer in ER than HC. No group diff in P100 nor N250
(2007) HC (N = 16) Stimuli SZ exhibited smaller N170 responses
Response to neutral faces was smaller (N170)
Patients had reduced P300
Dawson et al. Review. ASD and HC. P Face recognition ASD showed impairments in face discrimination and ERP: Neural system that mediates face processing is
(2005) recognition. disrupted by age three and persist in adulthood.
Use of atypical strategies for processing faces Early (encoding) and later (representation) stages of face
characterized by processing affected
reduced attention to the eyes and piecemeal rather than impairments in perception of facial expression of
holistic strategies. emotions
Abnormal gamma band activity during processing of
upright and inverted faces suggesting decreased
perceptual binding and consistent with impairment of
holistic processing of faces/Abnormal regional brain
(fMRI) activity during face processing.
Buhlmann et al. BDD (N = 20) P Short Form of Benton BDD performed worse than HC in ER tasks. No group Not measured.
(2004) OCD (N = 20) Facial Recognition difference for face recognition. BDD were impaired in
HC (N = 20) Emotion recognition task recognizing disgusted expressions.
OCD showed an emotion recognition bias for angry
expressions.
Ellis et al. (1997) Capgras w Psychiatric Diagnostic P Recognition of familiar Capgras patients showed deficits in face processing tasks Not measured.
(N = 5) faces compared to HC, although they showed no difference in
Psychiatric Patients w/o Capgras Matching photos of SCR between familiar and unfamiliar faces.
(N = 5) unfamiliar faces
HC (N = 5) Recognition memory of
faces
Skin Conductance
Response (SCR)
Ellis et al. (1993) Capgras delusion (N = 3) P Pictures of objects and Reversal in normal asymmetry for the Capgras group in Not measured.
Paranoid SZ (N = 3) faces shown on the face recognition (HC showed left visual field advantage
HC right visual field; left and in Capgras this was reversed).
visual field and bilateral
F: Field (neurology or psychiatry). AD: Alzheimer’s disease; bvFTD:behavioral variant frontotemporal dementia; SD: semantic dementia; PNFA: progressive nonfluent aphasia; CSF: cerebrospinal fluid biomarkers; nfv-PPA: non
fluent/agrammatic nonsemantic primary progressive aphasia; lv-PPA: logopenic non-semantic primary progressive aphasia; CBS: corticobasal syndrome; NMO: neuromielitis optica; ALS: Amiotrophic lateral sclerosis; CP:
congenital prosopagnosia; MS: Multiple sclerosis; ASD: Autism spectrum disorder; DLB: Capgras syndrome in Lewy body dementia; MCI: mild cognitive impairment; SZ: schizophrenia; BD: bipolar disorder; OCD: obsessive
compulsive disorder; BDD: body dysmorphic disorder; HD: Huntington’s disease; PSP: progressive supranuclear palsy; ADHD: Attention deficit hyperactivity disorder; HC: healthy controls; FER: facial emotion recognition; ER:
emotion recognition; TASIT: The Awareness of Social Inference Test; VBM: voxel-based morphometry; DTI: diffusion tensor imaging; SCR: skin conductance response.

respectively. Moreover, relatively similar affectation of
early brain markers of FER is observed across psychiatric
conditions (Ibanez et al., 2014).
FER dysfunctions are ubiquitously observed across
neurological and psychiatric conditions (Table 1).
Across individuals and patient groups, dimensional dif-
ferences are observed in various stimulus-related (arou-
sal, valence, types of emotions) and performance-
related (accuracy, reaction times) variables. Similarly,
imaging results show different degrees of damage in
relevant neural hubs (fusiform, amygdala, insula), while
electromagnetic techniques evidence alterations in
either early or late brain dynamics (Ibanez et al.,
2012). These dimensional differences are transnosologi-
cally observed within and across neurological and psy-
chiatric diseases. Also, the deficits in question may
involve similar (e.g., N170 amplitude/latency alterations)
as well as differential (neurodegeneration, focal lesions,
aberrant connectivity) mechanisms. No empirical com-
parisons of these dimensions are available across con-
ditions and related neural mechanisms, reducing the
chances of developing multilevel models addressing
different outcomes. Moreover, little is known about
how similar FER deficits impacts everyday behaviors
across conditions. Thus, future research is required to
integrate behavioral and cerebral measures of FER with
clinical associations across diseases.
Empathy
Empathy is the ability to understand and experience
other people’s emotional states (Decety & Jackson,
2004). Some research programs distinguish between
affective and cognitive empathy. The former (which
usually includes empathic concern and personal dis-
tress) refers to the ability to adequately express or
recognize emotions in response to others’ mental
states. Cognitive empathy, sometimes identified with
ToM (see below), refers more specifically to the capacity
to imagine and understand others’ perspectives or
mental states. Several cognitive and affective functions
are involved in this process, which engages the insula,
the somatosensory cortex, the periaqueductal gray, and
the anterior cingulate cortex (ACC) (Decety & Jackson,
2004; Decety & Lamm, 2006; Jackson, Rainville, &
Decety, 2006; Melloni, Lopez, & Ibanez, 2013). The
amygdala and related frontotemporal networks are cri-
tical for the detection of intentional harm in empathy-
for-pain paradigms (Hesse et al., 2016). Empathy is one
of the most widely compromised social cognition
domains across a range of neurodegenerative (Rankin
et al., 2006), cerebrovascular (Leigh et al., 2013), psy-
chiatric (Derntl, Seidel, Schneider, & Habel, 2012), and
SOCIAL NEUROSCIENCE 9
neurodevelopmental (Baron-Cohen, 2009) conditions
(Table 2).
Empathy deficits are noteworthy and consistent in
bvFTD (Baez & Ibanez, 2014b; Eslinger, Moore,
Anderson, & Grossman, 2011; Lough et al., 2006;
Rankin et al., 2006; Rankin, Kramer, & Miller, 2005),
which involves atrophy in frontotemporal networks
extending throughout the above structures (Cerami
et al., 2014b; Eslinger et al., 2011; Rankin et al., 2005).
Loss of empathy in this population has been related
to early impairment in social functioning (Piguet
et al., 2011). Suggestively, core (affective) deficits in
empathic concern appear to be unrelated to execu-
tive dysfunction (Baez & Ibanez, 2014b) and triggered
by regions of early atrophy, such as the OFC and the
amygdala (Baez et al., 2016).
Research on other neurological conditions (Table 2)
largely supports a network-based conceptualization of
empathy (Cerami et al., 2014a; Kraemer et al., 2013;
Leigh et al., 2013; Narme et al., 2013; Rankin et al.,
2006; Shamay-Tsoory, Tomer, Goldsher, Berger, &
Aharon-Peretz, 2004). For instance, cognitive and
affective empathy are doubly dissociated following
lesions to the ventromedial prefrontal cortex
(vmPFC) and the inferior frontal gyrus, respectively
(S. G. Shamay-Tsoory, Aharon-Peretz, & Perry, 2009).
Similarly, a comparison among neurodegenerative
conditions (Rankin et al., 2005) suggests that affective
empathy is likely mediated by temporal structures,
whereas cognitive empathy is partially mediated by
frontal structures. These studies align with previous
evidence in showing that several neuroanatomical loci
play a role in this vast functional network (Kennedy &
Adolphs, 2012).
Empathy impairments have also been reported innu-
merous psychiatric disorders (Table 2), such as SZ
(Derntl et al., 2009; McCormick et al., 2012; Montag,
Heinz, Kunz, & Gallinat, 2007), BD (Cusi, Macqueen, &
McKinnon, 2010; Seidel et al., 2012; Shamay-Tsoory,
Harari, Szepsenwol, & Levkovitz, 2009), and ASD (Baez
& Ibanez, 2014a; Baez et al., 2012; Baron-Cohen &
Wheelwright, 2004; Dziobek et al., 2008). Despite the
variability in associated neural abnormalities (Derntl
et al., 2012; Di Martino et al., 2009; Fakra, Salgado-
Pineda, Delaveau, Hariri, & Blin, 2008; Gur et al., 2007;
Habel et al., 2010; Pugliese et al., 2009), they rely on a
partially shared network. For example, studies on SZ
point to abnormal frontoinsular-temporal systems as a
key correlate of empathy deficits (Benedetti et al., 2009;
Lee et al., 2010). Such impairments can be tapped
through ecological methods involving implicit cues,
which more closely replicate real-life settings (Baez,
Herrera, Villarin, et al. 2013; Torralva et al., 2012).
 10

Table 2. Empathy in neurological and psychiatric conditions.

Study Subjects F Task Behavioral findings Biomarker
Jiang et al. (2014) Idiopathic generalized N Interpersonal Reactivity Index and eye emotion Impaired eye emotion recognition and cognitive Not measured.
epilepsy (N = 42); controls recognition tasks. empathy abilities. Preserved affective empathy.
(N = 47)
Baez and BvFTD (N = 37); controls N Empathy-for-pain task. Deficits in affective cognitive and moral aspects of Not measured.
Ibanez (2014b) (N = 30) empathy. Empathic concern was the only aspect
not related to deficits in EFs or other social
cognition domains.
A. IBÁÑEZ ET AL.

Yeh and Tsai (2014) Stroke patients (N = 34); N Verbal and nonverbal empathy tasks. On the subscale of cognitive empathy, the right Not measured.
controls (N = 40) stroke group had poorer performance on
perspective-taking.
Fujino et al. (2014) MDD (N = 11); controls P Videos showing human hands in painful Lower pain ratings for the painful videos. Reduced cerebral activation (fMRI) in the left
(N = 11) situations. Subjective pain ratings. middle cingulate cortex and the right
somatosensory-related cortices. Greater
cerebral activation in the left inferior frontal
gyrus.
Corbera, Ikezawa, Bell, SZ (N = 19); controls (N = 18) P Pictures. Subjective ratings. Empathic self-reports. Lower ratings of perspective taking and higher Decreased responses to pictures of others in pain
& Wexler, (2014) ratings of personal distress related to decreased (EEG/ERP). Decreased modulation by attention
modulation of late-cognitive empathic of late-cognitive ERPs related to behavioral
responses. deficits.
Abu-Akel, Fischer- SZ (N = 28); controls (N = 27) P Pain evaluation task with oxytocin administration. Absence of empathy bias toward conflictual out- Not measured.
Shofty, Levkovitz, group members.
Decety, & Shamay-
Tsoory, (2014)
Schroeter et al. (2008) BvFTD (N = 417); Controls N Meta-analysis. Anatomical and activation Empathy processing impairments. Compromised networks were associated with
(N = 408) likelihood estimates. emotion and reward processing, empathy, and
executive functions (mainly inhibition)
Cerami et al. (2014b) BvFTD (N = 18); controls N Intention attribution and emotion attribution Intention attribution and emotion attribution Emotion attribution correlated with gray-matter
(N = 36) using non-verbal test. impairments. reduction in the right amygdala, left insula,
and posterior-superior temporal sulcus.
Cerami et al. (2014a) ALS (N = 20); controls (N = 56) N Attribution of emotional versus cognitive states in Defective emotional empathy attribution. Deficit correlated with reduced grey-matter
comic strips. density in the anterior cingulate cortex and
right inferior frontal gyrus.
Kraemer et al. (2013) RRMS (N = 25); controls N Baron-Cohen’s Empathy Quotient Significantly lower level of empathy in the self- Not measured.
(N = 25) rating questionnaire.
Narme et al. (2013) PD (N = 23); controls (N = 46) N Interpersonal Reactivity Index PD patients showed lower levels of empathy Not measured.
Leigh et al. (2013) Stroke patients (N = 27); N Videos and stories. Impairment in affective empathy. Acute impairment of affective empathy was
controls (N = 24) associated with infarcts in the temporal pole
and anterior insula.
Wojakiewicz, Januel, SZ (N = 29); controls (N = 27) P Sensitivity to expressions of pain (STEP) test. Pain Significant differences in all three measures. Not measured.
Braha, Prkachin, Video. Situational pain questionnaire (SPQ)
Danziger, &
Bouhassira, (2013).
Driscoll, Dal Monte, Vietnam combat veterans N Balanced Emotional Empathy Scale. Diminished emotional empathy. Voxel-based lesion-symptom mapping revealed
Solomon, Krueger, & with focal penetrating damage in ventrolateral prefrontal cortex, left
Grafman, (2012) traumatic brain injuries and right temporal lobes, and insula, was
(N = 192); Non-injured associated with diminished emotional
veterans (N = 54) empathy.
Kang et al. (2012) OCD (N = 107); controls P Interpersonal Reactivity Index, Toronto Lower perspective taking, and higher personal Not measured.
(N = 130) Alexithymia Scale-20 and emotional perception distress, and higher alexithymia.
task of face expression.
McCormick et al. SZ (N = 25); controls (N = 22) P Interpersonal Reactivity Index and hand Higher affective empathy driven by personal Actively psychotic participants showed
(2012) movement observation task. distress subscale. significantly greater mu suppression over the
sensorimotor cortex (EEG). Abnormal “mirror”
activity was positively correlated with
psychotic symptoms.
(Continued )
Table2. (Continued).
Study Subjects F Task Behavioral findings Biomarker
Seidel et al. (2012) BD (N = 21); first-degree P Facial Identities, scenes showing social interaction, Significantly lower scores in patients for emotion Not measured.
relatives (N = 21); controls short written sentences describing situations, recognition and affective responsiveness.
(N = 21) and Interpersonal Reactivity Index
Baez et al. (2012) ASD (N = 15); controls P Empathy-for-pain task and Interpersonal Reactivity ASD scored higher on PD subscale and lower on PT Not measured.
(N = 15) Index (IRI) of IRI. ASD rated the intentional pain situations
with lower scores. No difference between scores
for intentional and accidental harm situations
(expected for controls).
Derntl, Finkelmeyer, et SZ (N = 15); controls (N = 15) P Questionnaire Measure of Emotional Empathy, the Significant empathic deficits in patients, reflected Hypoactivation in a fronto-temporoparietal
al. (2012) German Questionnaire for Assessment of in worse performance in all three domains: network including the amygdala in patients
Empathy, Social Attitude and Aggression, and emotion recognition, perspective-taking, and (fMRI). Moreover, amygdala activation
the Interpersonal Reactivity Index. Facial affective responsiveness. correlated negatively with severity of negative
Identities, Scenes showing social interaction, symptoms.
short written sentences describing situations.
Derntl, Finkelmeyer, et SZ (N = 24); BD (N = 24); + 24 P Facial identities depicting five basic emotions, SZ showed the strongest impairment in empathic Not measured.
al. (2012) MDD (N = 24); controls pictures depicting scenes showing social performance followed by BD, while MDD
(N = 24) interaction and short written sentences performed similar to controls, except for
describing real-life situations. affective responsiveness.
Eslinger et al. (2011) FTD (N = 26); controls N Interpersonal Reactivity Index BvFTD patients were significantly impaired on VBM revealed that reduced empathic
(N = 16) caregiver assessments of empathy, although perspective-taking was related to bilateral
self-ratings were normal. frontal and left anterior temporal atrophy,
whereas empathic emotions were related to
right medial frontal atrophy.
Cusi et al. (2010) BD (N = 20); controls (N = 20) P Interpersonal Reactivity Index and the Social Reduced perspective taking and higher personal Not measured.
Adjustment Scale Self-Report distress. Altered affective empathic abilities
correlated with reduced psychosocial
functioning and with increased symptom
severity.
Chen, Chen, Decety, Healthy participants from Visual stimuli depicting body parts being injured Older adults reported less dispositional emotional The response in anterior insula and anterior mid-
and Cheng (2014) three age groups (N = 65). and Interpersonal Reactivity Index empathy and their unpleasantness ratings were cingulate cortex showed an age-related
more sensitive to intentional harm. decline (fMRI).
Shamay-Tsoory, Harari, Stroke patients, ventromedial N Interpersonal Reactivity Index Patients with ventromedial lesions were impaired Not measured.
et al. (2009) lesions (N = 11); inferior in cognitive empathy compared to the HC and
frontal gyrus lesions other patient groups. Patients with IFG lesions
(N = 8); posterior lesions were impaired in emotional empathy compared
(N = 11); controls (N = 34) to the HC and the PC group.
Minio-Paluello, Baron- ASD (N = 16); neurotypical P Single-pulse transcranial magnetic stimulation Not measured. Contrary to controls, no amplitude reduction of
Cohen, Avenanti, controls (N = 20). during observation of painful and nonpainful motor-evoked potentials (EEG-ERP).
Walsh, & Aglioti, stimuli affecting another individual.
(2009)
Derntl et al. (2009) SZ (N = 24); controls (N = 24) P Facial identities, scenes showing social interaction Significant empathic deficits in patients, reflected Not measured.
and short written sentences describing in worse performance in emotion recognition,
situations. perspective taking and affective responsiveness
Questionnaire Measure of Emotional Empathy, as well as self-report empathy questionnaires.
German Questionnaire for Assessment of
Empathy, Social Attitude and Aggression, and
SOCIAL NEUROSCIENCE

Interpersonal Reactivity Index

Dziobek et al. (2008) ASD (N = 17); controls P Multifaceted Empathy Test Impairment in cognitive empathy. Not measured
(N = 18)
Montag et al. (2007) SZ (N = 45); controls (N = 45) P Interpersonal Reactivity Index Significantly lower scores in cognitive empathy. Not measured.
11

(Continued )
 12 A. IBÁÑEZ ET AL.

Investigations in both neurological and psychiatric

F: Field (neurology or psychiatry); SZ: schizophrenia; bvFTD: behavioral variant frontotemporal dementia; MS: Multiple sclerosis; SD: semantic dementia; BD: bipolar disorder; OCD: obsessive compulsive disorder; ASD: Autism
gyrus correlated with empathy score. Empathy

temporal structures in SD, and with subcallosal

score correlated positively with volume of right

AS activated the frontotemporal regions but not

Voxels in the right temporal pole, right fusiform
disorders point to a complex network subserving empa-

gyrus, right caudate, and right subcallosal

thy processing. Different dimensions (empathic con-

the amygdala when making mentalistic

cern, perspective taking, distress, intentionality) are

inferences from the eyes (fMRI).

affected to varying degrees across disorders and related
to different and distributed regions of the empathizing
Biomarker

gyrus volume in FTD. network. Moreover, other aspects of empathy, such as

the distinctions between cognitive and affective or
explicit and implicit dimensions, are not well character-
Not measured.

FTD and SD showed lower levels of empathy than Not measured.

Patients with prefrontal lesions and patients with Not measured.

Not measured.
ized at transnosological level. Thus, despite the initial
step showing pervasive impairment of this function
across neurological and psychiatric conditions, further

spectrum disorder; MDD: major depressive disorder; AD: Alzheimer’s disease; HD: Hungtington’s disease; PD: Parkinson’s disease; RRMS: Relapsing remitting multiple sclerosis.
right parietal lesions were significantly impaired
research is required to tackle the above constructs
transnosologically.
showed disruption of cognitive empathy only.
both emotional and cognitive empathy. FTDs
Lower empathy scores for FTD and SD patients.

either ADs or NCs. SDs showed disruption of

in both cognitive and affective empathy.

Reduced empathy as rated by caregivers.

Theory of mind
Behavioral findings

The ability to infer other people’s mental states is

Significantly lower scores for AS.

Significantly worse performance.

known as ToM (Premack & Woodruff, 1978). It impli-

cates several areas, including the medial prefrontal cor-
tex (PFC), the bilateral temporoparietal junction, and
the medial parietal cortex. ToM tasks involve various
levels of complexity and recruit several cognitive pro-
cesses (Ahmed & Stephen Miller, 2011). For example,
the Reading-the-Mind-in-the-Eyes Test only requires
identifying an emotional state associated to a gaze;
instead, the faux pass test is considerably more
N Questionnaire Measure of Emotional Empathy

ASD (N = 6); controls (N = 12) P Inference of mental states with photographs.

FTD (N = 18); SD (N = 19); AD N Interpersonal Reactivity Index by first-degree

(QMEE) and Interpersonal Reactivity Index

demanding, as it engages the ability to implicitly inte-

grate cognitive inferences about mental states together
with emotion understanding (Stone, Baron-Cohen, &
Knight, 1998).
N Empathy reports by caregivers.
N Interpersonal Reactivity Index
Task

ToM is especially relevant for the clinical character-

ization and prognosis of bvFTD, as it is more impaired
in this disease (Gregory et al., 2002; Henry, Phillips, &
P Empathy quotient

Von Hippel, 2014) than in other neurodegenerative

relatives.

conditions (J. D. Henry, Phillips, Crawford, Ietswaart, &

Summers, 2006). BvFTD patients have difficulties infer-
ring others’ intentions (cognitive ToM) and emotional
states (affective ToM) (Gregory et al., 2002; Schroeter,
F

PNFA (N = 8); AD (N = 38);

CBD (N = 15); PSP (N = 6);

Raczka, Neumann, & Von Cramon, 2008). These deficits

(N = 16); controls (N = 10)

lesions (N = 15); controls

lesions (N = 36); parietal
FTD (N = 30); SD (N = 26);

Stroke patients, prefrontal

may reflect damage to the frontomedian network

BvFTD (N = 18); controls

ASD (N = 90); controls

(including the anterior PFC, the ACC, the subcallosal/

controls (N = 20)
Subjects

septal area, and the gyrus rectus) (Bruning, Konrad, &

Herpertz-Dahlmann, 2005; Couto et al., 2013), altera-
(N = 13)

(N = 19)

(N = 90)

tions in the anterior medial frontal cortex—Brodmann

areas (BAs) 9 and 32—hypometabolism in the right
lateral PFC (Le Bouc et al., 2012), and perfusion in the
Table2. (Continued).

Wheelwright, (2004)

left rostral medial PFC (BA 10) (Bertoux, Volle, et al.

Shamay-Tsoory et al.
Rankin et al. (2006)

Rankin et al. (2005)

Lough et al. (2006)

Baron-Cohen et al.

2014).
Baron-Cohen &

ToM impairments are also pervasive in other neuro-

logical conditions such as semantic dementia, temporal
(2004)

(1999)
Study

lobe epilepsy (Hennion et al., 2014), MS (Roca et al.,

2014), focal brain lesions, and Parkinson’s disease

(Poletti, Vergallo, Ulivi, Sonnoli, & Bonuccelli, 2013).
Notably, AD patients feature impairments in the most
complex levels of ToM—correlated with hypometabo-
lism in the left temporoparietal junction (Le Bouc et al.,
2012), with preservation of intermediate and simple
levels (Castelli et al., 2011). Similar deficits are observed
in stroke patients with temporal and medial frontal
damage (Duval et al., 2012).
Psychiatric conditions also involve ToM deficits. This
is true of non-remitted and remitted patients diagnosed
with SZ (Bora, Yucel, & Pantelis, 2009; Brune, 2005;
Harrington, Siegert, & McClure, 2005; Huepe et al.,
2012; Sprong, Schothorst, Vos, Hox, & Van Engeland,
2007) and BD (Samamé, Martino, & Strejilevich, 2012;
Van Rheenen & Rossell, 2013). ASD individuals are not
the exception (Yirmiya, Erel, Shaked, & Solomonica-Levi,
1998), although their impairments may be limited to
implicit aspects of the domain (Schneider, Slaughter,
Bayliss, & Dux, 2013). Complex ToM abilities are com-
promised in other conditions such as OCD (Sayın, Oral,
Utku, Baysak, & Candansayar, 2010). Social anxiety dis-
order patients stand apart from the previous popula-
tions in that they attribute greater emotional content
and meaningfulness to others’ mental states than con-
trols (Hezel & McNally, 2014). Finally, context-sensitive
tasks have revealed subtle ToM impairments in psycho-
paths (Sharp & Vanwoerden, 2014) and BPD patients
(Preissler, Dziobek, Ritter, Heekeren, & Roepke, 2010). In
the latter population, such deficits are partially
explained by an incapacity to integrate social cues
(Baez et al., 2014, Baez & Ibanez, 2014b).
ToM impairments figure prominently in various neuro-
logical and psychiatric diseases (Table 3). At a dimensional
level, complex or high-order ToM deficits are more
extended than those affecting basic ToM abilities.
Although the latter are usually affected in very severe
conditions, they are sometimes preserved after focal
stroke, early stage neurodegeneration or even diffuse
alterations, including connectivity aberrations. Also, these
basic levels tend to be more affected in conditions with
strong and extended social cognition impairments (e.g.,
bvFTD, SZ) than in those conditions with more restrictive
social impairments (e.g., PD, AD, OCD). Similarly, implicit
ToM tasks which depend on more extended brain net-
works are often more sensitive than explicit paradigms
across neuropsychiatric conditions. Besides, the review
shows that different pathophysiological mechanisms can
originate these deficits. Not only core (e.g., direct compro-
mise following lesions or atrophy of prefrontal or temporal
regions) but also distributed or unspecific brain distur-
bances can induce ToM impairments. Similarly, different
affective (e.g., empathy) and cognitive (e.g., intelligence)
domains impacts in ToM performance (Ibanez et al., 2013).
SOCIAL NEUROSCIENCE 13
Also, complex ToM skills are more sensitive to impairments
in non-social mechanisms such as language or executive
functions. Regarding the multiple neural mechanisms of
ToM subtypes (emotional, cognitive, high-level mentaliz-
ing, irony, figurative language, perspective taking), more
systematic research is needed. Dimensional and transno-
sological comparisons across ToM components and asso-
ciated neural substrates are also missing.
Moral judgment
Morality can be defined as the code of values and
customs conventionally accepted within a social group
(Marazziti, Baroni, Landi, Ceresoli, & Dell’Osso, 2013).
Moral cognition consists in using such codes to guide
culturally adequate social behavior (Moll, Zahn, De
Oliveira-Souza, Krueger, & Grafman, 2005), by virtue of
cognitive, emotion-related, and ToM processes (Decety
& Howard, 2013; Decety, Michalska, & Kinzler, 2012).
These domains converge, for example, in the passing
of moral judgment (Anderson, Bechara, Damasio,
Tranel, & Damasio, 1999), via both cortical (OFC, ante-
rior PFC, dorsolateral PFC, vmPFC, anterior temporal
lobes, superior temporal sulcus) and subcortical (amyg-
dala, ventromedial hypothalamus, septal area and
nuclei, basal forebrain) structures (Moll et al., 2005).
Moral judgment is typically impaired in bvFTD
patients (Lough et al., 2006), who lack moral emotional
reactions, favor utilitarian decisions in personal dilem-
mas, and approve emotion-guided moral violations
(Mendez, Anderson, & Shapira, 2005; Mendez &
Shapira, 2009). Moreover, these patients have difficulty
inferring the intentionality of others’ actions (Baez et al.,
2014, 2016), and tend to base their moral decisions
exclusively on outcomes rather than on the integration
of intentions and outcomes (Baez et al., 2014). This
impairment is triggered by atrophy of extended net-
works (but not focalized regions) implicated in moral
processing (Baez et al., 2015). In healthy participants,
moral judgment tasks engage areas comprised by FTD
atrophy such as the lateral OFC and the medial PFC
(during transgressions of social norms) (Berthoz,
Armony, Blair, & Dolan, 2002) and the posterior cingu-
late gyrus, the amygdala, and the vmPFC (in moral
dilemma solving) (J. D. Greene, Nystrom, Engell,
Darley, & Cohen, 2004; Greene, Sommerville, Nystrom,
Darley, & Cohen, 2001).
Deficits in moral judgment are pervasive across neu-
rological conditions. Subsequent to vmPFC damage,
stroke patients fail to generate skin conductance
responses before endorsing personal moral violations
(Ciaramelli, Muccioli, Làdavas, & Di Pellegrino, 2007;
Moretto, Làdavas, Mattioli, & Di Pellegrino, 2010). In
 14

Table 3. Moral cognition in neurological and psychiatric conditions.

Study Subjects F Tasks Behavioral findings Biomarkers
Baez and Ibanez BvFTD (N = 37) and HC (N = 30) N Animated scenarios that involves BvFTD (a) rated neutral situations as more incorrect than HC Not measured.
(2014) the perception of intentional and rated neutral situations higher than controls; (b)
and accidental harm presented deficits in moral aspects of empathy.
Baez et al. (2014) PFC damage (N = 8), bvFTD N Moral judgment task (a) Differences in attempted harm between patients and HC; No differences in patients with vmPFC stroke, other frontal
(N = 19) and HC (N = 37) (b) differences in accidental harm between bvFTD and HC. stroke or frontotemporal atrophy.
Njomboro et al. Neurological damage with N Moral sense test—foreseen and (a) Intended harm: significant differences between patients Not measured.
A. IBÁÑEZ ET AL.

(2014) apathy symptoms (N = 7) intended harm dimensions with apathy, HC and patients without apathy; (b) Foreseen
and without apathy harm: significant differences between HC and patients
symptoms (N = 7) and HC with apathy.
(N = 17)
Beauchamp et al. Mild-to-Severe TBI (N = 25) and N So-Moral and So-Mature (a) TBI had significantly lower levels of moral reasoning Not measured.
(2013) Typically-developing peers maturity; (b) empathy correlated positively with moral
(N = 66) reasoning abilities.
Gleichgerrcht, BvFTD (N = 22) (13—NO group, N Personal moral dilemmas BvFTD patients who performed utilitarian responses (YES Not measured.
Ibanez, Roca, 9—YES group) group) in front of high-emotional scenarios showed
Torralva, & significantly lower scores on affective ToM relative to
Manes, (2010) those bvFTD patients who did not (NO group).
Calder et al. HD (N = 19) and HC (N = 14) N Photographs of a male or female The HD patients show the largest discrepancy from HC for Not measured.
(2010) model (select which emotional scenarios relating to upper lip curl, the face linked more
expression constituted the most to moral disgust.
appropriate facial reaction)
Miller et al. Anterior-Resected (N = 3), N Reasoning task that required verbal Full and partial callosotomy patients based their moral Not measured.
(2010) complete callosotomy moral judgments judgments primarily on actions “outcomes, disregarding
patients (N = 3) and HC agents” beliefs.
(N = 22)
Young et al. Bilateral vmPFC damage N Moral dilemmas vmPFC patients: (a) judged attempted harms, including Not measured.
(2010) (N = 9), brain damage attempted murder, as more morally permissible relative to
(N = 7) and HC (N = 8) HC; (b) judged attempted harms as more permissible than
accidental harms.
Mendez and FTD (N = 21), AD (N = 21) and N Moral dilemmas (reasoned and FTD patients: (a) retention of knowledge for moral behavior Among the FTD patients, the altered moral judgments
Shapira (2009) HC (N = 21) emotional) and the ability to make reasoned moral judgments; (b) corresponded to right hemisphere frontotemporal
were altered in their ability to make emotional moral involvement (functional neuroimaging).
judgments.
Moretto et al. vmPFC bilateral focal damage N Moral dilemmas and skin vmPFC patients approved more personal moral violations vmPFC patients failed to generate SCRs before endorsing
(2010) (N = 8), damage sparing FC conductance response (SCR) than did HC. personal moral violations; SCRs correlated negatively
(N = 7) and HC (N = 18) with the frequency of utilitarian judgments in normal
participants.
Ciaramelli et al. vmPFC damage (N = 7) and HC N Moral dilemmas (personal and VmPFC patients were more willing to judge personal moral Not measured.
(2007) (N = 12) impersonal) and non-moral violations as acceptable behaviors in personal moral
dilemmas dilemmas, and they did so more quickly.
Koenigs et al. Bilateral, adult-onset vmPFC N Moral dilemmas (high and low Significant differences emerged for the high-conflict Not measured.
(2007) damage (N = 6), brain conflict scenarios) scenarios: The vmPFC group was more likely to endorse
damage (N = 12) and HC the proposed action than either the HC or brain damage
(N = 12) group, with no difference between the HC and brain-
damage participants.
Lough et al. FvFTD (N = 18) and HC (N = 13) N The Moral/Conventional distinction FvFTD patients: (a) moral reasoning was defective; (b) Not measured.
(2006) task executive function was impaired in this group, and
compromised aspects of moral reasoning.
(Continued )
Table3. (Continued).
Study Subjects F Tasks Behavioral findings Biomarkers
Mendez et al. FvFTD (N = 26), AD (N = 26) N Inventory of moral knowledge and FTD patients were impaired in their ability to make Not measured.
(2005) and HC (N = 26) moral dilemmas immediate, emotionally based moral judgments
compared with the patients with AD and the HC subjects.
Anderson et al. Early PFC (N = 2) damage, N Moral dilemmas and social The two patients had defective social and moral reasoning. Not measured.
(1999) adult-onset PFC damage situations Thus early-onset PFC resulted in a syndrome resembling
(N = 6) and HC (N = 7) psychopathy.
Bear (1979) Right focal TE (N = 15), left N Five questionnaire items, true–false Some TLE patients exhibit hypermoralism, religiosity and Not measured.
focal TE (N = 12), contrasted in five questionnaire items, true– excessive rumination over the social consequences of
HC (N = 12) and severe false in format actions.
Neuromuscular or ND (N = 9)
Carmona-Perera Alcohol-dependent individuals P Moral judgment task Alcohol-dependent individuals: (a) were more likely to Not measured.
et al. (2014) (N = 31) and HC (N = 34) endorse utilitarian choices in personal moral dilemmas; (b)
poorer decoding of fear and disgust significantly
predicted utilitarian biases in personal moral dilemmas.
Epa, Czyzowska, BD patients (N = 43) and HC. P Defining Issue Test (DIT) BD patients: (a) significantly less often than HC chose Not measured.
Dudek, Siwek, (N = 43) answers indicating the post-conventional thinking; (b)
& Gierowski, patients in mania less often than persons in euthymia
(2014) chose answers indicating the final stage of moral thinking.
Escobar et al. ESD individuals (n19) and P Intentional Inference Task No significant differences between groups on externalizing ESD: (a) atypical early and late frontal cortical markers
(2014) Controls non-adopted and internalizing problems and no between-group associated with attribution of intentionality; (b) reduced
adolescents (N = 18) differences were observed in accuracy measure. activity in the right prefrontal cortex and insula and
bilaterally in vmPFC.
Verdejo-Garcia Cocaine-dependent individuals P Moral dilemmas Cocaine-dependent and HC subjects provided similar Cocaine-dependent subjects: (a) reduced activation
et al. (2014) (N = 10) and nondrug using responses to moral dilemmas, as both study groups did involving frontolimbic structures: (b) less resting-state
controls (N = 14) not differ in the proportion of positive and negative functional connectivity between ACC, thalamus, insula,
responses. and brain stem.
Whitton et al. OCD (N = 23), non-OCD anxiety P Moral dilemmas: benign, OCD: (a) fewer utilitarian responses to impersonal moral Not measured.
(2014) (N = 21) and HC (N = 24) impersonal, personal dilemmas; (b) poorer cognitive flexibility was associated
with fewer utilitarian responses to impersonal dilemmas;
(c) greater trait disgust was associated with increased
utilitarian responding to personal dilemmas.
de Achával et al. SZ patients (N = 13), unaffected P Deontological or utilitarian All participants made the same proportion of utilitarian and Brain activation induced by moral decisions was different
(2013) siblings (N = 13) and HC decisions deontological decisions. in HC, SZ patients, and nonpsychotic siblings in regards
(N = 13) to areas directly concerned with emotion processing.
Gleichgerrcht HFA/AS adults (N = 36) and HC P Moral dilemmas with low and high (a) HFA/AS participants more frequently delivered the Not measured.
et al. (2013) (N = 36) emotional saliency utilitarian judgment; (b) utilitarian HFA/AS participants
showed a decreased ability to infer other people’s
thoughts and to understand their intentions.
Khemiri et al. Alcohol-dependent individuals P Moral dilemmas (personal and AD patients generated increased utilitarian moral judgment Not measured.
(2012) (N = 20) and HC (N = 20) impersonal) and non-moral compared to controls when faced with moral personal
dilemmas dilemmas.
Koenigs et al. Low-anxious psychopaths P Moral dilemmas (a) Both groups of psychopaths were significantly more likely Not measured.
(2012) (N = 12), high-anxious to endorse the impersonal actions; (b) only the low-
psychopaths (N = 12) and HC anxious psychopaths were significantly more likely to
(N = 12) endorse the personal harms when commission of the
harm would maximize aggregate welfare-the “utilitarian”
SOCIAL NEUROSCIENCE

choice.
(Continued )
15
 16
A. IBÁÑEZ ET AL.

Table3. (Continued).
Study Subjects F Tasks Behavioral findings Biomarkers
Pujol et al. (2012) Criminals psychopaths (N = 22) P Moral dilemmas Psychopathic individuals and control subjects provided (a) The network subserving moral judgment is underactive
and HC (N = 22) similar responses to most moral dilemmas; the responses in psychopathic individuals during moral dilemma
were all in the same direction psychopaths were more situations; (b) a baseline network alteration with a
likely to endorse the harmful action. functional disconnection between emotional and
cognitive elements that jointly construct moral
judgment.
Zalla et al. (2011) HFA/AS (N = 20) and HC P Transgression scenarios followed HFA/AS failed to distinguish moral and disgust Not measured.
(N = 33) by questions about transgressions along the seriousness dimension and were
permissibility, seriousness, unable to provide appropriate welfare based moral
authority contingency and justifications.
justification
Franklin et al. OCD (N = 20) and HC (N = 18) P Moral dilemmas OCD: The higher patients’ scores on the Responsibility Not measured.
(2009) Attitude Scale, the less likely they were to act to kill one
person to save the lives of others.
Takeda et al. HFPDD students (N = 23)(6– P Human External Action and its HFPDD scored significantly lower on Internal Moral Not measured.
(2007) 14 years old) and HC internal Reasoning Type (HEART) Reasoning than control students.
students (N = 23)
Blair (1995) Psychopaths (N = 10) and HC P Moral stories used to measure the Psychopaths fail to make the moral/conventional distinction Not measured.
(N = 10) moral/conventional distinction and they are significantly less likely to make reference to
the welfare of others.
Benson (1980) SZ (N = 40) and HC (aged P Kohlberg Moral Judgment SZ scored lower than controls on all measures. Not measured.
14–26) Interview
Campagna and 44 (normal and sociopathic P Kohlberg’s Moral Development Level of moral reasoning was higher for normal than for Not measured.
Harter (1975) children) Interview sociopathic children at both mental age levels.
F: Field (neurology or psychiatry); SZ: schizophrenia; bvFTD: behavioral variant frontotemporal dementia; fvFTD frontal variant frontotemporal dementia; MS: Multiple sclerosis; SD: semantic dementia; BD: bipolar disorder; OCD:
obsessive compulsive disorder; ASD: Autism spectrum disorder; HFA/AS: high-functioning autism/Asperger’s syndrome; MDD: major depressive disorder; AD: Alzheimer’s disease; HD: Huntington’s disease; PD: Parkinson’s
disease; RRMS: Relapsing remitting multiple sclerosis; HFPDD: high-functioning pervasive developmental disorder; PFC: prefrontal cortex; TBI: traumatic brain injury; VM: ventromedial; ESD: early social deprivation; FC: frontal
cortex. TE: temporal epilepsy; ND: neuropathic disorder.

addition, when judging harmful intent, these patients
base their moral judgments preferentially on action
outcomes (Baez & Ibanez, 2014; Young et al., 2010).
Although many studies have emphasized the role of
the vmPFC in intuitive/affective moral judgment, similar
impairments are observed following frontal stroke, with
or without vmPFC involvement (Baez et al., 2014;
Njomboro, Humphreys, & Deb, 2014; Young et al.,
2010) or partial callosotomy (M. B. Miller et al., 2010).
In neurodegenerative diseases such as HD, impairments
in recognizing facial expressions correlate with viola-
tions of socio-moral norms (Calder et al., 2010) and
moral emotions (e.g., schadenfreude) are also affected
(Baez et al., 2016). During normal brain ontogeny, early
PFC lesions compromise the development of moral
skills (Anderson et al., 1999); indeed, children with trau-
matic brain injury evince immature socio-moral reason-
ing (Beauchamp, Dooley, & Anderson, 2013).
Similar impairments in moral judgment have also
been observed in psychiatric disorders. Psychopaths
fail to make the moral/conventional distinction (Blair,
1995) and more frequently endorse utilitarian choices
when facing personal dilemmas (Koenigs, Kruepke,
Zeier, & Newman, 2012). The same occurs in individuals
with addictions (Carmona-Perera, Clark, Young, Pérez-
García, & Verdejo-García, 2014; Khemiri, Guterstam,
Franck, Jayaram-Lindström, & García, 2012). Such pat-
terns are related to functional alterations in the PFC and
other regions (Koob & Volkow, 2010; Verdejo-Garcia
et al., 2014). Adults with ASD judge conventional and
disgust transgressions as more serious than do controls,
while failing to distinguish between disgust and moral
transgressions (Moran et al., 2011; Zalla, Barlassina,
Buon, & Leboyer, 2011). They also favor utilitarian judg-
ments in moral dilemmas tasks (Gleichgerrcht et al.,
2013) and show a dissociation between moral knowl-
edge and moral judgment. The opposite pattern has
been observed in OCD (Franklin, McNally, & Riemann,
2009). Furthermore, immature moral reasoning has
been detected across age groups in social deprivation
(Escobar et al., 2014), sociopathic conditions
(Campagna & Harter, 1975), high-functioning pervasive
developmental disorders (Takeda, Kasai, & Kato, 2007),
and SZ (Benson, 1980). In psychopaths, addicts, socio-
pathic children, and socially deprived adolescents,
moral dilemma tasks yield reduced activation patterns
in several areas, including the PFC, the cingulate gyrus,
and the insula.
In sum, moral judgment is compromised across neu-
rological and psychiatric conditions (Table 4), although
current research is difficult to integrate given the diver-
sity of tasks employed, the different moral domains
being assessed, and the dearth of systematic
SOCIAL NEUROSCIENCE 17
comparisons across conditions. As this function
depends on an extended neural network (Moll &
Schulkin, 2009; Moll et al., 2005), which is differentially
affected at different levels, several conditions present
both similar and dissimilar impairments. Also, subtle
differences among moral sensitivity, emotions, reason-
ing, and dilemmas are not well understood. We do not
yet know how these different dimensions interact and
manifest each condition. Dimensionality in a single
domain must also be considered within specific groups.
For instance, in studies of moral dilemmas, different
patient populations present non-absolute differential
patterns of utilitarian and deontological responses.
Not all patients with bvFTD develop aberrant moral
judgments, and not all OCD patients present hyper-
moralistic judgments. Moral cognition impairments are
very variable across individuals (within and between
diseases). Thus, future neuroscience research should
point at individual differences (Dubois & Adolphs,
2016) as a strategy to provide a better dimensional
characterization across conditions. Also, some areas
that have been rarely explored (e.g., moral emotions)
should be assessed together with other moral pro-
cesses. Thus, a challenge for future neuropsychiatric
research into moral cognition is to assess individual
and group variability across relevant processes and
test multilevel models considering different pathophy-
siological mechanisms.
Ecological assessment of social context
Human interaction and social cognition are multifar-
iously influenced by context, namely, the relevant cir-
cumstances surrounding a cognitive event (Adolphs,
2009; Barrett, Lindquist, & Gendron, 2007). Integrating
contextual information with our appraisal of others’
intentions is critical to deploy adequate social behaviors
and access social meaning (Adolph, Meister, & Pause,
2013; Adolphs, 2009; Baez, Herrera, Villarin, et al. 2013;
Ibanez & Manes, 2012). Context-dependent effects have
been documented in low-level domains—such as visual
perception (Bar, 2004)—and in high-level social cogni-
tion—including prediction and understanding of
others’ intentions and meanings (Baez et al., 2016,
2013; Baez & Ibanez, 2014b; Baez et al., 2012; Ibanez &
Manes, 2012).
BvFTD clearly illustrates that social cognition impair-
ments result from a general inability to integrate con-
textual information (Ibanez & Manes, 2012). Such
deficits are present since early stages of the disease
and probably reflect abnormalities in a frontotemporo-
insular network (Ibanez & Manes, 2012), although they
are not easily captured in classical and routine
Table 4. ToM in neurological and psychiatric conditions.
18

Subjects F Task Behavioral findings Biomarker

Gregory et al. FvFTD (N = 19); AD patients N NPI, first and second order false belief, Faux Pas FvFTD impaired on all tests of TOM. AD failed in Not measured.
(2002) (N = 12) and HC (N = 16) Test and RMET second-order false belief (heavy demands on
working memory).
Torralva et al. Early/mild fvFTD patients N ToM tasks and IGT FvFTD group impaired in both ToM tasks and IGT. Not measured.
(2009) (N = 20) and HC (N = 10)
Henry et al. TBI patients (N = 16) and HC N RMET, faces and verbal fluency (FAS). In TBI participants significantly reduced: Recognition Deficits in some aspects of EF may partially underlie
(2006) (N = 17) of basic emotions and capacity for mental state deficits in social cognition following TBI
attribution.
A. IBÁÑEZ ET AL.

Schroeter et al. Meta-analysis: 9 studies. FTD N Meta-analysis of neuroimaging data Not measured. Frontomedian network impaired
(2008) patients (N = 132) and HC
(N = 166)
Adenzato, Review N Multiple neuroimaging tasks ToM deficits Link between the progressive degeneration of the
Cavallo, & anterior regions of medial frontal structures
Enrici, (2010) characterizing the early stages of the bvFTD and
the ToM deficits.
Castelli et al. AD patients (N = 16) and HC N RMET and strange stories Complex ToM levels are impaired in AD patients. Not measured.
(2011) (N = 16)
Allain et al. HD patients (N = 18) and HC N Intention test, RMET and EF Significant impairment of ToM abilities in HD patients Cortico–subcortical circuits are underlying higher
(2011) (N = 18) social functions such as ToM.
Duval et al. SD patients (N = 15) and HC N Memory tasks, intention test, false-belief task, Cognitive and affective ToM impairment. ToM deficit was consistent with the patients’ atrophy
(2012) (N = 36) RMET and “Tom’s taste” in the left temporal lobe and hypometabolism in
the temporal lobes and the medial frontal cortex.
Eddy & Rickards, HD patients (N = 16) and HC N Social recognition of inappropriate behavior, HD associated with deficits in ToM Not measured.
(2012) (N = 16) RMET, verbal fluency, working memory,
inhibition, and Problem Behaviors
Assessment-short form.
Le Bouc et al. BvFTD (N = 11); AD patients N Belief-reasoning task, EF and clinical AD patients had deficit in inferring someone else’s Beliefs task correlated with hypometabolism in the
(2012) (N = 12) and HC (N = 20) assessment belief, whereas patients with BvFTD were impaired left TPJ. Self-perspective inhibition correlated with
in inhibiting their own mental perspective. hypometabolism in the right LPFC.
Mike et al. (2013) MS patients (N = 49) and HC N MRI images; tests of recognition of mental Areas of emotion of (right and left fusiform face area,
(N = 24) states and emotions from facial expressions frontal eye filed and right entorhinal cortex) and
and eye gazes socially relevant information (left temporal pole).
Roca, Cerebellar stroke patients N FPT and EF Focal cerebellar lesions do not affect ToM Not measured.
Gleichgerrcht, (N = 11)
Ibáñez,
Torralva, &
Manes, (2013)
Hennion et al. TLE patients (N = 50) and HC N FPT, sarcastic remarks & mentalistic actions Cognitive and affective ToM processes impaired in TLE Not measured.
(2014) (N = 50) patients
Roca et al. (2014) Mild relapsing-remitting MS N FPT and EF Cognitive but not affective ToM deficits in mild Not measured.
(N = 18) and HC (N = 16) relapsing-remitting MS
Henry et al. Meta-analysis: 15 studies. N Meta-analysis of ToM tasks ToM deficit. Not measured.
(2014) BvFTD (N = 312); AD
patients (N = 163) and HC
(N = 325).
Bertoux, Volle, BvFTD patients (N = 20) N Mini-SEA Not measured. Detection of Faux pas was related to rostral mPFC
et al. (2014) perfusion (BA 10) while recognition of emotion
involved more dorsal regions within the mPFC (BA
9).
Yeh & Tsai (2014) CVA patients (N = 34) and HC N Tasks testing verbal and nonverbal ToM and CVA patients were impaired in both cognitive and The right hemisphere may play an important role in
(N = 40) empathy. affective ToM. Poorer performance in patients with decoding nonverbal cues to infer others’ minds as
right stroke on the cognitive component of well as the processing of empathy.
nonverbal ToM.
(Continued )
Table4. (Continued).
Subjects F Task Behavioral findings Biomarker
Brüne, Blank, HD patients (N = 25); SZ N/P ToM and neurocognitive functions HD impairment in ToM relative to HC and deficits in Not measured.
Witthaus, & (N = 25) and HC (N = 25) ToM similar to SZ.
Saft, (2011)
Hezel and SAD patients (N = 40) and HC P RMET and MASC SAD patients attribute more intense emotions and Not measured.
McNally (2014) (N = 40) greater meaning to what others were thinking and
feeling.
Baez, Marengo, BPD patients (N = 15) and HC P EF, emotion recognition, and ToM BPD adults exhibited deficits in the three domains. Not measured.
et al. (2014) (N = 15)
Schneider et al. High-functioning ASD P ToM scale, Strange Stories test, implicit ToM Impaired implicit false-belief in ASD patients. Not measured.
(2013) patients (N = 24) and HC movies
(N = 20)
Van Rheenen and BD patients (N = 49) and HC P Picture sequencing Task. ToM impairment in BD Not measured.
Rossell (2013) (N = 49)
Das, Lagopoulos, SZ patients (N = 20) and HC P Functional MRI images + intention test Not measured. Patients with schizophrenia had significantly
Coulston, (N = 19) diminished activity in the right superior temporal
Henderson, gyrus at the TPJ and bilaterally within the inferior
and Malhi frontal gyri.
(2012)
Samamé et al. Review and meta-analysis of P Meta-analysis ToM tasks Emotion processing and ToM deficits in remitted BD. Not measured.
(2012) BD
Sayın et al. (2010) OCD patients (N = 30) and P First and second order false belief, hinting task Significant reduction in their “advanced” ToM abilities Not measured.
HC (N = 30) and double-bluff task, verbal memory in OCD patients, which seem related to their
processes test, Weschler memory test, and reduced memory capacities.
Stroop test
Preissler et al. BPD patients (N = 64) and HC P MASC and RMET Impaired abilities in BPD patients in MASC not in Not measured.
(2010) (N = 38) RMET
Bora et al. (2009) Meta-analysis: 36 studies. SZ P Meta-analysis of ToM tasks ToM impairment in remission phase suggests Not measured.
patients (combined mentalizing impairments in schizophrenia
N = 1,181) and HC
(combined N = 936)
Sprong et al. Meta-analysis: 29 studies. SZ P Meta-analysis of ToM tasks Mentalizing impairments in SZ even in remission Not measured.
(2007) patients (combined
N = 1518)
Adolph et al. Nonclinical students (N = 40) P Emotional recognition under relax and stress High-anxiety participants were highly sensitive to the Not measured.
(2013) divided in high and lower full conditions. contextual anxiety signals
social anxiety groups
F: Field (neurology or psychiatry). SZ: schizophrenia; BvFTD: behavioral variant frontotemporal dementia; fvFTD: frontal variant frontotemporal dementia; CVA: cerebrovascular accident; MS: Multiple sclerosis; SD: semantic
dementia; TBI: traumatic brain injury; HC: human controls; BPD: borderline personality disorder; BD: bipolar disorder; OCD: obsessive compulsive disorder; ASD: Autism spectrum disorder; SAD: social anxiety disorder; TLE:
temporal lobe epilepsy; AD: Alzheimer’s disease; HD: Huntington’s disease; RMET: Reading-the-mind-in-the-Eyes Test; MASC: movie for the assessment of social cognition; EF: executive functions; FPT: faux pas test; Mini Sea:
Social cognition & Emotional Assessment; IGT: Iowa Gambling Task; TPJ: temporoparietal junction; MPFC: medial prefrontal cortex; LPFC: lateral prefrontal cortex.
SOCIAL NEUROSCIENCE
19
20 A. IBÁÑEZ ET AL.
neuropsychological assessment. An aberrant frontotem-
poro-insular network predicts social cognition deficits in
bvFTD (Sedeño et al., 2016). The same holds for frontal
lobe lesion patients (Mesulam, 1986). Deficits in this
population can be tapped via more ecological tasks
with implicit contextual cues (Burgess, Alderman,
Volle, Benoit, & Gilbert, 2009). By the same token, dur-
ing short-term contextual processing tasks, patients
with prefrontal compromise exhibit abnormal beha-
vioral and electrophysiological responses (Fogelson,
Shah, Scabini, & Knight, 2009). Both, bvFTD and frontal
lesion patients present difficulties to develop context-
sensitive strategies for successful social bargaining.
These deficits are associated not only with atrophy
and lesions of prefrontal regions, but also with fronto-
temporal aberrant oscillations during social offers as
well as fronto-posterior functional connectivity abnorm-
alities (Melloni et al., 2016). The crucial role of context
for social cognition is further highlighted by studies on
HD. Here, deficits in the appraisal of disgust
(Sprengelmeyer et al., 1996) and other negative emo-
tions (Johnson et al., 2007) during FER are reduced
when contextual clues are provided (Aviezer et al.,
2009; Baez et al., 2015).
Similar difficulties have been observed in psychiatric
disorders. In SZ, inefficient integration of situational
information (Amoruso, Cardona, Melloni, Sedeno, &
Ibanez, 2012; Guerra et al., 2009; Ibáñez, Riveros, et al.
2011) may influence emotion recognition (Green,
Waldron, & Coltheart, 2007; Green, Waldron, Simpson,
& Coltheart, 2008; Monkul et al., 2007), supporting the
idea that social context processing is impaired (Cohen,
Barch, Carter, & Servan-Schreiber, 1999; Riveros et al.,
2010). Also, frontal activity engaged in predictive cod-
ing of upcoming information is also affected in ADHD
and ASD (Gonzalez-Gadea et al., 2015). Similar to
bvFTD, SZ features deficits to contextually update social
decisions during bargaining (Billeke et al., 2015). Also,
ADHD and ASD presents reduced and aberrant markers
of social cooperation (Gonzalez-Gadea et al., 2016),
respectively. Notably, such deficits, which affect both
social and non-social domains (Chung & Barch, 2011),
become more marked in ecological tasks (Baez, Herrera,
Villarin, et al. 2013), highlighting the need for novel
context-sensitive approaches (Chung & Barch, 2011).
Comparable deficits have been reported in BD research,
although these are not so severe (Baez, Herrera, Villarin,
et al. 2013; Brambilla et al., 2007). Also, in ASD, aberrant
implicit recognition of contextual clues (Senju, 2012)
triggers impairments in social cognition (Baez &
Ibanez, 2014a; Baez et al., 2012; Schneider et al., 2013;
Senju, Southgate, White, & Frith, 2009). Finally,
attentional demands in complex scenarios increase
emotion-related deficits in psychopaths (Newman,
Curtin, Bertsch, & Baskin-Sommers, 2010; Sadeh et al.,
2013) and young offenders (Gonzalez-Gadea, Herrera,
et al., 2014).
Altogether, the above findings highlight distur-
bances of implicit contextual appraisal as one further
commonality between neurological and psychiatric
conditions (Table 5). As predicted by the social context
network model (Baez et al., 2012; Ibanez & Manes,
2012), prefrontal areas would support focused predic-
tions by dynamically updating associations in a specific
context (Amoruso et al., 2016, 2014; Bar, 2004; Friston,
2012; Torralva, Gleichgerrcht, Ibanez, & Manes, 2016).
Also, target-context links subserved by temporal
regions would be integrated with feature-based infor-
mation subserved by frontal regions (A. J. Greene,
Gross, Elsinger, & Rao, 2006) (Bar, 2004). Finally, the
insular cortex would be critical to merge emotional
and high-level signals related to the coordination
between external and internal milieus (Canales-
Johnson et al., 2015; Couto et al., 2015, 2015, 2014,
2013; García-Cordero et al., 2016; Garfinkel & Critchley,
2013; Melloni et al., 2013; Sedeño et al., 2014; Uddin,
Kinnison, Pessoa, & Anderson, 2014; Yoris et al., 2015).
Thus, deficits in contextual social cognition will emerge
upon compromise to any of these three main hubs.
However, no dimensional study has revealed the speci-
fic contributions of these hubs (frontal, insular, and
temporal) to each subprocess or their interactions dur-
ing relevant tasks. Also, there is no information about
how distinct pathophysiological mechanisms differen-
tially impact this network across neuropsychiatric con-
ditions. Finally, most current tasks fail to capture the
influence of implicit contextual information on socio-
cognitive performance. In this sense, further research is
needed based on ecological interactive paradigms (A.
M. García & Ibáñez, 2014) and situated cross-domain
tasks (García & Ibáñez, 2016).
A triangulation with social neuroscience
Nearly all neurological and psychiatric disorders involve
some form of impairment in the above domains, all of
which are systematically assessed by social neu-
roscience. Despite the relative youth and internal pro-
blems of this field, we argue that it is prime time to
triangulate its efforts with those of neurology and psy-
chiatry. Moreover, basic principles which guide current
social neuroscience can provide fruitful advances if they
are applied to neuropsychiatry, as described below.
Table 5. Social context sensitivity in neurological and psychiatric conditions.
Study Subjects F Task Behavioral findings Biomarker
Aviezer et al. HD patients (N = 21) N Recognition of emotional scenes and body HD displayed intact recognition of emotion from non- Not measured.
(2009) and controls (N = 27) language facial visual stimuli.
Recognition of isolated facial expressions HD participants were impaired in disgust recognition.
Couto, Sedeño, et Focal stroke (N = 2) and controls N Multimodal basic emotion recognition tests The insular lesion patient showed delayed reaction times. Not measured.
al. (2013) (N = 10) Emotional inference disambiguation task using The subcortical lesion patient was impaired in
contextual social clues multimodal aversive emotion recognition, and was
variously impaired in subtasks of empathy and
contextual inference of emotions.
Fogelson et al. Unilateral focal PFC stroke (N = 7) and N Visual stimuli (targets) Faster reaction time for controls in predicted targets. No Not measured.
(2009) controls (N = 7) reaction-time differences among targets for PFC
patients.
Barcelo & Knight Prefrontal injured (N = 10) and HC N Predictable and unpredictable task context Deficits in both the selection and the suppression of Disrupted frontocortical and
(2007) (N = 10) (targets). familiar versus novel contextual information. frontosubcortical
connectivity.
Fogelson et al. SZ (N = 20); HC (N = 20) and N/P Visual discrimination task. SZ were significantly less accurate than controls. Not measured.
(2013) PD (N = 15) No differences for PD and controls.
Baez & Ibanez Review P Executive function assessments. Social cognition deficits in ASD imply a reduced ability to Not measured.
(2014) Emotional recognition and social interference implicitly encode and integrate contextual cues
tasks (contextual integration) needed to access social meaning
Gonzalez-Gadea, AO (N = 30) and HC (N = 15) P High and low context-sensitive measure: facial Offenders had a significantly poorer performance in High Not measured.
Herrera, et al. emotion recognition. context-sensitive measure.
(2014) Fluid intelligence and EF.
Dwyer, Peters, Formal thought SZ (N = 18) and HC P Semantic processing in emotional salient No differences in emotional manipulation but more Not measured.
McKenna, (N = 15) sentences and sensibility-judgments. errors on sense-judgments and repetition than the
David, and other two groups.
McCarthy
(2014)
Schneider et al. High-functioning ASD (N = 24) and HC P Explicit and implicit ToM measure. Funneled Deficits in implicit ToM recognition. Not measured.
(2013) (N = 20) debriefing
Baez, Herrera, SZ (N = 15); BP (N = 15); HC (N = 30) P Executive functions (EF) assessments. EF was deficit for SZ and BD relative to controls; similarly Not measured.
Villarin, et al. Emotional recognition and social interference was for disgust and fear recognition and contextual
(2013) tasks (contextual integration) integration performance.
Adolph et al. Nonclinical students (N = 40) divided P Emotional recognition under relaxed and High-anxiety participants were highly sensitive to the Not measured.
(2013) in high and low social anxiety stressful conditions contextual anxiety signals.
Yang, Tadin, BP (N = 16) and HC (N = 23) P Visual context processing (luminance, contrast, No differences with controls. Stronger motion and Not measured.
Glasser, Wook size, orientation, and motion direction) orientation context effects correlated with worse
Hong, Blake, clinical symptoms.
and Park
(2013)
Fogelson et al. SZ (N = 32) and HC (N = 30) P Visual discrimination task No score differences. Context-dependent P3b deficits
(2011)
Senju et al. (2009) AS subjects (N = 19) and HC (N = 17) P Eye-tracking task In ASD individuals, eye movements did not anticipate an Not measured.
actor’s intention.
Brambilla et al. BD patients (N = 15) and HC (N = 26) P Visual context interference BD showed a context processing deficit relative to Not measured.
(2007) healthy controls.
Green et al. SZ (N = 20) and HC (N = 22) P Target facial expressions preceded by vignettes Patients shown deficit in facial recognition and vignettes Not measured.
(2007) integration.
SOCIAL NEUROSCIENCE

Cohen et al. SZ, UD and HC P Attentional interference test (Stroop) and lexical Accentuation of deficits in patients with schizophrenia in Not measured.
(1999) disambiguation task context-sensitive conditions.
F: Field (neurology or psychiatry). HD: Huntington’s Disease; PFC: prefrontal cortex; SZ: Schizophrenic Patients; PD: Parkinson’s disease; ASD: Autism spectrum disorder; AS: Asperger’s syndrome; EF: executive functions; ToM:
Theory of mind; BD: bipolar disorder; UP: unipolar depression; P3b: P300 event-related potential (ERP) component.
21
22 A. IBÁÑEZ ET AL.

Tracking the synergies between brain structures leading to behavioral inadequacies (Cryan & Kaupmann,
and functions 2005; Krystal et al., 2002; Lupien, McEwen, Gunnar, &
Heim, 2009; Maguire & Mody, 2008) and illness
In both neurological and psychiatric disorders, social
(Segerstrom & Miller, 2004). Indeed, soluble mediators
cognition deficits emerge from disturbances of net-
released by immune cells can affect the central nervous
works spanning multiple neural locations. Modern
system and alter behavior (Irwin & Cole, 2011;
imaging techniques reveal intimate and complemen-
Segerstrom & Miller, 2004). In addition, mood and anxi-
tary connections between brain anatomy and function
ety disorders can be the early manifestation of broader
(Northoff, 2008). In the same vein, diseases and phar-
diseases, or they can index a disruption of neural net-
macotherapy may alter not just brain functions, but
works supporting interpersonal and emotional pro-
also neural structures proper. Building upon these
cesses (Cacioppo, Cacioppo, Dulawa, & Palmer, 2014;
findings, cognitive neuroscience conceives mental
Davidson, Pizzagalli, Nitschke, & Putnam, 2002).
processes as emerging from coordinated neural activ-
Accompanying social deficits might promote stressful
ity over multiple regions (see below). Across disorders,
interactions and contribute to a multilevel vicious circle
different substrates (from neuronal channels and
(Bartolomucci et al., 2005; Cacioppo, Cacioppo, Dulawa,
genes to global ensembles) subserve specific cogni-
et al. 2014; Meyer-Lindenberg, 2014). Social stress may
tive functions through various interactions (Millan
even have an impact on genetic regulation (Cacioppo,
et al., 2012). Moreover, in neuropsychiatric conditions,
Cacioppo, Dulawa, et al. 2014; Cole, Hawkley, Arevalo, &
social cognition impairments are not consistently
Cacioppo, 2011). In particular, perceived social isolation
associated with well-defined structural atypicalities
(loneliness) modifies the expression of genes driving
(Dickinson & Harvey, 2009). At the same time, func-
inflammation, one of the first responses of the immune
tional abnormalities in psychiatric patients have been
system (Cole et al., 2011). Molecular changes induced
associated with aberrant brain structure (Millan et al.,
by perceived or real social isolation may duplicate the
2012). Thus, the interplay among structures and func-
chances of developing dementia (Wilson et al., 2007)
tions in both neurological and psychiatric conditions
and increases mortality (Cacioppo, Cacioppo, Capitanio,
should be thoroughly studied. This agenda would also
& Cole, 2015).
help to understand how macroanatomical (e.g., focal
In turn, pure pathophysiological conditions can
lesions or specific neurotransmitter abnormalities
directly affect social and emotional processes. This
affecting whole-brain dynamics) and microanatomical
occurs in cases of premenstrual dysphoric disorder (a
(e.g., channelopathies compromising in neural net-
disturbance of lifestyle including symptoms of irritabil-
work dynamics) phenomena impact social cognition
ity, tension, dysphoria, and mood lability) (Steiner,
functions. Similarly, we can study how classically func-
1997), toxic psychosis (a substance-related disorder),
tional conditions are associated with enduring struc-
and MS (where the feelings of depression and fatigue
tural atrophy and how changes in aberrant
are common and detrimental to life quality (Krupp,
connectivity induce structural changes. As shown by
Alvarez, LaRocca, & Scheinberg, 1988; Marrie et al.,
social neuroscience, in between and around such con-
2015)). The same is true of a wide range of neurode-
structs lie multiple interacting dimensions that chal-
generative diseases (Levenson, Sturm, & Haase, 2014;
lenge one-to-one associations between structural
Neary et al., 1998). In FTD, pathology involves complex
damage and neurological disorders, one the one
interrelations among genetic, neural, and behavioral
hand, and functional alterations and psychiatric con-
levels, which challenges straightforward conceptualiza-
ditions, on the other.
tions of the disease. Just as an example, the same
mutation in gene C9orf72 can lead to either bvFTD
(with its typical social cognition impairments) or a pre-
Multilevel brain mechanisms for social cognition
dominant motor disease (such as ALS) (Bruijn, Miller, &
impairments
Cleveland, 2004; Mahoney et al., 2012).
Diseases are not monolithic entities; rather, they result Over the years, scientists have garnered convergent
from the interaction of social, neural, hormonal, cellular, information from different levels (genetics, neurobiol-
molecular, and genetic mechanisms underlying and ogy, behavior, social environment). Yet, this mosaic
surrounding cognitive processes (Caspi & Moffitt, strategy has not yet provided an adequate picture of
2006). Social and psychological phenomena have a neuropsychiatric conditions, let alone their vast varia-
profound impact on multiple neural levels, which in bility (Devor et al., 2013). Correlating mental disorders
turn affect the former in various ways. For instance, with brain activity patterns in critical regions is only a
stress can induce molecular and cellular brain changes first step toward specifying the mechanisms behind

nervous disorders (Cacioppo, Cacioppo, Dulawa, et al.
2014). An adequate picture of neuropsychiatric condi-
tions requires connecting the dots from all these
dimensions (Devor et al., 2013).
The multilevel view of social cognition poses addi-
tional challenges for triangulation. Although some of
them are beyond current agenda of social neu-
roscience, a number of steps can be taken in that
direction. The development of multimodal assess-
ments of interaction across levels can be boosted by
the direct comparison of pathophysiological mechan-
isms. To this end, it would be crucial to expand the
visibility of triangulated approaches via special issues,
specific funding opportunities, and explicit discussion
fora. Finally, recent data-driven methods of social
neuroscience (Adolphs, Nummenmaa, Todorov, &
Haxby, 2016) can capitalize on large datasets, find
patterns across levels, and provide a better character-
ization of the transdimensional nature of social
cognition.
How to promote dimensional and transnosological
research via a brain network approach
Social cognition impairments attributed to a specific
substrate can be supported by spatiotemporal integra-
tion of neural hubs. Today, we know that adequate
cognitive states depend on the spatial and temporal
organization of long-range networks (Sporns, 2014).
This is especially true of the social brain (Kennedy &
Adolphs, 2012). Some network attributes, such as small-
world properties, are associated to similar impairments
in both neurological and psychiatric disorders (Bullmore
& Sporns, 2009). However, dissimilar pathophysiological
processes impact differentially in network properties
(García-Cordero et al., 2015; Sedeño et al., 2016).The
default mode network (DMN), which is implicated in
social cognition processes, actually constitutes a trans-
diagnostic marker across these diseases. The DMN is
impaired in AD, SZ, ASD, and many other disorders.
Further research characterizing the similarities and dif-
ferences across conditions regarding the role of the
DMN in social cognition will offer finer grained insights
than those currently available. This will also allow
answering whether damage to specific hubs lead to
similar social cognition deficits across disorders. Also,
the network dynamics can be used to investigate how
specific social cognition mechanisms (e.g., the salience
network) interact with other non-social mechanisms
(e.g., frontoparietal network). Finally, modifications in
the connectivity of affected hubs (Silasi & Murphy,
2014) may afford future strategies for treatment.
SOCIAL NEUROSCIENCE 23
Neuropsychiatry informing social neuroscience
In the review section, we assessed available evidence
for dimensional and transdiagnostic social cognition
impairments in neurological and psychiatric conditions.
This evidence provides a fruitful agenda for new ques-
tions, as listed at the end of each subsection therein.
Here, we detail how the triangulation can advance a
deeper understanding of the social impairments.
Different models of the social brain
Parallel models of the social brain emerge from each
level of impairment. For example, the study of moral
cognition can thrive by considering patients with loca-
lized vmPFC damage (Koenigs et al., 2007; Young et al.,
2010). Despite this straightforward association, a more
extended anatomy may be postulated for moral sensi-
tivity by considering diffuse frontotemporal damage in
neurodegeneration (Baez, Baez et al., 2014; Ibanez &
Manes, 2012). Moreover, white-matter connectivity
models of moral cognition can be advanced by refer-
ence to complete and partial callosotomy (M. B. Miller
et al., 2010).
Additional evidence may be garnered from disorders
lacking precise neuroanatomical foundations.
Psychopathy, ASD, and Williams syndrome present par-
tially opposite social phenotypes which inform dissocia-
tions within the social cognition domain. Furthermore,
models of moral cognition may stem from research on
aberrant neurotransmission in relevant diseases, includ-
ing mesolimbic dopaminergic dysfunction (Khemiri et al.,
2012; Koob & Volkow, 2010) and serotonergic dysregula-
tion (Koob & Volkow, 2010; Whitton, Henry, & Grisham,
2014). In sum, different pathogenetic processes across
neuropsychiatric conditions can provide separate yet
compatible avenues to build complex models of the
social brain. One simple way to organize a research pro-
gram consists in advancing empirical comparisons of a
social cognition domain (e.g., moral cognition) across
different patient populations with different physiopathol-
ogy, including focal damage of critical regions, diffuse
alterations of functional networks, disruption of anatomi-
cal tracts, and neurotransmitter dysregulation, among
others. In the future, this would help to clarify which
mechanisms are more critical to the target domain, how
they interact, and what alternative ways may be posed to
ameliorate specific disorders.
Social dysfunction at the center or the periphery
Social cognition can be impaired by primary or sec-
ondary disturbances such as executive or linguistic
24 A. IBÁÑEZ ET AL.
deficits. Empathy, as well as other abilities discussed
in above sections, relies on working memory (Ze,
Thoma, & Suchan, 2014), inhibitory control (Hansen,
2011; Ze et al., 2014), and other executive functions
(Rankin et al., 2005). Inhibition of one’s own perspec-
tive is a prerequisite for ToM (Samson, Apperly,
Kathirgamanathan, & Humphreys, 2005).
Furthermore, working memory is required in com-
plex social situations (Meyer, Spunt, Berkman,
Taylor, & Lieberman, 2012; Rankin et al., 2006).
Language disorders may also disrupt social function-
ing in an indirect way. Wernicke’s aphasics, being
mostly unable to recognize the unintelligibility of
their own speech, are prone to develop major para-
noid syndrome and even manifest antisocial beha-
vior (Damasio, 1998). Also, in high-functioning ASD,
ToM deficits are correlated with deficits to compre-
hend figurative language, including metaphors and
irony (Huang, Oi, & Taguchi, 2015). All in all, similar
impairments in social cognition can be triggered by
either specifically social deficits or other types of
cognitive dysfunction.
Thus, although we can identify some cases where
social cognition is more primarily or secondarily
affected, the systematic study of the differences
among these conditions is scarce. Further research is
needed to understand how underlying networks under-
lying primary or secondary functions overlap and
interact.
Inter-cognition: beyond instrumental parcellation
Classical assessments of cognitive processes are typi-
cally rooted in isolation paradigms (Becchio, Sartori, &
Castiello, 2010), experimental set-ups in which a single
participant views preprogrammed, decontextualized sti-
muli and repeatedly performs the same task on them.
However, in neurological disorders, such as PD
(Dirnberger & Jahanshahi, 2013), NMO (Cardona et al.,
2014), and ALS (Watermeyer et al., 2015), social cogni-
tion impairments are typically concomitant with deficits
in other cognitive domains. The same is true of psychia-
tric conditions (Dere, Pause, & Pietrowsky, 2010). ASD
involves impairments in central components of social
cognition, including ToM and empathy (Geschwind,
2009), but these deficits also depend on executive dys-
function (Robinson, Goddard, Dritschel, Wisley, &
Howlin, 2009) and even sensory deficiencies. Likewise,
BD, SZ, MMD, OCD, ADHD, and post-traumatic stress
disorder are characterized by both cognitive (e.g., work-
ing memory, memory systems, executive functions, pro-
cessing speed) and social cognition impairments (Millan
et al., 2012). Moreover, higher levels of cognitive
variability are observed across disorders (e.g.,
Gonzalez-Gadea et al., 2013; Gonzalez-Gadea, Herrera
et al. 2014).
Unlike what experimental paradigms and ensuing the-
ories imply, neuropsychiatric disorders do not involve
deficits in a single domain. To incorporate intercognitive
deficits in the agenda of neuroscientific research, less
fragmentary methodologies must be developed. In the
future, classical experimental approaches that denatura-
lize participants’ cognitive processes by prioritizing fixed,
oversimplified, and isolated tasks should be complemen-
ted by more naturalistic tasks engaging interconnected
cognitive processes (J. D. Henry, Cowan, Lee, & Sachdev,
2015). Current advances of “second-person” (Schilbach
et al., 2013) or “two-person” (Liu & Pelowski, 2014) neu-
roscience assessing brain-to-brain coupling (Hasson,
Ghazanfar, Galantucci, Garrod, & Keysers, 2012) and active
forms of social interaction (Pfeiffer, Timmermans,
Vogeley, Frith, & Schilbach, 2013), together with multi-
source recording technologies, cameras, and mobile
devices (e.g., wearable eye trackers), will be key compo-
nents of this prospective tool kit. In brief, we need to
move from isolated, disembodied, and passive assess-
ments of social processes to more ecological approxima-
tions (Barutta, Aravena, & Ibáñez, 2010; Barutta, Cornejo,
& Ibáñez, 2011; Cosmelli & Ibáñez, 2008; Ibanez &
Cosmelli, 2008).
Social neuroscience informing neuropsychiatry
Historically, several neurological and psychiatric disor-
ders have been assessed with an emphasis on specific
symptomatology (mostly based on behavioral and
mood-related observations, respectively). Little atten-
tion has been paid to the patients’ social dysfunc-
tions, which are equally prominent and affect real-
world functioning (Cacioppo, Capitanio, & Cacioppo,
2014). Social cognition deficits can be detrimental to
functional performance, particularly as regards instru-
mental activities of daily living. Indeed, several neu-
ropsychiatric conditions involve a disproportion
between global cognitive function and daily function-
ing. Social cognition domains have to be assessed
taking into consideration the clinical characterization
and questions about patients’ everyday difficulties.
Hence, social cognition measures may be more appro-
priate surrogate markers of functional efficiency for
many patients. Through a combination of behavioral
measures, experimental manipulations, and physiolo-
gical recordings, social neuroscience may sow the
seeds for a new conception of neuropsychiatric dis-
orders and a novel approach to clinical practice.

Dimensional and transdiagnostic cross talk in
psychiatry and neurology
Social cognition impairments in major clinical entities
from neurology and psychiatry could be better under-
stood by providing transnosological research. The need
for new approaches to classify mental disorders has
been addressed by the Research Domain Criteria
(RDoC) project. The same dimensional and transdiag-
nostic principles are more difficult to implement in
neurology, but some developments have begun (e.g.,
(Carter & Ffytche, 2015)), specially under the guidance
of social neuroscience (Brugger & Lenggenhager, 2014).
The RDoC begins with, but is not limited to, symptoms.
A further advance may crystallize upon joint considera-
tion of biobehavioral dimensions cutting across multi-
ple levels of analysis. Neurocognitive states cannot be
properly conceived if framed separately from concomi-
tant socio-affective processes (Casey, Oliveri, & Insel,
2014; Insel, 2014).
Renewing clinical assessment and professional
training
Social neuroscience implies a renewed approach to
clinical assessment and professional training.
Improvements in socio-cognitive performance and
interaction are beneficial to patients’ life quality
(Cacioppo, Capitanio, et al. 2014; Millan et al., 2012).
By including social cognition assessments, clinical
practice would capitalize on an expert research area
with major translational potential. To this end, clinical
training should emphasize contributions from social
neuroscience with a view to broadening current
assessment standards. In other words, to ensure excel-
lence in clinical practice, both neurologists and psy-
chiatrists should be trained in a dimensional and
transdiagnostic approach to social cognition.
Currently, residency programs in neuropsychiatry (in
the U.S.A. and Europe) rarely include an in-depth study
of social cognition in their curricula, especially during
early stages of professional education. Training in dif-
ferent social cognitive domains, including behavioral
assessment, knowledge of underlying neural
dynamics, and current know-how from social neu-
roscience is crucial to increase the awareness of social
cognition in neuropsychiatry and facilitate exchanges
among neurologists and psychiatrists. A common
approach to social neuroscience and neuropsychiatry
may ameliorate the adverse effects of subspecializa-
tion and separation of clinical disciplines (Aminoff,
2008).
SOCIAL NEUROSCIENCE 25
Pharmacological therapeutics
Stabilization of chemical alterations underlying social
disturbances may have positive effects across disease
types. The neuroprotective effect of oxytocin treat-
ment may impact social interaction and social cogni-
tion performance not only in ASD (Bakermans-
Kranenburg & Van, 2013) but also in other disorders
such as stroke (Karelina et al., 2011), genetic diseases
(Francis et al., 2014), autism and seizures (Durand,
Pampillo, Caruso, & Lasaga, 2008), Prader–Willi syn-
drome (Meziane et al., 2014), anxiety (Milrod et al.,
2014), BPD (Stanley & Siever, 2010), depression and
chronic stress (Durand et al., 2008), and notably
bvFTD (Finger, 2011). While not yet approved, multi-
ple pharmacological treatments could prove benefi-
cial for social behavior in different conditions. The
comparison of clinical outcomes, long-lasting and
side effects, as well as other treatment-related vari-
ables could provide a better understanding of the
benefits and generalizability of specific drugs for
social cognition improvement.
The challenges ahead: how to bring the
framework to institutional life
In the above sections, we have updated how social
neuroscience has an active impact in triangulating neu-
rology and psychiatry. Nevertheless, the greatest long-
term challenge is how to formally implement this
approach. Bringing this framework to life in academic
and clinical settings calls for major institutional devel-
opments. A typical problem for clinical training pro-
grams and professional practice is to establish a
particular assessment/evaluation/treatment for a speci-
fic disorder. Clinical, funding, and academic programs
typically target highly specialized training, focus on a
particular condition, and support only specific research
programs. This is inconsistent with current knowledge
of social impairments, as it calls for expertise in many
conditions through theoretically heterogeneous train-
ing. A new institutional rationale must be forged for
this to happen. First, potential funding sources, both in
the public and private sectors, should open their
options for field-specific financing to dimensional psy-
chiatric and neurological projects. Funds made avail-
able for psychiatric research, for instance, should not
be denied to viable projects on the grounds that they
include both neurological and psychiatric conditions.
Second, faculties and departments specialized in either
discipline should be formally encouraged to incorpo-
rate literature and courses aimed to show the continu-
ities among both types of dysfunction.
26 A. IBÁÑEZ ET AL.
World experts must come together to produce
groundbreaking journals and handbooks which foster
developments within a dimensional and integrative
social neuroscience approach to neuropsychiatry.
Clinical institutions should mirror such synergistic
actions in their training programs and ongoing prac-
tices. Thus, a systematic triangulation can only become
concrete if major educational and political changes are
progressively made. Even if shared social cognition
impairments in neurological and psychiatric disorders
are already broadly acknowledged, implementing this
conception at an institutional level will constitute a
major challenge. The framework presently outlined
seeks to inspire more integrative training, funding,
and academic opportunities.
Conclusions
Since the first descriptions of neurocognitive diseases in
ancient Egypt (Santoro et al., 2009) and pre-Hippocratic
Greece (York & Steinberg, 2001), the history of nervous
diseases has been marked by exclusionary (sometimes
indexed as biological or psychological) explanations
(Barutta, Cornejo, & Ibáñez, 2011; Barutta,
Gleichgerrcht, Cornejo, & Ibáñez, 2010; Mikulan,
Reynaldo, & Ibanez, 2014). Current neuroscientific
views partially circumvent this tradition but still face
several difficulties to gain a deeper understanding of
social cognition impairments. Social neuroscience offers
a dimensional and transdiagnostic triangulation to
advance toward a better grasp of the impaired social
brain.
Review criteria
References for this Review were identified through
searches of PubMed from 2000 until January 2015,
with the terms “social neuroscience”, “social cognition”,
“emotion”, “facial emotions”, “empathy”, “theory of
mind”, “context/contextual and social”, and “psychia-
try/psychiatric” or “neurology/neurological”. Articles
were also identified through searches of the authors’
own files. Each hit was set aside for in-depth analysis.
Only papers published in English were reviewed. The
final reference list was generated on the basis of rele-
vance to the topics covered in this Review.
Acknowledgments
This work was partially supported by grants from CONICET,
CONICYT/FONDECYT Regular (1130920), FONDAP 15150012,
FONCyT-PICT 2012-0412, 2012-1309, and the INECO Foundation.
Disclosure statement
No potential conflict of interest was reported by the authors.
Funding
This work was supported by grants from CONICET, CONICYT/
FONDECYT Regular [1130920], FONDAP [15150012], FONCyT-
PICT [2012-0412], [2012-1309], and the INECO Foundation.
ORCID
Agustín Ibáñez http://orcid.org/0000-0001-6758-5101
References
Abu-Akel, A., Fischer-Shofty, M., Levkovitz, Y., Decety, J.,
Shamay-Tsoory, S. (2014). The role of oxytocin in empathy
to the pain of conflictual out-group members among
patients with schizophrenia. Psychological Medicine, 44(16),
3523–3532. doi:10.1017/S003329171400097X.
Adenzato, M., Cavallo, M., & Enrici, I. (2010). Theory of mind
ability in the behavioural variant of frontotemporal demen-
tia: an analysis of the neural, cognitive, and social levels.
Neuropsychologia, 48(1), 2–12. doi:10.1016/j.
neuropsychologia.2009.08.001.
Allain, P., Gaura, V., Fasotti, L., Chauviré, V., Prundean, A.,
Sherer-Gagou, C., … Verny, C. (2011). The neural substrates
of script knowledge deficits as revealed by a PET study in
Huntington's disease. Neuropsychologia, 49(9), 2673–2684.
doi:10.1016/j.neuropsychologia
Adolph, D., Meister, L., & Pause, B. M. (2013). Context counts!
social anxiety modulates the processing of fearful faces in
the context of chemosensory anxiety signals. Frontiers in
Human Neuroscience, 7, 283. doi:10.3389/fnhum.2013.00283
Adolphs, R. (2002). Recognizing emotion from facial expres-
sions: Psychological and neurological mechanisms.
Behavioral and Cognitive Neuroscience Reviews, 1(1), 21–62.
doi:10.1177/1534582302001001003
Adolphs, R. (2009). The social brain: Neural basis of social
knowledge. Annual Review of Psychology, 60, 693–716.
doi:10.1146/annurev.psych.60.110707.163514
Adolphs, R., Nummenmaa, L., Todorov, A., & Haxby, J. V.
(2016). Data-driven approaches in the investigation of
social perception. Philosophical Transactions of the Royal
Society B: Biological Sciences, 371(1693), 20150367.
doi:10.1098/rstb.2015.0367
Adolphs, R., Tranel, D., & Damasio, A. R. (2003). Dissociable
neural systems for recognizing emotions. Brain and
Cognition, 52(1), 61–69. doi:10.1016/S0278-2626(03)00009-5
Ahmed, F. S., & Stephen Miller, L. (2011). Executive function
mechanisms of theory of mind. Journal of Autism and
Developmental Disorders, 41(5), 667–678. doi:10.1007/
s10803-010-1087-7
Allison, T., Puce, A., Spencer, D. D., & McCarthy, G. (1999).
Electrophysiological studies of human face perception. I:
Potentials generated in occipitotemporal cortex by face
and non-face stimuli. Cerebral Cortex, 9(5), 415–430.
doi:10.1093/cercor/9.5.415

Aminoff, M. J. (2008). Training in neurology. Neurology, 70(20),
1912–1915. doi:10.1212/01.wnl.0000312287.53064.d2
Amoruso, L., Cardona, J., Melloni, M., Sedeno, L., & Ibanez, A.
(2012). Contextual impairments in Schizophrenia and the
FN400. Frontiers in Human Neuroscience, 6, 191.
doi:10.3389/fnhum.2012.00191
Amoruso, L., Ibáñez, A., Fonseca, B., Gadea, S., Sedeño, L.,
Sigman, M., . . . Fraiman, D. (2016). Variability in functional
brain networks predicts expertise during action observa-
tion. Neuroimage. doi:10.1016/j.neuroimage.2016.09.041
Amoruso, L., Sedeño, L., Huepe, D., Tomio, A., Kamienkowski,
J., Hurtado, E., . . . Ibáñez, A. (2014). Time to Tango: Expertise
and contextual anticipation during action observation.
Neuroimage, 98, 366–385. doi:10.1016/j.neuroimage.
2014.05.005
Anderson, S. W., Bechara, A., Damasio, H., Tranel, D., &
Damasio, A. R. (1999). Impairment of social and moral
behavior related to early damage in human prefrontal
cortex. Nature Neuroscience, 2(9), 820–824. doi:10.1038/
12194
Aoki, Y., Cortese, S., & Tansella, M. (2014). Neural bases of
atypical emotional face processing in autism: A meta-ana-
lysis of fMRI studies. The World Journal of Biological
Psychiatry : the Official Journal of the World Federation of
Societies of Biological Psychiatry, 1–10. doi:10.3109/
15622975.2014.957719
Association, A. P. (2000). Diagnostic and statistical manual of
mental disorders, fourth edition, text revision (DSM-IV-TR)
(Vol. IV). Arlington, TX: American Psychiatric Publishing.
Atkinson, A. P., & Adolphs, R. (2011). The neuropsychology of
face perception: Beyond simple dissociations and func-
tional selectivity. Philosophical Transactions of the Royal
Society B: Biological Sciences, 366(1571), 1726–1738.
doi:10.1098/rstb.2010.0349
Aviezer, H. B. S., Hassin, R. R., Meschino, W., Kennedy, J.,
Grewal, S., Esmail, E., . . . Moscovitch, H. (2009). Not on the
face alone: Perception of contextualized face expressions in
Huntington’s disease. Brain, 132, 1633–1644. doi:10.1093/
brain/awp067
Baez, S., Couto, B., Herrera, E., Bocanegra, Y., Trujillo-Orrego,
N., Madrigal-Zapata, L., . . . Villegas, A. (2013). Tracking the
cognitive, social, and neuroanatomical profile in early neu-
rodegeneration: Type III cockayne syndrome. Frontiers in
Aging Neuroscience, 5, 80. doi:10.3389/fnagi.2013.00080
Baez, S., Couto, B., Torralva, T., Sposato, L. A., Huepe, D.,
Montanes, P., . . . Ibanez, A. (2014). Comparing moral judg-
ments of patients with frontotemporal dementia and fron-
tal stroke. JAMA Neurology, 71(9), 1172–1176. doi:10.1001/
jamaneurol.2014.347
Baez, S., García, A. M., & Ibanez, A. (2016). The social context
network model in psychiatric and neurological diseases.
Current Topics in Behavioral Neurosciences. doi:10.1007/
7854_2016_443
Baez, S., Herrera, E., Gershanik, O., Garcia, A. M., Bocanegra, Y.,
Kargieman, L., . . . Ibanez, A. (2015). Impairments in negative
emotion recognition and empathy for pain in Huntington’s
disease families. Neuropsychologia, 68, 158–167.
doi:10.1016/j.neuropsychologia.2015.01.012
Baez, S., Herrera, E., Villarin, L., Theil, D., Gonzalez-Gadea, M. L.,
Gomez, P., . . . Ibanez, A. (2013). Contextual social cognition
impairments in schizophrenia and bipolar disorder. PLoS
One, 8(3), e57664. doi:10.1371/journal.pone.0057664
SOCIAL NEUROSCIENCE 27
Baez, S., & Ibanez, A. (2014a). The effects of context processing
on social cognition impairments in adults with Asperger’s
syndrome. Frontiers in Neuroscience, 8, 270. doi:10.3389/
fnins.2014.00270
Baez, S., & Ibanez, A. (2014b). The effects of context proces-
sing on social cognition impairments in adults with
Asperger’s syndrome. Front Neurosci, 8. doi:10.3389/
fnins.2014.00270
Baez, S., Kanske, P., Matallana, D., Montanes, P., Reyes, P.,
Slachevsky, A., . . . Ibanez, A. (2015). Integration of intention
and outcome for moral judgment in frontotemporal
dementia: Brain structural signatures. Neurodegenerative
Diseases. doi:10.1159/000441918
Baez, S., Manes, F., Huepe, D., Torralva, T., Fiorentino, N.,
Richter, F., . . . Ibanez, A. (2014). Primary empathy deficits
in frontotemporal dementia. Frontiers in Aging
Neuroscience, 6, 262. doi:10.3389/fnagi.2014.00262
Baez, S., Marengo, J., Perez, A., Huepe, D., Font, F. G., Rial, V., . . .
Ibanez, A. (2014). Theory of mind and its relationship with
executive functions and emotion recognition in borderline
personality disorder. Journal of Neuropsychology.
doi:10.1111/jnp.12046
Baez, S., Morales, J. P., Slachevsky, A., Torralva, T., Matus, C.,
Manes, F., & Ibanez, A. (2016). Orbitofrontal and limbic
signatures of empathic concern and intentional harm in
the behavioral variant frontotemporal dementia. Cortex,
75, 20–32. doi:10.1016/j.cortex.2015.11.007
Baez, S., Rattazzi, A., Gonzalez-Gadea, M. L., Torralva, T.,
Vigliecca, N. S., Decety, J., . . . Ibanez, A. (2012). Integrating
intention and context: Assessing social cognition in adults
with Asperger syndrome. Frontiers in Human Neuroscience,
6, 302. doi:10.3389/fnhum.2012.00302
Baez, S., Santamaría-García, H., Orozco, J., Fittipaldi, S., García,
A., Pino, M., & Ibáñez, A. (2016). Your misery is no longer
my pleasure: Reduced schadenfreude in Huntington’s dis-
ease families. Cortex, 83, 78–85. doi:10.1016/j.
cortex.2016.07.009
Bakermans-Kranenburg, M. J., & Van, I. J. M. H. (2013). Sniffing
around oxytocin: Review and meta-analyses of trials in
healthy and clinical groups with implications for pharma-
cotherapy. Translational Psychiatry, 21(3), 34.
Bar, M. (2004). Visual objects in context. Nature Reviews.
Neuroscience, 5(8), 617–629. doi:10.1038/nrn1476
Barcelo, F., & Knight, R. T. (2007). An information-theoretical
approach to contextual processing in the human brain:
Evidence from prefrontal lesions. Cerebral Cortex, 17 Suppl
1, i51–60.
Baron-Cohen, S. (2009). Autism: The empathizing-systemizing
(E-S) theory. Annals of the New York Academy of Sciences,
1156, 68–80. doi:10.1111/j.1749-6632.2009.04467.x
Baron-Cohen, S., & Wheelwright, S. (2004). The empathy quo-
tient: An investigation of adults with Asperger syndrome or
high functioning autism, and normal sex differences.
Journal of Autism and Developmental Disorders, 34(2), 163–
175. doi:10.1023/B:JADD.0000022607.19833.00
Barrett, L. F., Lindquist, K. A., & Gendron, M. (2007). Language
as context for the perception of emotion. Trends in
Cognitive Sciences, 11(8), 327–332. doi:10.1016/j.
tics.2007.06.003
Bartolomucci, A., Palanza, P., Sacerdote, P., Panerai, A. E.,
Sgoifo, A., Dantzer, R., & Parmigiani, S. (2005). Social factors
and individual vulnerability to chronic stress exposure.
28 A. IBÁÑEZ ET AL.
Neuroscience & Biobehavioral Reviews, 29(1), 67–81.
doi:10.1016/j.neubiorev.2004.06.009
Barutta, J., Aravena, P., & Ibáñez, A. (2010). The machine
paradigm and alternative approaches in cognitive science.
Integrative Psychological and Behavioral Science, 44(2), 176–
183. doi:10.1007/s12124-010-9116-9
Barutta, J., Cornejo, C., & Ibáñez, A. (2011). Theories and
theorizers: A contextual approach to theories of cognition.
Integrative Psychological and Behavioral Science, 45(2), 223–
246. doi:10.1007/s12124-011-9156-9
Barutta, J., Gleichgerrcht, E., Cornejo, C., & Ibáñez, A. (2010).
Neurodynamics of mind: The arrow illusion of conscious
intentionality as downward causation. Integrative
Psychological and Behavioral Science, 44(2), 127–143.
doi:10.1007/s12124-010-9117-8
Barutta, J., Hodges, J., Ibanez, A., Gleichgerrcht, E., & Manes, F.
(2011). Argentina’s early contributions to the understand-
ing of frontotemporal lobar degeneration. Cortex, 47(5),
621–627. doi:10.1016/j.cortex.2010.05.006
Beauchamp, M. H., Dooley, J. J., & Anderson, V. (2013). A
preliminary investigation of moral reasoning and empa-
thy after traumatic brain injury in adolescents. Brain
Injury, 27(7–8), 896–902. doi:10.3109/02699052.2013.
775486
Bear, D. M. (1979). Temporal lobe epilepsy–a syndrome of
sensory-limbic hyperconnection. Cortex, 15(3), 357–84.
Becchio, C., Sartori, L., & Castiello, U. (2010). Toward you: The
social side of actions. Current Directions in Psychological
Science, 19(3), 183–188. doi:10.1177/0963721410370131
Bediou, B., Ryff, I., Mercier, B., Milliery, M., Hénaff, M. A.,
D'Amato, T., … Krolak-Salmon, P. (2009). Impaired social
cognition in mild Alzheimer disease. Journal of Geriatric
Psychiatry and Neurology, 22(2), 130–140. doi:10.1177/
0891988709332939.
Benedetti, F., Bernasconi, A., Bosia, M., Cavallaro, R.,
Dallaspezia, S., Falini, A., . . . Smeraldi, E. (2009). Functional
and structural brain correlates of theory of mind and empa-
thy deficits in schizophrenia. Schizophrenia Research, 114(1–
3), 154–160. doi:10.1016/j.schres.2009.06.021
Benson, A. L. (1980). Morality of schizophrenic adolescents.
Journal of Abnormal Psychology, 89(5), 674–677.
doi:10.1037/0021-843X.89.5.674
Berthoz, S., Armony, J. L., Blair, R. J., & Dolan, R. J. (2002). An
fMRI study of intentional and unintentional (embarrassing)
violations of social norms. Brain, 125(8), 1696–1708.
doi:10.1093/brain/awf190
Bertoux, M., De Souza, L. C., Sarazin, M., Funkiewiez, A.,
Dubois, B., & Hornberger, M. (2014). How preserved is
emotion recognition in Alzheimer disease compared with
behavioral variant frontotemporal dementia? Alzheimer
Disease & Associated Disorders, 1. doi:10.1097/
WAD.0000000000000023
Bertoux, M., Volle, E., De Souza, L. C., Funkiewiez, A., Dubois,
B., & Habert, M. O. (2014). Neural correlates of the mini-SEA
(Social cognition and Emotional Assessment) in behavioral
variant frontotemporal dementia. Brain Imaging and
Behavior, 8(1), 1–6. doi:10.1007/s11682-013-9261-0
Bertoux, M., Volle, E., Funkiewiez, A., De Souza, L. C., Leclercq,
D., & Dubois, B. (2012). Social Cognition and Emotional
Assessment (SEA) is a marker of medial and orbital frontal
functions: A voxel-based morphometry study in behavioral
variant of frontotemporal degeneration. Journal of the
International Neuropsychological Society : JINS, 18(6), 972–
985. doi:10.1017/S1355617712001300
Billeke, P., Armijo, A., Castillo, D., Lopez, T., Zamorano, F.,
Cosmelli, D., & Aboitiz, F. (2015). Paradoxical expectation:
Oscillatory brain activity reveals social interaction impair-
ment in schizophrenia. Biological Psychiatry, 78(6), 421–431.
doi:10.1016/j.biopsych.2015.02.012
Blair, R. J. (1995). A cognitive developmental approach to
mortality: Investigating the psychopath. Cognition, 57(1),
1–29. doi:10.1016/0010-0277(95)00676-P
Bora, E., Yucel, M., & Pantelis, C. (2009). Theory of mind
impairment in schizophrenia: Meta-analysis. Schizophrenia
Research, 109(1–3), 1–9. doi:10.1016/j.schres.2008.12.020
Braak, H., & Braak, E. (1991). Neuropathological stageing of
Alzheimer-related changes. Acta Neuropathologica, 82(4),
239–259. doi:10.1007/BF00308809
Brambilla, P., Macdonald, A. W., III, Sassi, R. B., Johnson, M. K.,
Mallinger, A. G., Carter, C. S., & Soares, J. C. (2007). Context
processing performance in bipolar disorder patients.
Bipolar Disorders, 9(3), 230–237. doi:10.1111/j.1399-
5618.2007.00398.x
Bruen, P. D., McGeown, W. J., Shanks, M. F., & Venneri, A.
(2008). Neuroanatomical correlates of neuropsychiatric
symptoms in Alzheimer’s disease. Brain, 131(9), 2455–
2463. doi:10.1093/brain/awn151
Brugger, P., & Lenggenhager, B. (2014). The bodily self and its
disorders: Neurological, psychological and social aspects.
Current Opinion in Neurology, 27(6), 644–652. doi:10.1097/
WCO.0000000000000151
Bruijn, L. I., Miller, T. M., & Cleveland, D. W. (2004). Unraveling
the mechanisms involved in motor neuron degeneration in
ALS. Annual Review of Neuroscience, 27, 723–749.
doi:10.1146/annurev.neuro.27.070203.144244
Brune, M. (2005). “Theory of mind” in schizophrenia: A review
of the literature. Schizophrenia Bulletin, 31(1), 21–42.
doi:10.1093/schbul/sbi002
Brüne, M., Blank, K., Witthaus, H., & Saft, C. (2011). “Theory of
mind” is impaired in Huntington's disease. Movement
Disorders, 26(4), 671–678. doi:10.1002/mds.23494.
Bruning, N., Konrad, K., & Herpertz-Dahlmann, B. (2005).
Relevance and results of theory of mind research for autism
and other psychiatric disorders. Zeitschrift Für Kinder- Und
Jugendpsychiatrie Und Psychotherapie, 33(2), 77–88.
doi:10.1024/1422-4917.33.2.77
Buhlmann, U., McNally, R. J., Etcoff, N. L., Tuschen-Caffier, B., &
Wilhelm, S. (2004). Emotion recognition deficits in body
dysmorphic disorder. Journal of Psychiatric Research, 38(2),
201–206. doi:10.1016/S0022-3956(03)00107-9
Bullmore, E., & Sporns, O. (2009). Complex brain networks:
Graph theoretical analysis of structural and functional sys-
tems. Nature Reviews. Neuroscience, 10(3), 186–198.
doi:10.1038/nrn2575
Burgess, P. W., Alderman, N., Volle, E., Benoit, R. G., & Gilbert, S.
J. (2009). Mesulam’s frontal lobe mystery re-examined.
Restorative Neurology and Neuroscience, 27(5), 493–506.
doi:10.3233/RNN-2009-0511
Cacioppo, J. T., Cacioppo, S., Capitanio, J. P., & Cole, S. W.
(2015). The neuroendocrinology of social isolation. Annual
Review of Psychology, 66, 733–767. doi:10.1146/annurev-
psych-010814-015240
Cacioppo, J. T., Cacioppo, S., Dulawa, S., & Palmer, A. A. (2014).
Social neuroscience and its potential contribution to

psychiatry. World Psychiatry, 13(2), 131–139. doi:10.1002/
wps.20118
Cacioppo, S., Capitanio, J. P., & Cacioppo, J. T. (2014). Toward a
neurology of loneliness. Psychological Bulletin, 140(6), 1464–
1504. doi:10.1037/a0037618
Calder, A. J., Keane, J., Young, A. W., Lawrence, A. D., Mason, S.,
& Barker, R. A. (2010). The relation between anger and
different forms of disgust: Implications for emotion recog-
nition impairments in Huntington’s disease.
Neuropsychologia, 48(9), 2719–2729. doi:10.1016/j.
neuropsychologia.2010.05.019
Campagna, A. F., & Harter, S. (1975). Moral judgment in socio-
pathic and normal children. Journal of Personality and Social
Psychology, 31(2), 199–205. doi:10.1037/h0076318
Canales-Johnson, A., Silva, C., Huepe, D., Rivera-Rei, Á.,
Noreika, V., Garcia, M. D. C., . . . Bekinschtein, T. A. (2015).
Auditory feedback differentially modulates behavioral and
neural markers of objective and subjective performance
when tapping to your heartbeat. Cerebral Cortex (New
York, N.Y. : 1991), 25, 4490–4503. doi:10.1093/cercor/bhv076
Cardona, J. F., Sinay, V., Amoruso, L., Hesse, E., Manes, F., &
Ibanez, A. (2014). The impact of neuromyelitis optica on the
recognition of emotional facial expressions: A preliminary
report. Social Neuroscience, 9(6), 633–638.
Carmona-Perera, M., Clark, L., Young, L., Pérez-García, M., &
Verdejo-García, A. (2014). Impaired decoding of fear and
disgust predicts utilitarian moral judgment in alcohol-depen-
dent individuals. Alcoholism, Clinical and Experimental
Research, 38(1), 179–185. doi:10.1111/acer.12245
Carter, R., & Ffytche, D. H. (2015). On visual hallucinations and
cortical networks: A trans-diagnostic review. Journal of
Neurology, 13, 13.
Casey, B. J., Oliveri, M. E., & Insel, T. (2014). A neurodevelop-
mental perspective on the research domain criteria (RDoC)
framework. Biological Psychiatry, 76(5), 350–353.
doi:10.1016/j.biopsych.2014.01.006
Caspi, A., & Moffitt, T. E. (2006). Gene-environment interac-
tions in psychiatry: Joining forces with neuroscience.
Nature Reviews. Neuroscience, 7(7), 583–590. doi:10.1038/
nrn1925
Castelli, I., Pini, A., Alberoni, M., Liverta-Sempio, O., Baglio, F.,
Massaro, D., . . . Nemni, R. (2011). Mapping levels of theory
of mind in Alzheimer’s disease: A preliminary study. Aging &
Mental Health, 15(2), 157–168. doi:10.1080/
13607863.2010.513038
Cerami, C., Dodich, A., Canessa, N., Crespi, C., Iannaccone, S.,
Corbo, M., . . . Cappa, S. F. (2014a). Emotional empathy in
amyotrophic lateral sclerosis: A behavioural and voxel-
based morphometry study. Amyotrophic Lateral Sclerosis
and Frontotemporal Degeneration, 15(1–2), 21–29.
doi:10.3109/21678421.2013.785568
Cerami, C., Dodich, A., Canessa, N., Crespi, C., Marcone, A.,
Cortese, F., . . . Cappa, S. F. (2014b). Neural correlates of
empathic impairment in the behavioral variant of fronto-
temporal dementia. Alzheimer’s & Dementia, 10, 827–834.
doi:10.1016/j.jalz.2014.01.005
Chen, Y. C., Chen, C. C., Decety, J., & Cheng, Y. (2014). Aging is
associated with changes in the neural circuits underlying
empathy. Neurobiology of Aging, 35(4), 827–836.
doi:10.1016/j.neurobiolaging.2013.10.080
Chung, Y. S., & Barch, D. M. (2011). The effect of emotional
context on facial emotion ratings in schizophrenia.
SOCIAL NEUROSCIENCE 29
Schizophrenia Research, 131(1–3), 235–241. doi:10.1016/j.
schres.2011.05.028
Ciaramelli, E., Muccioli, M., Làdavas, E., & Di Pellegrino, G.
(2007). Selective deficit in personal moral judgment follow-
ing damage to ventromedial prefrontal cortex. Social
Cognitive and Affective Neuroscience, 2(2), 84–92.
doi:10.1093/scan/nsm001
Cohen, J. D., Barch, D. M., Carter, C., & Servan-Schreiber, D.
(1999). Context-processing deficits in schizophrenia:
Converging evidence from three theoretically motivated
cognitive tasks. Journal of Abnormal Psychology, 108(1),
120–133. doi:10.1037/0021-843X.108.1.120
Cole, S. W., Hawkley, L. C., Arevalo, J. M., & Cacioppo, J. T.
(2011). Transcript origin analysis identifies antigen-present-
ing cells as primary targets of socially regulated gene
expression in leukocytes. Proceedings of the National
Academy of Sciences, 108(7), 3080–3085. doi:10.1073/
pnas.1014218108
Corbera, S., Ikezawa, S., Bell, M. D., Wexler, B. E. (2014).
Physiological evidence of a deficit to enhance the empathic
response in schizophrenia. European Psychiatry, 29(8), 463–
72. doi:10.1016/j.eurpsy.2014.01.005.
Cosmelli, D., & Ibáñez, A. (2008). Human cognition in context:
On the biologic, cognitive and social reconsideration of
meaning as making sense of action. Integrative
Psychological and Behavioral Science, 42(2), 233–244.
doi:10.1007/s12124-008-9060-0
Couto, B., Adolfi, F., Sedeño, L., Salles, A., Canales-Johnson, A.,
Alvarez-Abut, P., . . . Ibanez, A. (2015). Disentangling inter-
oception: Insights from focal strokes affecting the percep-
tion of external and internal milieus. Frontiers in Psychology,
6(503). doi:10.3389/fpsyg.2015.00503
Couto, B., Adolfi, F., Velasquez, M., Mesow, M., Feinstein, J.,
Canales-Johnson, A., . . . Ibanez, A. (2015). Heart evoked
potential triggers brain responses to natural affective
scenes: A preliminary study. Autonomic Neuroscience, 193,
132–137. doi:10.1016/j.autneu.2015.06.006
Couto, B., Manes, F., Montañés, P., Matallana, D., Reyes, P.,
Velasquez, M., . . . Ibáñez, A. (2013). Structural neuroima-
ging of social cognition in progressive non-fluent aphasia
and behavioral variant of frontotemporal dementia.
Frontiers in Human Neuroscience, 7, 467. doi:10.3389/
fnhum.2013.00467
Couto, B., Salles, A., Sedeño, L., Peradejordi, M., Barttfeld, P.,
Canales-Johnson, A., . . . Ibanez, A. (2014). The man who
feels two hearts: The different pathways of interoception.
Social Cognitive and Affective Neuroscience, 9(9), 1253–1260.
doi:10.1093/scan/nst108
Couto, B., Sedeño, L., Sposato, L. A., Sigman, M., Riccio, P. M.,
Salles, A., . . . Ibanez, A. (2013). Insular networks for emo-
tional processing and social cognition: Comparison of two
case reports with either cortical or subcortical involvement.
Cortex, 49(5), 1420–1434. doi:10.1016/j.cortex.2012.08.006
Cowan, W. M., Harter, D. H., & Kandel, E. R. (2000). The emer-
gence of modern neuroscience: Some implications for neu-
rology and psychiatry. Annual Review of Neuroscience, 23,
343–391. doi:10.1146/annurev.neuro.23.1.343
Crespi, C., Cerami, C., Dodich, A., Canessa, N., Arpone, M.,
Iannaccone, S., . . . Cappa, S. F. (2014). Microstructural
white matter correlates of emotion recognition impairment
in amyotrophic lateral sclerosis. Cortex, 53, 1–8.
doi:10.1016/j.cortex.2014.01.002
30 A. IBÁÑEZ ET AL.
Cryan, J. F., & Kaupmann, K. (2005). Don’t worry ‘B’happy!: A
role for GABA B receptors in anxiety and depression. Trends
in Pharmacological Sciences, 26(1), 36–43. doi:10.1016/j.
tips.2004.11.004
Cusi, A., Macqueen, G. M., & McKinnon, M. C. (2010). Altered
self-report of empathic responding in patients with bipolar
disorder. Psychiatry Research, 178(2), 354–358. doi:10.1016/j.
psychres.2009.07.009
Damasio, A. R. (1998). 2 - Signs of aphasia. In M. T. Sarno (Ed.),
Acquired aphasia (3rd ed., pp. 25–41). San Diego: Academic
Press.
Das, P., Lagopoulos, J., Coulston, C. M., Henderson, A. F., &
Malhi, G. S. (2012). Mentalizing impairment in schizophre-
nia: A functional MRI study. Schizophrenia Research, 134(2–
3), 158–164. doi:10.1016/j.schres.2011.08.019.
Davidson, R. J., Pizzagalli, D., Nitschke, J. B., & Putnam, K.
(2002). Depression: Perspectives from affective neu-
roscience. Annual Review of Psychology, 53, 545–574.
doi:10.1146/annurev.psych.53.100901.135148
Dawson, G., Webb, S. J., & McPartland, J. (2005).
Understanding the nature of face processing impairment
in autism: Insights from behavioral and electrophysiological
studies. Developmental Neuropsychology, 27(3), 403–424.
doi:10.1207/s15326942dn2703_6
de Achával, D., Villarreal, M. F., Salles, A., Bertomeu, M. J.,
Costanzo, E. Y., Goldschmidt, M., … Guinjoan, S. M. (2013).
Activation of brain areas concerned with social cognition
during moral decisions is abnormal in schizophrenia
patients and unaffected siblings. Journal of Psychiatric
Research, 47(6), 774–782. doi:10.1016/j.
jpsychires.2012.12.018.
De Renzi, E. (1986). Prosopagnosia in two patients with CT
scan evidence of damage confined to the right hemisphere.
Neuropsychologia, 24(3), 385–389. doi:10.1016/0028-3932
(86)90023-0
De Renzi, E, Perani, D., Carlesimo, G. A., Silveri, M. C., Fazio, F.
(1994). Prosopagnosia can be associated with damage
confined to the right hemisphere–an MRI and PET study
and a review of the literature. Neuropsychologia, 32(8),
893–902.
Decety, J., & Howard, L. H. (2013). The role of affect in the
neurodevelopment of morality. Child Development
Perspectives, 7, 49–54. doi:10.1111/cdep.12020
Decety, J., & Jackson, P. L. (2004). The functional architecture
of human empathy. Behavioral and Cognitive Neuroscience
Reviews, 3(2), 71–100. doi:10.1177/1534582304267187
Decety, J., & Lamm, C. (2006). Human empathy through the
lens of social neuroscience. The Scientific World Journal, 6,
1146–1163. doi:10.1100/tsw.2006.221
Decety, J., Michalska, K. J., & Kinzler, K. D. (2012). The con-
tribution of emotion and cognition to moral sensitivity: A
neurodevelopmental study. Cerebral Cortex, 22(1), 209–220.
doi:10.1093/cercor/bhr111
Dere, E., Pause, B. M., & Pietrowsky, R. (2010). Emotion and
episodic memory in neuropsychiatric disorders. Behavioural
Brain Research, 215(2), 162–171. doi:10.1016/j.
bbr.2010.03.017
Derntl, B., Finkelmeyer, A., Toygar, T. K., Hülsmann, A.,
Schneider, F., Falkenberg, D. I., & Habel, U. (2009).
Generalized deficit in all core components of empathy in
schizophrenia. Schizophrenia Research, 108(1–3), 197–206.
doi:10.1016/j.schres.2008.11.009
Derntl, B., Finkelmeyer, A., Voss, B., Eickhoff, S. B., Kellermann,
T., Schneider, F., & Habel, U. (2012). Neural correlates of the
core facets of empathy in schizophrenia. Schizophrenia
Research, 136(1–3), 70–81. doi:10.1016/j.schres.2011.12.018
Derntl, B., Seidel, E.-M., Schneider, F., & Habel, U. (2012). How
specific are emotional deficits? A comparison of empathic
abilities in schizophrenia, bipolar and depressed patients.
Schizophrenia Research, 142(1–3), 58–64. doi:10.1016/j.
schres.2012.09.020
Devor, A., Bandettini, P. A., Boas, D. A., Bower, J. M., Buxton, R.
B., Cohen, L. B., . . . Yodh, A. G. (2013). The challenge of
connecting the dots in the B.R.A.I.N. Neuron, 80(2), 270–274.
doi:10.1016/j.neuron.2013.09.008
Di Martino, A., Ross, K., Uddin, L. Q., Sklar, A. B., Castellanos, F.
X., & Milham, M. P. (2009). Functional brain correlates of
social and nonsocial processes in autism spectrum disor-
ders: An activation likelihood estimation meta-analysis.
Biological Psychiatry, 65(1), 63–74. doi:10.1016/j.
biopsych.2008.09.022
Dickerson, B. C. (2015). Dysfunction of social cognition and
behavior. Continuum (Minneap Minn), 21(3 Behavioral
Neurology and Neuropsychiatry), 660–677. doi:10.1212/01.
CON.0000466659.05156.1d
Dickinson, D., & Harvey, P. D. (2009). Systemic hypotheses for
generalized cognitive deficits in schizophrenia: A new take
on an old problem. Schizophrenia Bulletin, 35(2), 403–414.
doi:10.1093/schbul/sbn097
Dirnberger, G., & Jahanshahi, M. (2013). Executive dysfunction in
Parkinson’s disease: A review. Journal of Neuropsychology, 7
(2), 193–224. doi:10.1111/jnp.2013.7.issue-2
Djukic, A., Rose, S. A., Jankowski, J. J., & Feldman, J. F. (2014).
Rett syndrome: Recognition of facial expression and its
relation to scanning patterns. Pediatric Neurology, 51, 650–
656. doi:10.1016/j.pediatrneurol.2014.07.022
Driscoll, D. M., Dal Monte, O., Solomon, J., Krueger, F.,
Grafman, J. (2012). Empathic deficits in combat veterans
with traumatic brain injury: Avoxel-based lesion-symptom
mapping study. Cognitive and Behavioral Neurology, 25(4),
160–166. doi:10.1097/WNN.0b013e318280cf4e.
Donix, M., Jurjanz, L., Meyer, S., Amanatidis, E. C., Baeumler, D.,
Huebner, T., … Holthoff, V. A. (2013). Functional imaging
during recognition of personally familiar faces and places in
Alzheimer's disease. Archives of Clinical Neuropsychology, 28
(1), 72–80. doi:10.1093/arclin/acs093.
Dubois, J., & Adolphs, R. (2016). Building a science of indivi-
dual differences from fMRI. Trends in Cognitive Sciences, 20
(6), 425–443. doi:10.1016/j.tics.2016.03.014
Durand, D., Pampillo, M., Caruso, C., & Lasaga, M. (2008). Role
of metabotropic glutamate receptors in the control of neu-
roendocrine function. Neuropharmacology, 55(4), 577–583.
doi:10.1016/j.neuropharm.2008.06.022
Duval, C., Bejanin, A., Piolino, P., Laisney, M., De La Sayette, V.,
Belliard, S., . . . Desgranges, B. (2012). Theory of mind impair-
ments in patients with semantic dementia. Brain, 135(1),
228–241. doi:10.1093/brain/awr309
Dwyer, K., Peters, E., McKenna, P., David, A., & McCarthy, R.
(2014). Verbatim recall in formal thought disorder in schi-
zophrenia: A study of contextual influences. Cognitive
Neuropsychiatry, 19(4), 337–358. doi:10.1080/
13546805.2013.870069.
Dziobek, I., Rogers, K., Fleck, S., Bahnemann, M., Heekeren, H.
R., Wolf, O. T., & Convit, A. (2008). Dissociation of cognitive

and emotional empathy in adults with Asperger syndrome
using the Multifaceted Empathy Test (MET). Journal of
Autism and Developmental Disorders, 38(3), 464–473.
doi:10.1007/s10803-007-0486-x
Eddy, C. M., & Rickards, H. E. (2015). Cognitive deficits predict
poorer functional capacity in Huntington's disease: but
what is being measured? Neuropsychology, 29(2), 268–273.
doi:10.1037/neu0000134.
Editorial, N. N. (2012). Focus on social neuroscience. Nature
Neuroscience, 15(5), 645. doi:10.1038/nn0512-645
Ellis, H. D., De Pauw, K. W., Christodoulou, G. N., Papageorgiou,
L., Milne, A. B., & Joseph, A. B. (1993). Responses to facial
and non-facial stimuli presented tachistoscopically in either
or both visual fields by patients with the Capgras delusion
and paranoid schizophrenics. Journal of Neurology,
Neurosurgery & Psychiatry, 56(2), 215–219. doi:10.1136/
jnnp.56.2.215
Ellis, H. D., Young, A. W., Quayle, A. H., & De Pauw, K. W.
(1997). Reduced autonomic responses to faces in Capgras
delusion. Proceedings of the Royal Society B: Biological
Sciences, 264(1384), 1085–1092. doi:10.1098/
rspb.1997.0150
Epa, R., Czyzowska, N., Dudek, D., Siwek, M., & Gierowski, J. K.
(2014). Profile of moral reasoning in persons with bipolar
affective disorder. Polish Psychiatry, 48(3), 489–502.
Escobar, M. J., Huepe, D., Decety, J., Sedeño, L., Messow, M. K.,
Baez, S., . . . Ibánez, A. (2014). Brain signatures of moral
sensitivity in adolescents with early social deprivation.
Scientific Reports, 4, 5354. doi:10.1038/srep05354
Escobar, M. J., Rivera-Rei, A., Decety, J., Huepe, D., Cardona, J.
F., Canales-Johnson, A., . . . García, A. V. (2013). Attachment
patterns trigger differential neural signature of emotional
processing in adolescents. PLoS One, 8(8), e70247.
doi:10.1371/journal.pone.0070247
Eslinger, P. J., Moore, P., Anderson, C., & Grossman, M. (2011).
Social cognition, executive functioning, and neuroimaging
correlates of empathic deficits in frontotemporal dementia.
Journal of Neuropsychiatry, 23(1), 74–82. doi:10.1176/appi.
neuropsych.23.1.74
Fakra, E., Salgado-Pineda, P., Delaveau, P., Hariri, A. R., & Blin, O.
(2008). Neural bases of different cognitive strategies for facial
affect processing in schizophrenia. Schizophrenia Research,
100(1–3), 191–205. doi:10.1016/j.schres.2007.11.040
Falquez, R., Couto, B., Ibanez, A., Freitag, M. T., Berger, M.,
Arens, E. A., . . . Barnow, S. (2014). Detaching from the
negative by reappraisal: The role of right superior frontal
gyrus (BA9/32). Frontiers in Behavioral Neuroscience, 8, 165.
doi:10.3389/fnbeh.2014.00165
Fernandez-Duque, D., & Black, S. E. (2005). Impaired recogni-
tion of negative facial emotions in patients with frontotem-
poral dementia. Neuropsychologia, 43(11), 1673–1687.
doi:10.1016/j.neuropsychologia.2005.01.005
Fett, A. K., Shergill, S. S., & Krabbendam, L. (2015). Social
neuroscience in psychiatry: Unravelling the neural mechan-
isms of social dysfunction. Psychological Medicine, 45(6),
1145–1165. doi:10.1017/s0033291714002487
Feuerriegel, D., Churches, O., Hofmann, J., & Keage, H. A.
(2014). The N170 and face perception in psychiatric and
neurological disorders: A systematic review. Clinical
Neurophysiology : Official Journal of the International
Federation of Clinical Neurophysiology. doi:10.1016/j.
clinph.2014.09.015
SOCIAL NEUROSCIENCE 31
Fiacconi, C. M., Barkley, V., Finger, E. C., Carson, N., Duke, D.,
Rosenbaum, R. S., . . . KÃhler, S. (2014). Nature and extent of
person recognition impairments associated with Capgras
syndrome in Lewy body dementia. Frontiers in Human
Neuroscience, 8, 726. doi:10.3389/fnhum.2014.00726
Finger, E. C. (2011). New potential therapeutic approaches in
frontotemporal dementia: Oxytocin, vasopressin, and social
cognition. Journal of Molecular Neuroscience : MN, 45(3),
696–701. doi:10.1007/s12031-011-9550-2
Fogelson, N., Li, L., Li, Y., Fernandez-Del-Olmo, M., Santos-
Garcia, D., & Peled, A. (2013). Functional connectivity
abnormalities during contextual processing in schizophre-
nia and in Parkinson's disease. Brain and Cognition, 82(3),
243–253. doi:10.1016/j.bandc.2013.05.001.
Fogelson, N., Ribolsi, M., Fernandez-Del-Olmo, M., Rubino, I. A.,
Romeo, D., Koch, G., & Peled, A. (2011). Neural correlates of
local contextual processing deficits in schizophrenic
patients. Psychophysiology, 48(9), 1217–1226. doi:10.1111/
j.1469-8986.2011.01195.x.
Fogelson, N., Shah, M., Scabini, D., & Knight, R. T. (2009).
Prefrontal cortex is critical for contextual processing:
Evidence from brain lesions. Brain, 132(11), 3002–3010.
doi:10.1093/brain/awp230
Fonville, L., Giampietro, V., Surguladze, S., Williams, S., &
Tchanturia, K. (2014). Increased BOLD signal in the fusiform
gyrus during implicit emotion processing in anorexia ner-
vosa. NeuroImage: Clinical, 4, 266–273. doi:10.1016/j.
nicl.2013.12.002
Francis, S. M., Sagar, A., Levin-Decanini, T., Liu, W., Carter, C. S.,
& Jacob, S. (2014). Oxytocin and vasopressin systems in
genetic syndromes and neurodevelopmental disorders.
Brain Research, 1580, 199–218. doi:10.1016/j.
brainres.2014.01.021
Franklin, S. A., McNally, R. J., & Riemann, B. C. (2009). Moral
reasoning in obsessive-compulsive disorder. Journal of
Anxiety Disorders, 23(5), 575–577. doi:10.1016/j.
janxdis.2008.11.005
Friston, K. J. (2012). The history of the future of the Bayesian
brain. Neuroimage, 62(2), 1230–1233. doi:10.1016/j.
neuroimage.2011.10.004
Fujino, J., Yamasaki, N., Miyata, J., Kawada, R., Sasaki, H.,
Matsukawa, N., … Murai, T. (2014). Altered brain response
to others‫ ׳‬pain in major depressive disorder. Journal of
Affective Disorders, 165, 170–175. doi:10.1016/j.
jad.2014.04.058
Fujiwara, H., Yassin, W., & Murai, T. (2014). Neuroimaging
studies of social cognition in schizophrenia. Psychiatry and
Clinical Neurosciences. doi:10.1111/pcn.12258
García, A., & Ibáñez, A. (2016). A touch with words: Dynamic
synergies between manual actions and language.
Neuroscience & Biobehavioral Reviews, 68, 59–95.
doi:10.1016/j.neubiorev.2016.04.022
García, A. M., & Ibáñez, A. (2014). Two-person neuroscience
and naturalistic social communication: The role of language
and linguistic variables in brain-coupling research. Frontiers
in Psychiatry, 5. doi:10.3389/fpsyt.2014.00124
García-Cordero, I., Sedeño, L., De La Fuente, L., Slachevsky, A.,
Forno, G., Klein, F., . . . Ibañez, A. (2016). Feeling, learning
from, and being aware of inner states: Interoceptive dimen-
sions in neurodegeneration and stroke. Philosophical
Transactions of the Royal Society of London. Series B,
Biological Sciences. doi:10.1098/rstb.2016-0006
32 A. IBÁÑEZ ET AL.
García-Cordero, I., Sedeño, L., Fraiman, D., Craiem, D., De La
Fuente, L. A., Salamone, P., . . . Ibañez, A. (2015). Stroke and
neurodegeneration induce different connectivity aberra-
tions in the insula. Stroke, 46(9), 2673–2677. doi:10.1161/
STROKEAHA.115.009598
Garfinkel, S. N., & Critchley, H. D. (2013). Interoception, emo-
tion and brain: New insights link internal physiology to
social behaviour. Commentary on:: “Anterior insular cortex
mediates bodily sensibility and social anxiety” by Terasawa
et al. (2012). Social Cognitive and Affective Neuroscience, 8
(3), 231–234. doi:10.1093/scan/nss140
Geschwind, D. H. (2009). Advances in autism. Annual Review of
Medicine, 60, 367–380. doi:10.1146/annurev.
med.60.053107.121225
Gleichgerrcht, E., Ibanez, A., Roca, M., Torralva, T., & Manes, F.
(2010). Decision-making cognition in neurodegenerative
diseases. Nature Reviews. Neurology, 6(11), 611–623.
doi:10.1038/nrneurol.2010.148
Gleichgerrcht, E., Torralva, T., Rattazzi, A., Marenco, V., Roca,
M., & Manes, F. (2013). Selective impairment of cognitive
empathy for moral judgment in adults with high function-
ing autism. Social Cognitive and Affective Neuroscience, 8(7),
780–788. doi:10.1093/scan/nss067
Gomez-Ibanez, A., Urrestarazu, E., & Viteri, C. (2014).
Recognition of facial emotions and identity in patients
with mesial temporal lobe and idiopathic generalized epi-
lepsy: An eye-tracking study. Seizure, 23, 892–898.
doi:10.1016/j.seizure.2014.08.012
Gonzalez-Gadea, M. L., Baez, S., Torralva, T., Castellanos, F. X.,
Rattazzi, A., Bein, V., . . . Ibanez, A. (2013). Cognitive varia-
bility in adults with ADHD and AS: Disentangling the roles
of executive functions and social cognition. Research in
Developmental Disabilities, 34(2), 817–830. doi:10.1016/j.
ridd.2012.11.009
Gonzalez-Gadea, M. L., Chennu, S., Bekinschtein, T. A., Rattazzi,
A., Beraudi, A., Tripicchio, P., . . . Ibanez, A. (2015). Predictive
coding in autism spectrum disorder and attention deficit
hyperactivity disorder. Journal of Neurophysiology, 114(5),
2625–2636. doi:10.1152/jn.00543.2015
Gonzalez-Gadea, M. L., Herrera, E., Parra, M., Gomez Mendez,
P., Baez, S., Manes, F., & Ibanez, A. (2014). Emotion recogni-
tion and cognitive empathy deficits in adolescent offenders
revealed by context-sensitive tasks. Frontiers in Human
Neuroscience, 8, 850. doi:10.3389/fnhum.2014.00850
Gonzalez-Gadea, M. L., Ibanez, A., Damm, J., Ramirez Romero,
D. A., Abrevaya, S., Manes, F., . . . Roca, M. (2014). Different
levels of implicit emotional recognition in posterior cortical
atrophy (PCA). Neurocase, 1–8. doi:10.1080/
13554794.2014.919325
Gonzalez-Gadea, M. L., Sigman, M., Rattazzi, A., Lavin, C., Rivera-
Rei, A., Marino, J., . . . Ibanez, A. (2016). Neural markers of
social and monetary rewards in children with Attention-
Deficit/Hyperactivity disorder and autism spectrum disorder.
Scientific Reports, 6, 30588. doi:10.1038/srep30588
Gonzalez-Gadea, M. L., Tripicchio, P., Rattazzi, A., Baez, S., Marino,
J., Roca, M., . . . Ibanez, A. (2014). Inter-individual cognitive
variability in children with Asperger’s syndrome. Frontiers in
Human Neuroscience, 8. doi:10.3389/fnhum.2014.00575
Green, M. J., Waldron, J. H., & Coltheart, M. (2007). Emotional
context processing is impaired in schizophrenia. Cognitive
Neuropsychiatry, 12(3), 259–280. doi:10.1080/
13546800601051847
Green, M. J., Waldron, J. H., Simpson, I., & Coltheart, M. (2008).
Visual processing of social context during mental state
perception in schizophrenia. Journal of Psychiatry &
Neuroscience : JPN, 33(1), 34–42.
Greene, A. J., Gross, W. L., Elsinger, C. L., & Rao, S. M. (2006). An
FMRI analysis of the human hippocampus: Inference, con-
text, and task awareness. Journal of Cognitive Neuroscience,
18(7), 1156–1173. doi:10.1162/jocn.2006.18.7.1156
Greene, J. D., Nystrom, L. E., Engell, A. D., Darley, J. M., &
Cohen, J. D. (2004). The neural bases of cognitive conflict
and control in moral judgment. Neuron, 44(2), 389–400.
doi:10.1016/j.neuron.2004.09.027
Greene, J. D., Sommerville, R. B., Nystrom, L. E., Darley, J. M., &
Cohen, J. D. (2001). An fMRI investigation of emotional
engagement in moral judgment. Science, 293(5537), 2105–
2108. doi:10.1126/science.1062872
Gregory, C., Lough, S., Stone, V., Erzinclioglu, S., Martin, L.,
Baron-Cohen, S., & Hodges, J. R. (2002). Theory of mind in
patients with frontal variant frontotemporal dementia and
Alzheimer’s disease: Theoretical and practical implications.
Brain, 125(4), 752–764. doi:10.1093/brain/awf079
Guerra, S., Ibanez, A., Martin, M., Bobes, M. A., Reyes, A.,
Mendoza, R., . . . Sosa, M. V. (2009). N400 deficits from
semantic matching of pictures in probands and first-degree
relatives from multiplex schizophrenia families. Brain
and Cognition, 70(2), 221–230. doi:10.1016/j.
bandc.2009.02.004
Gur, R. E., Loughead, J., Kohler, C. G., Elliott, M. A., Lesko, K.,
Ruparel, K., . . . Gur, R. C. (2007). Limbic activation associated
with misidentification of fearful faces and flat affect in
schizophrenia. Archives of General Psychiatry, 64(12), 1356–
1366. doi:10.1001/archpsyc.64.12.1356
Habel, U., Chechko, N., Pauly, K., Koch, K., Backes, V., Seiferth,
N., . . . Kellermann, T. (2010). Neural correlates of emotion
recognition in schizophrenia. Schizophrenia Research, 122
(1–3), 113–123. doi:10.1016/j.schres.2010.06.009
Hansen, S. (2011). Inhibitory control and empathy-related
personality traits: Sex-linked associations. Brain and
Cognition, 76(3), 364–368. doi:10.1016/j.bandc.2011.04.004
Harrington, L., Siegert, R. J., & McClure, J. (2005). Theory of mind
in schizophrenia: A critical review. Cognitive Neuropsychiatry,
10(4), 249–286. doi:10.1080/13546800444000056
Hasson, U., Ghazanfar, A. A., Galantucci, B., Garrod, S., &
Keysers, C. (2012). Brain-to-brain coupling: A mechanism
for creating and sharing a social world. Trends in Cognitive
Sciences, 16(2), 114–121. doi:10.1016/j.tics.2011.12.007
Hennion, S., Delbeuck, X., Duhamel, A., Lopes, R., Semah, F.,
Tyvaert, L., . . . Szurhaj, W. (2014). Characterization and pre-
diction of theory of mind disorders in temporal lobe epi-
lepsy. Neuropsychology. doi:10.1037/neu0000126
Henry, A., Tourbah, A., Chaunu, M. P., Rumbach, L., Montreuil,
M., & Bakchine, S. (2011). Social cognition impairments in
relapsing-remitting multiple sclerosis. Journal of the
International Neuropsychological Society : JINS, 17(6), 1122–
1131. doi:10.1017/S1355617711001147
Henry, J. D., Cowan, D. G., Lee, T., & Sachdev, P. (2015). A
review of different methods of assessing social cognitive
function in clinical settings. Current Opinion in Psychiatry, 1.
doi:10.1097/yco.0000000000000139
Henry, J. D., Phillips, L. H., Crawford, J. R., Ietswaart, M., &
Summers, F. (2006). Theory of mind following traumatic
brain injury: The role of emotion recognition and executive

dysfunction. Neuropsychologia, 44(10), 1623–1628.
doi:10.1016/j.neuropsychologia.2006.03.020
Henry, J. D., Phillips, L. H., & Von Hippel, C. (2014). A meta-
analytic review of theory of mind difficulties in behavioural-
variant frontotemporal dementia. Neuropsychologia, 56, 53–
62. doi:10.1016/j.neuropsychologia.2013.12.024
Hesse, E., Mikulan, E., Decety, J., Sigman, M., Garcia, M. D. C.,
Silva, W., . . . Ibanez, A. (2016). Early detection of intentional
harm in the human amygdala. Brain, 139(Pt 1), 54–61.
doi:10.1093/brain/awv336
Hezel, D. M., & McNally, R. J. (2014). Theory of mind impair-
ments in social anxiety disorder. Behavior Therapy, 45(4),
530–540. doi:10.1016/j.beth.2014.02.010
Hot, P., Klein-Koerkamp, Y., Borg, C., Richard-Mornas, A.,
Zsoldos, I., Paignon Adeline, A., Thomas Antérion, C.,
Baciu, M. (2013). Fear recognition impairment in early-
stage Alzheimer's disease: When focusing on the eyes
region improves performance. Brain and Cognition, 82(1),
25–34. doi:10.1016/j.bandc.2013.02.001.
Horinek, D., Varjassyova, A., & Hort, J. (2007). Magnetic reso-
nance analysis of amygdalar volume in Alzheimer’s disease.
Current Opinion in Psychiatry, 20(3), 273–277. doi:10.1097/
YCO.0b013e3280ebb613
Huang, S. F., Oi, M., & Taguchi, A. (2015). Comprehension of
figurative language in Taiwanese children with autism: The
role of theory of mind and receptive vocabulary. Clinical
Linguistics & Phonetics, 24, 1–12.
Huepe, D., Riveros, R., Manes, F., Couto, B., Hurtado, E.,
Cetkovich, M., . . . Ibanez, A. (2012). The relationship of
clinical, cognitive and social measures in schizophrenia: A
preliminary finding combining measures in probands and
relatives. Behavioural Neurology, 25(2), 137–150.
doi:10.1155/2012/194159
Hyman, S. E. (2007). Can neuroscience be integrated into the
DSM-V? Nature Reviews. Neuroscience, 8(9), 725–732.
doi:10.1038/nrn2218
Ibanez, A., Aguado, J., Baez, S., Huepe, D., Lopez, V., Ortega, R.,
. . . Manes, F. (2014). From neural signatures of emotional
modulation to social cognition: Individual differences in
healthy volunteers and psychiatric participants. Social
Cognitive and Affective Neuroscience, 9(7), 939–950.
doi:10.1093/scan/nst067
Ibanez, A., & Cosmelli, D. (2008). Moving beyond computa-
tional cognitivism: Understanding intentionality, intersub-
jectivity and ecology of mind. Integrative Psychological and
Behavioral Science, 42(2), 129–136. doi:10.1007/s12124-007-
9045-4
Ibáñez, A., Gleichgerrcht, E., Hurtado, E., González, R., Haye, A.,
& Manes, F. (2010). Early neural markers of implicit atti-
tudes: N170 modulated by intergroup and evaluative con-
texts in IAT. Frontiers in Human Neuroscience, 4, 188.
doi:10.3389/fnhum.2010.00188
Ibanez, A., Huepe, D., Gempp, R., Gutiérrez, V., Rivera-Rei, A., &
Toledo, M. I. (2013). Empathy, sex and fluid intelligence as
predictors of theory of mind. Personality and Individual
Differences, 54(5), 616–621. doi:10.1016/j.paid.2012.11.022
Ibáñez, A., Hurtado, E., Riveros, R., Urquina, H., Cardona, J. F.,
Petroni, A., . . . Manes, F. (2011). Facial and semantic emotional
interference: A pilot study on the behavioral and cortical
responses to the dual valence association task. Behavioral
and Brain Functions, 7(1), 8. doi:10.1186/1744-9081-7-8
SOCIAL NEUROSCIENCE 33
Ibanez, A., Kotz, S. A., Barrett, L., Moll, J., & Ruz, M. (2014).
Situated affective and social neuroscience. Frontiers in
Human Neuroscience, 8, 547. doi:10.3389/fnhum.2014.00547
Ibanez, A., Kuljis, R. O., Matallana, D., & Manes, F. (2014).
Bridging psychiatry and neurology through social neu-
roscience. World Psychiatry, 13(2), 148–149. doi:10.1002/
wps.20125
Ibanez, A., & Manes, F. (2012). Contextual social cognition and
the behavioral variant of frontotemporal dementia.
Neurology, 78(17), 1354–1362. doi:10.1212/
WNL.0b013e3182518375
Ibanez, A., Melloni, M., Huepe, D., Helgiu, E., Rivera-Rei, A.,
Canales-Johnson, A., . . . Moya, A. (2012). What event-related
potentials (ERPs) bring to social neuroscience? Social
Neuroscience, 7(6), 632–649. doi:10.1080/
17470919.2012.691078
Ibáñez, A., Petroni, A., Urquina, H., Torrente, F., Torralva, T.,
Hurtado, E., . . . Manes, F. (2011). Cortical deficits of emo-
tional face processing in adults with ADHD: Its relation to
social cognition and executive function. Social
Neuroscience, 6(5–6), 464–481. doi:10.1080/
17470919.2011.620769
Ibáñez, A., Riveros, R., Aravena, P., Vergara, V., Cardona, J. F.,
García, L., . . . Manes, F. (2011). When context is difficult to
integrate: Cortical measures of congruency in schizophre-
nics and healthy relatives from multiplex families.
Schizophrenia Research, 126(1–3), 303–305. doi:10.1016/j.
schres.2010.04.008
Ibanez, A., Riveros, R., Hurtado, E., Gleichgerrcht, E., Urquina,
H., Herrera, E., . . . Manes, F. (2012). The face and its emotion:
Right N170 deficits in structural processing and early emo-
tional discrimination in schizophrenic patients and rela-
tives. Psychiatry Research, 195(1–2), 18–26. doi:10.1016/j.
psychres.2011.07.027
Ibanez, A., Urquina, H., Petroni, A., Baez, S., Lopez, V., Do
Nascimento, M., . . . Baune, B. T. (2012). Neural processing
of emotional facial and semantic expressions in euthymic
bipolar disorder (BD) and its association with theory of
mind (ToM). PLoS One, 7(10), e46877. doi:10.1371/journal.
pone.0046877
Ibanez, A., Velasquez, M. M., Caro, M. M., & Manes, F. (2013).
Implicit emotional awareness in frontotemporal dementia.
Cognitive Neuroscience, 4(3–4), 204–206. doi:10.1080/
17588928.2013.854756
Insel, T. R. (2014). The NIMH Research Domain Criteria (RDoC)
Project: Precision medicine for psychiatry. American Journal
of Psychiatry, 171(4), 395–397. doi:10.1176/appi.
ajp.2014.14020138
Insel, T. R., & Quirion, R. (2005). Psychiatry as a clinical neu-
roscience discipline. Jama, 294(17), 2221–2224. doi:10.1001/
jama.294.17.2221
Irwin, M. R., & Cole, S. W. (2011). Reciprocal regulation of the
neural and innate immune systems. Nature Reviews.
Immunology, 11(9), 625–632. doi:10.1038/nri3042
Jablensky, A. (2005). Categories, dimensions and prototypes:
Critical issues for psychiatric classification. Psychopathology,
38(4), 201–205. doi:10.1159/000086092
Jackson, P. L., Rainville, P., & Decety, J. (2006). To what extent
do we share the pain of others? Insight from the neural
bases of pain empathy. Pain, 125(1), 5–9. doi:10.1016/j.
pain.2006.09.013
34 A. IBÁÑEZ ET AL.
Jiang, Y., Hu, Y., Wang, Y., Zhou, N., Zhu, L., & Wang, K. (2014).
Empathy and emotion recognition in patients with idio-
pathic generalized epilepsy. Epilepsy & Behavior, 37, 139–
144. doi:10.1016/j.yebeh.2014.06.005
Johnson, S. A., Stout, J. C., Solomon, A. C., Langbehn, D. R.,
Aylward, E. H., Cruce, C. B., . . . Paulsen, J. S. (2007). Beyond
disgust: Impaired recognition of negative emotions prior to
diagnosis in Huntington’s disease. Brain, 130(7), 1732–1744.
doi:10.1093/brain/awm107
Kang, J. I., Namkoong, K., Yoo, S. W., Jhung, K., & Kim, S. J.
(2012). Abnormalities of emotional awareness and percep-
tion in patients with obsessive-compulsive disorder. Journal
of Affective Disorders, 141(2–3), 286–293. doi:10.1016/j.
jad.2012.04.001
Karelina, K., Stuller, K. A., Jarrett, B., Zhang, N., Wells, J.,
Norman, G. J., & DeVries, A. C. (2011). Oxytocin mediates
social neuroprotection after cerebral ischemia. Stroke, 42
(12), 3606–3611. doi:10.1161/STROKEAHA.111.628008
Kendler, K. S. (1990). Toward a scientific psychiatric nosology.
Strengths and limitations. Archives of General Psychiatry, 47
(10), 969–973. doi:10.1001/archpsyc.1990.01810220085011
Kennedy, D. P., & Adolphs, R. (2012). The social brain in
psychiatric and neurological disorders. Trends in Cognitive
Sciences, 16(11), 559–572. doi:10.1016/j.tics.2012.09.006
Key, A. P., Jones, D., & Dykens, E. M. (2013). Social and emo-
tional processing in Prader-Willi syndrome: Genetic subtype
differences. Journal of Neurodevelopmental Disorders, 5(1), 7.
doi:10.1186/1866-1955-5-7
Khemiri, L., Guterstam, J., Franck, J., Jayaram-Lindström, N., &
García, A. V. (2012). Alcohol dependence associated with
increased utilitarian moral judgment: A case control study.
PLoS One, 7(6), e39882. doi:10.1371/journal.pone.0039882
Kipps, C. M., Nestor, P. J., Acosta-Cabronero, J., Arnold, R., &
Hodges, J. R. (2009). Understanding social dysfunction in
the behavioural variant of frontotemporal dementia: The
role of emotion and sarcasm processing. Brain, 132(3), 592–
603. doi:10.1093/brain/awn314
Klein-Koerkamp, Y., Beaudoin, M., Baciu, M., & Hot, P. (2012).
Emotional decoding abilities in Alzheimer’s disease: A
meta-analysis. Journal of Alzheimer’s Disease : JAD, 32(1),
109–125. doi:10.3233/JAD-2012-120553
Koenigs, M., Kruepke, M., Zeier, J., & Newman, J. P. (2012).
Utilitarian moral judgment in psychopathy. Social Cognitive
and Affective Neuroscience, 7(6), 708–714. doi:10.1093/scan/
nsr048
Koenigs, M., Young, L., Adolphs, R., Tranel, D., Cushman, F.,
Hauser, M., & Damasio, A. (2007). Damage to the prefrontal
cortex increases utilitarian moral judgements. Nature, 446
(7138), 908–911. doi:10.1038/nature05631
Kohler, C. G., Martin, E. A., Stolar, N., Barrett, F. S., Verma, R.,
Brensinger, C., . . . Gur, R. C. (2008). Static posed and evoked
facial expressions of emotions in schizophrenia.
Schizophrenia Research, 105(1–3), 49–60. doi:10.1016/j.
schres.2008.05.010
Koob, G. F., & Volkow, N. D. (2010). Neurocircuitry of addiction.
Neuropsychopharmacology, 35(1), 217–238. doi:10.1038/
npp.2009.110
Kraemer, M., Herold, M., Uekermann, J., Kis, B., Wiltfang, J.,
Daum, I., . . . Abdel-Hamid, M. (2013). Theory of mind and
empathy in patients at an early stage of relapsing remitting
multiple sclerosis. Clinical Neurology and Neurosurgery, 115
(7), 1016–1022. doi:10.1016/j.clineuro.2012.10.027
Krupp, L. B., Alvarez, L. A., LaRocca, N. G., & Scheinberg, L. C.
(1988). Fatigue in multiple sclerosis. Archives of Neurology,
45(4), 435–437. doi:10.1001/archneur.1988.0052028
0085020
Krystal, J., Sanacora, G., Blumberg, H., Anand, A., Charney, D.,
Marek, G., . . . Mason, G. F. (2002). Glutamate and GABA
systems as targets for novel antidepressant and mood-
stabilizing treatments. Molecular Psychiatry, 7, S71–S80.
doi:10.1038/sj.mp.4001021
Kumfor, F., Irish, M., Hodges, J. R., Piguet, O., & Kilner, J. (2013).
Discrete Neural Correlates for the Recognition of Negative
Emotions: Insights from Frontotemporal Dementia. PLoS
One, 8(6), e67457. doi:10.1371/journal.pone.0067457
Kumfor, F., Miller, L., Lah, S., Hsieh, S., Savage, S., Hodges, J. R.,
& Piguet, O. (2011). Are you really angry? The effect of
intensity on facial emotion recognition in frontotemporal
dementia. Social Neuroscience, 6(5–6), 502–514.
doi:10.1080/17470919.2011.620779
Kumfor, F., & Piguet, O. (2013). Emotion recognition in the
dementias: Brain correlates and patient implications.
Neurodegenerative Disease Management, 3(3), 277–288.
doi:10.2217/nmt.13.16
Kumfor, F., Sapey-Triomphe, L.-A., Leyton, C. E., Burrell, J. R.,
Hodges, J. R., & Piguet, O. (2014). Degradation of emotion
processing ability in corticobasal syndrome and Alzheimer’s
disease. Brain, 137(11), 3061–3072. doi:10.1093/brain/
awu246
Lavenu, I., & Pasquier, F. (2005). Perception of emotion on
faces in frontotemporal dementia and Alzheimer’s disease:
A longitudinal study. Dementia and Geriatric Cognitive
Disorders, 19(1), 37–41. doi:10.1159/000080969
Le Bouc, R., Lenfant, P., Delbeuck, X., Ravasi, L., Lebert, F.,
Semah, F., & Pasquier, F. (2012). My belief or yours?
Differential theory of mind deficits in frontotemporal
dementia and Alzheimer’s disease. Brain, 135(10), 3026–
3038. doi:10.1093/brain/aws237
Lee, S. J., Kang Do, H., Kim, C.-W., Gu, B. M., Park, J.-Y., Choi, C.-
H., . . . Kwon, J. S. (2010). Multi-level comparison of empathy
in schizophrenia: An fMRI study of a cartoon task. Psychiatry
Research: Neuroimaging, 181(2), 121–129. doi:10.1016/j.
pscychresns.2009.08.003
Leigh, R., Oishi, K., Hsu, J., Lindquist, M., Gottesman, R. F.,
Jarso, S., . . . Hillis, A. E. (2013). Acute lesions that impair
affective empathy. Brain, 136(8), 2539–2549. doi:10.1093/
brain/awt177
Levenson, R. W., Sturm, V. E., & Haase, C. M. (2014). Emotional
and behavioral symptoms in neurodegenerative disease: A
model for studying the neural bases of psychopathology.
Annual Review of Clinical Psychology, 10, 581–606.
doi:10.1146/annurev-clinpsy-032813-153653
Linden, S. C., Jackson, M. C., Subramanian, L., Wolf, C., Green,
P., Healy, D., & Linden, D. E. J. (2010). Emotion-cognition
interactions in schizophrenia: Implicit and explicit effects of
facial expression. Neuropsychologia, 48(4), 997–1002.
doi:10.1016/j.neuropsychologia.2009.11.023
Liu, T., & Pelowski, M. (2014). Clarifying the interaction types in
two-person neuroscience research. Frontiers in Human
Neuroscience, 8. doi:10.3389/fnhum.2014.00276
Liu, T. T., & Behrmann, M. (2014). Impaired holistic processing
of left-right composite faces in congenital prosopagnosia.
Frontiers in Human Neuroscience, 8, 750. doi:10.3389/
fnhum.2014.00750

Lough, S., Kipps, C. M., Treise, C., Watson, P., Blair, J. R., &
Hodges, J. R. (2006). Social reasoning, emotion and empa-
thy in frontotemporal dementia. Neuropsychologia, 44(6),
950–958. doi:10.1016/j.neuropsychologia.2005.08.009
Lupien, S. J., McEwen, B. S., Gunnar, M. R., & Heim, C. (2009).
Effects of stress throughout the lifespan on the brain,
behaviour and cognition. Nature Reviews. Neuroscience, 10
(6), 434–445. doi:10.1038/nrn2639
Maguire, J., & Mody, I. (2008). GABA A R plasticity during
pregnancy: Relevance to postpartum depression. Neuron,
59(2), 207–213. doi:10.1016/j.neuron.2008.06.019
Mahoney, C. J., Beck, J., Rohrer, J. D., Lashley, T., Mok, K.,
Shakespeare, T., . . . Warren, J. D. (2012). Frontotemporal
dementia with the C9ORF72 hexanucleotide repeat
expansion: Clinical, neuroanatomical and neuropathologi-
cal features. Brain, 135(3), 736–750. doi:10.1093/brain/
awr361
Manes, F. (2012). Psychiatric conditions that can mimic early
behavioral variant frontotemporal dementia: The impor-
tance of the new diagnostic criteria. Current Psychiatry
Reports, 14(5), 450–452. doi:10.1007/s11920-012-0294-7
Manes, F. F., Torralva, T., Roca, M., Gleichgerrcht, E.,
Bekinschtein, T. A., & Hodges, J. R. (2010). Frontotemporal
dementia presenting as pathological gambling. Nature
Reviews. Neurology, 6(6), 347–352. doi:10.1038/
nrneurol.2010.34
Marazziti, D., Baroni, S., Landi, P., Ceresoli, D., & Dell’Osso, L.
(2013). The neurobiology of moral sense: Facts or hypoth-
eses? Annals of General Psychiatry, 12(1), 6. doi:10.1186/
1744-859X-12-6
Marrie, R. A., Reingold, S., Cohen, J., Stuve, O., Trojano, M.,
Sorensen, P. S., . . . Reider, N. (2015). The incidence and
prevalence of psychiatric disorders in multiple sclerosis: A
systematic review. Multiple Sclerosis (Houndmills,
Basingstoke, England). doi:10.1177/1352458514564487
Martin, J. B. (2002). The integration of neurology, psychiatry,
and neuroscience in the 21st century. American Journal of
Psychiatry, 159(5), 695–704. doi:10.1176/appi.ajp.159.5.695
McCleery, A., Lee, J., Joshi, A., Wynn, J. K., Hellemann, G. S., &
Green, M. F. (2014). Meta-analysis of face processing event-
related potentials in schizophrenia. Biological Psychiatry, 5
(14), 015.
McCormick, L. M., Brumm, M. C., Beadle, J. N., Paradiso, S.,
Yamada, T., & Andreasen, N. (2012). Mirror neuron function,
psychosis, and empathy in schizophrenia. Psychiatry
Research: Neuroimaging, 201(3), 233–239. doi:10.1016/j.
pscychresns.2012.01.004
McGorry, P., & Van Os, J. (2013). Redeeming diagnosis in
psychiatry: Timing versus specificity. The Lancet, 381(9863),
343–345. doi:10.1016/S0140-6736(12)61268-9
Melloni, M., Billeke, P., Baez, S., Hesse, E., De La Fuente, L.,
Forno, G., . . . Ibanez, A. (2016). Your perspective and my
benefit: Multiple lesion models of self-other integration
strategies during social bargaining. Brain, 26. 10.1093/
brain/aww1231
Melloni, M., Lopez, V., & Ibanez, A. (2013). Empathy and con-
textual social cognition. Cognitive, Affective & Behavioral
Neuroscience. doi:10.3758/s13415-013-0205-3
Melloni, M., Sedeño, L., Couto, B., Reynoso, M., Gelormini, C.,
Favaloro, R., . . . Ibanez, A. (2013). Preliminary evidence
about the effects of meditation on interoceptive sensitivity
SOCIAL NEUROSCIENCE 35
and social cognition. Behavioral and Brain Functions : BBF, 9,
47. doi:10.1186/1744-9081-9-47
Mendez, M. F., Anderson, E., & Shapira, J. S. (2005). An inves-
tigation of moral judgement in frontotemporal dementia.
Cognitive and Behavioral Neurology, 18(4), 193–197.
doi:10.1097/01.wnn.0000191292.17964.bb
Mendez, M. F., & Shapira, J. S. (2009). Altered emotional
morality in frontotemporal dementia. Cognitive
Neuropsychiatry, 14(3), 165–179. doi:10.1080/
13546800902924122
Mesulam, M. M. (1986). Frontal cortex and behavior. Annals of
Neurology, 19(4), 320–325. doi:10.1002/ana.410190403
Meyer, M. L., Spunt, R. P., Berkman, E. T., Taylor, S. E., &
Lieberman, M. D. (2012). Evidence for social working mem-
ory from a parametric functional MRI study. Proceedings of
the National Academy of Sciences, 109(6), 1883–1888.
doi:10.1073/pnas.1121077109
Meyer-Lindenberg, A. (2014). Social neuroscience and
mechanisms of risk for mental disorders. World Psychiatry,
13(2), 143–144. doi:10.1002/wps.20121
Meziane, H., Schaller, F., Bauer, S., Villard, C., Matarazzo, V., Riet,
F., . . . Muscatelli, F. (2014). An early postnatal oxytocin treat-
ment prevents social and learning deficits in adult mice
deficient for Magel2, a gene involved in prader-willi syn-
drome and autism. Biological Psychiatry, 20(14), 00887–00887.
Mike, A., Strammer, E., Aradi, M., Orsi, G., Perlaki, G., Hajnal, A.,
. . . Paul, F. (2013). Disconnection mechanism and regional
cortical atrophy contribute to impaired processing of facial
expressions and theory of mind in multiple sclerosis: A
structural MRI study. PLoS One, 8(12), e82422. doi:10.1371/
journal.pone.0082422
Mikulan, E. P., Reynaldo, L., & Ibanez, A. (2014). Homuncular
mirrors: Misunderstanding causality in embodied cognition.
Frontiers in Human Neuroscience, 8, 299. doi:10.3389/
fnhum.2014.00299
Millan, M. J., Agid, Y., Brüne, M., Bullmore, E. T., Carter, C. S.,
Clayton, N. S., . . . Young, L. J. (2012). Cognitive dysfunction
in psychiatric disorders: Characteristics, causes and the
quest for improved therapy. Nature Reviews. Drug
Discovery, 11(2), 141–168. doi:10.1038/nrd3628
Miller, L. A., Hsieh, S., Lah, S., Savage, S., Hodges, J. R., & Piguet,
O. (2012). One size does not fit all: Face emotion processing
impairments in semantic dementia, behavioural-variant
frontotemporal dementia and Alzheimer’s disease are
mediated by distinct cognitive deficits. Behavioural
Neurology, 25(1), 53–60. doi:10.1155/2012/683052
Miller, M. B., Sinnott-Armstrong, W., Young, L., King, D., Paggi,
A., Fabri, M., . . . Gazzaniga, M. S. (2010). Abnormal moral
reasoning in complete and partial callosotomy patients.
Neuropsychologia, 48(7), 2215–2220. doi:10.1016/j.
neuropsychologia.2010.02.021
Milrod, B., Markowitz, J. C., Gerber, A. J., Cyranowski, J.,
Altemus, M., Shapiro, T., . . . Glatt, C. (2014). Childhood
separation anxiety and the pathogenesis and treatment of
adult anxiety. American Journal of Psychiatry, 171(1), 34–43.
doi:10.1176/appi.ajp.2013.13060781
Minio-Paluello, I., Baron-Cohen, S., Avenanti, A., Walsh, V., &
Aglioti, S. M. (2009). Absence of embodied empathy during
pain observation in Asperger syndrome. Biological
Psychiatry, 65(1), 55–62. doi: 10.1016/j.
biopsych.2008.08.006.
36 A. IBÁÑEZ ET AL.
Moll, J., & Schulkin, J. (2009). Social attachment and aversion
in human moral cognition. Neuroscience & Biobehavioral
Reviews, 33(3), 456–465. doi:10.1016/j.
neubiorev.2008.12.001
Moll, J., Zahn, R., De Oliveira-Souza, R., Krueger, F., & Grafman,
J. (2005). Opinion: The neural basis of human moral cogni-
tion. Nature Reviews Neuroscience, 6(10), 799–809.
doi:10.1038/nrn1768
Monkul, E. S., Green, M. J., Barrett, J. A., Robinson, J. L.,
Velligan, D. I., & Glahn, D. C. (2007). A social cognitive
approach to emotional intensity judgment deficits in schi-
zophrenia. Schizophrenia Research, 94(1–3), 245–252.
doi:10.1016/j.schres.2007.03.023
Montag, C., Heinz, A., Kunz, D., & Gallinat, J. (2007). Self-
reported empathic abilities in schizophrenia. Schizophrenia
Research, 92(1–3), 85–89. doi:10.1016/j.schres.2007.01.024
Moran, J. M., Young, L. L., Saxe, R., Lee, S. M., O’Young, D.,
Mavros, P. L., & Gabrieli, J. D. (2011). Impaired theory of
mind for moral judgment in high-functioning autism.
Proceedings of the National Academy of Sciences, 108(7),
2688–2692. doi:10.1073/pnas.1011734108
Moretto, G., Làdavas, E., Mattioli, F., & Di Pellegrino, G. (2010).
A psychophysiological investigation of moral judgment
after ventromedial prefrontal damage. Journal of Cognitive
Neuroscience, 22(8), 1888–1899. doi:10.1162/
jocn.2009.21367
Narme, P., Mouras, H., Roussel, M., Duru, C., Krystkowiak, P., &
Godefroy, O. (2013). Emotional and cognitive social pro-
cesses are impaired in Parkinson’s disease and are related
to behavioral disorders. Neuropsychology, 27(2), 182–192.
doi:10.1037/a0031522
Neary, D., Snowden, J. S., Gustafson, L., Passant, U., Stuss, D.,
Black, S., . . . Benson, D. F. (1998). Frontotemporal lobar
degeneration: A consensus on clinical diagnostic criteria.
Neurology, 51(6), 1546–1554. doi:10.1212/WNL.51.6.1546
Newman, J. P., Curtin, J. J., Bertsch, J. D., & Baskin-Sommers, A.
R. (2010). Attention moderates the fearlessness of psycho-
pathic offenders. Biological Psychiatry, 67(1), 66–70.
doi:10.1016/j.biopsych.2009.07.035
Njomboro, P., Humphreys, G. W., & Deb, S. (2014). Exploring
social cognition in patients with apathy following acquired
brain damage. BMC Neurology, 14, 18. doi:10.1186/1471-
2377-14-18
Northoff, G. (2008). Neuropsychiatry. An old discipline in a
new gestalt bridging biological psychiatry, neuropsychol-
ogy, and cognitive neurology. European Archives of
Psychiatry and Clinical Neuroscience, 258(4), 226–238.
doi:10.1007/s00406-007-0783-6
Novak, M. J., Warren, J. D., Henley, S. M., Draganski, B.,
Frackowiak, R. S., & Tabrizi, S. J. (2012). Altered brain
mechanisms of emotion processing in pre-manifest
Huntington’s disease. Brain, 135(4), 1165–1179.
doi:10.1093/brain/aws024
Omar, R., Rohrer, J. D., Hailstone, J. C., & Warren, J. D. (2011).
Structural neuroanatomy of face processing in frontotem-
poral lobar degeneration. Journal of Neurology,
Neurosurgery & Psychiatry, 82(12), 1341–1343. doi:10.1136/
jnnp.2010.227983
Paradiso, S., Andreasen, N. C., Crespo-Facorro, B., O’Leary, D. S.,
Watkins, G. L., Boles Ponto, L. L., & Hichwa, R. D. (2003).
Emotions in unmedicated patients with schizophrenia dur-
ing evaluation with positron emission tomography.
American Journal of Psychiatry, 160(10), 1775–1783.
doi:10.1176/appi.ajp.160.10.1775
Pfeiffer, U. J., Timmermans, B., Vogeley, K., Frith, C., &
Schilbach, L. (2013). Towards a neuroscience of social inter-
action. Frontiers in Human Neuroscience, 7. doi:10.3389/
fnhum.2013.00022
Phillips, L. H., Scott, C., Henry, J. D., Mowat, D., & Bell, J. S.
(2010). Emotion perception in Alzheimer’s disease and
mood disorder in old age. Psychology and Aging, 25(1),
38–47. doi:10.1037/a0017369
Piguet, O., Hornberger, M., Mioshi, E., & Hodges, J. R. (2011).
Behavioural-variant frontotemporal dementia: Diagnosis,
clinical staging, and management. The Lancet Neurology,
10(2), 162–172. doi:10.1016/S1474-4422(10)70299-4
Piguet, O., Leyton, C. E., Gleeson, L. D., Hoon, C., & Hodges, J.
R. (2015). Memory and emotion processing performance
contributes to the diagnosis of non-semantic primary pro-
gressive aphasia syndromes. Journal of Alzheimer's Disease,
44(2), 541–547. doi:10.3233/JAD-141854.
Poletti, M., Vergallo, A., Ulivi, M., Sonnoli, A., & Bonuccelli, U.
(2013). Affective theory of mind in patients with Parkinson’s
disease. Psychiatry and Clinical Neurosciences, 67(4), 273–
276. doi:10.1111/pcn.12045
Preissler, S., Dziobek, I., Ritter, K., Heekeren, H. R., & Roepke, S.
(2010). Social cognition in borderline personality disorder:
Evidence for disturbed recognition of the emotions,
thoughts, and intentions of others. Frontiers in Behavioral
Neuroscience, 4, 182. doi:10.3389/fnbeh.2010.00182
Premack, D. W. G., & Woodruff, G. (1978). Does the chimpan-
zee have a theory of mind? Behavioral Brain Sciences, 1,
515–526. doi:10.1017/S0140525X00076512
Price, B. H., Adams, R. D., & Coyle, J. T. (2000). Neurology and
psychiatry: Closing the great divide. Neurology, 54(1), 8-8.
doi:10.1212/WNL.54.1.8
Pugliese, L., Catani, M., Ameis, S., Dell’Acqua, F., Thiebaut De
Schotten, M., Murphy, C., . . . Murphy, D. G. M. (2009). The
anatomy of extended limbic pathways in Asperger syn-
drome: A preliminary diffusion tensor imaging tractography
study. Neuroimage, 47(2), 427–434. doi:10.1016/j.
neuroimage.2009.05.014
Pujol, J., Batalla, I., Contreras-Rodríguez, O., Harrison, B. J.,
Pera, V., Hernández-Ribas, R., … Cardoner, N. (2012).
Breakdown in the brain network subserving moral judg-
ment in criminal psychopathy. Social Cognitive and Affective
Neuroscience, 7(8), 917–923. doi:10.1093/scan/nsr075
Rahman, S., Sahakian, B. J., Hodges, J. R., Rogers, R. D., &
Robbins, T. W. (1999). Specific cognitive deficits in mild
frontal variant frontotemporal dementia. Brain, 122(8),
1469–1493. doi:10.1093/brain/122.8.1469
Rankin, K. P., Gorno-Tempini, M. L., Allison, S. C., Stanley, C. M.,
Glenn, S., Weiner, M. W., & Miller, B. L. (2006). Structural
anatomy of empathy in neurodegenerative disease. Brain,
129(11), 2945–2956. doi:10.1093/brain/awl254
Rankin, K. P., Kramer, J. H., & Miller, B. L. (2005). Patterns of
cognitive and emotional empathy in frontotemporal lobar
degeneration. Cognitive and Behavioral Neurology, 18(1),
28–36. doi:10.1097/01.wnn.0000152225.05377.ab
Rascovsky, K., Hodges, J. R., Knopman, D., Mendez, M. F.,
Kramer, J. H., Neuhaus, J., . . . Miller, B. L., et, al. (2011).
Sensitivity of revised diagnostic criteria for the behavioural
variant of frontotemporal dementia. Brain, 134(9), 2456–
2477. doi:10.1093/brain/awr179

Reynolds, E. H. (1990). Structure and function in neurology
and psychiatry. The British Journal of Psychiatry, 157, 481–
490. doi:10.1192/bjp.157.4.481
Riveros, R., Manes, F., Hurtado, E., Escobar, M., Martin Reyes,
M., Cetkovich, M., & Ibañez, A. (2010). Context-sensitive
social cognition is impaired in schizophrenic patients and
their healthy relatives. Schizophrenia Research, 116(2–3),
297–298. doi:10.1016/j.schres.2009.10.017
Robinson, S., Goddard, L., Dritschel, B., Wisley, M., & Howlin, P.
(2009). Executive functions in children with autism spec-
trum disorders. Brain and Cognition, 71(3), 362–368.
doi:10.1016/j.bandc.2009.06.007
Roca, M., Gleichgerrcht, E., Ibáñez, A., Torralva, T., & Manes, F.
(2013). Cerebellar stroke impairs executive functions but
not theory of mind. Journal of Neuropsychiatry & Clinical
Neurosciences, 25(1), E48–49. doi:10.1176/appi.
neuropsych.12030057.
Roca, M., Manes, F., Gleichgerrcht, E., Ibáñez, A., Gonzalez De
Toledo, M. E., Marenco, V., . . . Sinay, V. (2014). Cognitive but
not affective theory of mind deficits in mild relapsing-
remitting multiple sclerosis. Cognitive and Behavioral
Neurology : Official Journal of the Society for Behavioral
and Cognitive Neurology, 27(1), 25–30. doi:10.1097/
WNN.0000000000000017
Rosen, H. J., Perry, R. J., Murphy, J., Kramer, J. H., Mychack, P.,
Schuff, N., . . . Miller, B. L. (2002). Emotion comprehension in
the temporal variant of frontotemporal dementia. Brain,
125(Pt 10), 2286–2295. doi:10.1093/brain/awf225
Rosen, H. J., Wilson, M. R., Schauer, G. F., Allison, S., Gorno-
Tempini, M.-L., Pace-Savitsky, C., . . . Miller, B. L. (2006).
Neuroanatomical correlates of impaired recognition of
emotion in dementia. Neuropsychologia, 44(3), 365–373.
doi:10.1016/j.neuropsychologia.2005.06.012
Rutishauser, U., Mamelak, A. N., & Adolphs, R. (2015). The
primate amygdala in social perception - insights from elec-
trophysiological recordings and stimulation. Trends in
Neurosciences, 38(5), 295–306. doi:10.1016/j.tins.2015.03.001
Sachse, M., Schlitt, S., Hainz, D., Ciaramidaro, A., Walter, H.,
Poustka, F., . . . Freitag, C. M. (2014). Facial emotion recogni-
tion in paranoid schizophrenia and autism spectrum dis-
order. Schizophrenia Research, 159, 509–514. doi:10.1016/j.
schres.2014.08.030
Sadeh, N., Spielberg, J. M., Heller, W., Herrington, J. D., Engels,
A. S., Warren, S. L., . . . Miller, G. A. (2013). Emotion disrupts
neural activity during selective attention in psychopathy.
Social Cognitive and Affective Neuroscience, 8(3), 235–246.
doi:10.1093/scan/nsr092
Samamé, C., Martino, D. J., & Strejilevich, S. A. (2012). Social
cognition in euthymic bipolar disorder: Systematic review
and meta-analytic approach. Acta Psychiatrica Scandinavica,
125(4), 266–280. doi:10.1111/j.1600-0447.2011.01808.x
Samson, D., Apperly, I. A., Kathirgamanathan, U., &
Humphreys, G. W. (2005). Seeing it my way: A case of a
selective deficit in inhibiting self-perspective. Brain, 128(Pt
5), 1102–1111. doi:10.1093/brain/awh464
Santamaría-García, H., Reyes, P., García, A., Baéz, S., Martinez,
A., Santacruz, J. M., . . . Ibañez, A. (2016). First symptoms and
neurocognitive correlates of behavioral variant frontotem-
poral dementia. Journal of Alzheimer’s Disease, 54, 957–970.
doi:10.3233/jad-160501
Santoro, G., Wood, M. D., Merlo, L., Anastasi, G. P., Tomasello,
F., & Germano, A. (2009). The anatomic location of the soul
SOCIAL NEUROSCIENCE 37
from the heart, through the brain, to the whole body, and
beyond: A journey through Western history, science, and
philosophy. Neurosurgery, 65(4), 633–643. doi:10.1227/01.
NEU.0000349750.22332.6A
Sayın, A., Oral, N., Utku, Ç., Baysak, E., & Candansayar, S. (2010).
Theory of mind in obsessive-compulsive disorder:
Comparison with healthy controls. European Psychiatry, 25
(2), 116–122. doi:10.1016/j.eurpsy.2009.09.002
Schepman, K., Taylor, E., Collishaw, S., & Fombonne, E. (2012).
Face emotion processing in depressed children and ado-
lescents with and without comorbid conduct disorder.
Journal of Abnormal Child Psychology, 40(4), 583–593.
doi:10.1007/s10802-011-9587-2
Schilbach, L., Timmermans, B., Reddy, V., Costall, A., Bente, G.,
Schlicht, T., & Vogeley, K. (2013). Toward a second-person
neuroscience. The Behavioral and Brain Sciences, 36(4), 393–
414. doi:10.1017/s0140525x12000660
Schneider, D., Slaughter, V. P., Bayliss, A. P., & Dux, P. E. (2013).
A temporally sustained implicit theory of mind deficit in
autism spectrum disorders. Cognition, 129(2), 410–417.
doi:10.1016/j.cognition.2013.08.004
Schroeter, M. L., Raczka, K., Neumann, J., & Von Cramon, D. Y.
(2008). Neural networks in frontotemporal dementia–a
meta-analysis. Neurobiology of Aging, 29(3), 418–426.
doi:10.1016/j.neurobiolaging.2006.10.023
Sedeño, L., Couto, B., García-Cordero, I., Melloni, M., Baez, S.,
Morales Sepúlveda, J. P., . . . Ibanez, A. (2016). Brain network
organization and social executive performance in fronto-
temporal dementia. Journal of the International
Neuropsychological Society : JINS, 22(2), 250–262.
doi:10.1017/S1355617715000703
Sedeño, L., Couto, B., Melloni, M., Canales-Johnson, A., Yoris,
A., Baez, S., . . . Soriano-Mas, C. (2014). How do you feel
when you can’t feel your body? Interoception, functional
connectivity and emotional processing in depersonaliza-
tion-derealization disorder. PLoS One, 9(6), e98769.
doi:10.1371/journal.pone.0098769
Segerstrom, S. C., & Miller, G. E. (2004). Psychological stress
and the human immune system: A meta-analytic study of
30 years of inquiry. Psychological Bulletin, 130(4), 601–630.
doi:10.1037/0033-2909.130.4.601
Seidel, E.-M., Habel, U., Finkelmeyer, A., Hasmann, A.,
Dobmeier, M., & Derntl, B. (2012). Risk or resilience?
Empathic abilities in patients with bipolar disorders
and their first-degree relatives. Journal of Psychiatric
Research, 46(3), 382–388. doi:10.1016/j.jpsychires.
2011.11.006
Senju, A. (2012). Spontaneous theory of mind and its absence
in autism spectrum disorders. The Neuroscientist, 18(2), 108–
113. doi:10.1177/1073858410397208
Senju, A., Southgate, V., White, S., & Frith, U. (2009). Mindblind
eyes: An absence of spontaneous theory of mind in
Asperger syndrome. Science, 325(5942), 883–885.
doi:10.1126/science.1176170
Shamay-Tsoory, S., Harari, H., Szepsenwol, O., & Levkovitz, Y.
(2009). Neuropsychological evidence of impaired cognitive
empathy in euthymic bipolar disorder. The Journal of
Neuropsychiatry and Clinical Neurosciences, 21(1), 59–67.
doi:10.1176/jnp.2009.21.1.59
Shamay-Tsoory, S. G., Aharon-Peretz, J., & Perry, D. (2009). Two
systems for empathy: A double dissociation between emo-
tional and cognitive empathy in inferior frontal gyrus
38 A. IBÁÑEZ ET AL.
versus ventromedial prefrontal lesions. Brain, 132(3), 617–
627. doi:10.1093/brain/awn279
Shamay-Tsoory, S. G., Tomer, R., Goldsher, D., Berger, B. D., &
Aharon-Peretz, J. (2004). Impairment in cognitive and affec-
tive empathy in patients with brain lesions: Anatomical and
cognitive correlates. Journal of Clinical and Experimental
Neuropsychology, 26(8), 1113–1127. doi:10.1080/
13803390490515531
Sharp, C., & Vanwoerden, S. (2014). Social cognition: empirical
contribution: The developmental building blocks of psy-
chopathic traits: Revisiting the role of theory of mind.
Journal of Personality Disorders, 28(1), 78–95. doi:10.1521/
pedi.2014.28.1.78
Silasi, G., & Murphy, T. H. (2014). Stroke and the connectome:
How connectivity guides therapeutic intervention. Neuron,
83(6), 1354–1368. doi:10.1016/j.neuron.2014.08.052
Sporns, O. (2014). Contributions and challenges for network
models in cognitive neuroscience. Nature Neuroscience, 17
(5), 652–660. doi:10.1038/nn.3690
Sprengelmeyer, R., Young, A. W., Calder, A. J., Karnat, A.,
Lange, H., Hömberg, V., . . . Rowland, D. (1996). Loss of
disgust. Perception of faces and emotions in Huntington’s
disease. Brain, 119(5), 1647–1665. doi:10.1093/brain/
119.5.1647
Sprong, M., Schothorst, P., Vos, E., Hox, J., & Van Engeland, H.
(2007). Theory of mind in schizophrenia: Meta-analysis. The
British Journal of Psychiatry, 191, 5–13. doi:10.1192/bjp.
bp.107.035899
Stanley, B., & Siever, L. J. (2010). The interpersonal dimension
of borderline personality disorder: Toward a neuropeptide
model. American Journal of Psychiatry, 167(1), 24–39.
doi:10.1176/appi.ajp.2009.09050744
Steiner, M. (1997). Premenstrual syndromes. Annual Review of
Medicine, 48, 447–455. doi:10.1146/annurev.med.48.1.447
Stone, V. E., Baron-Cohen, S., & Knight, R. T. (1998). Frontal
lobe contributions to theory of mind. Journal of Cognitive
Neuroscience, 10(5), 640–656. doi:10.1162/
089892998562942
Takeda, T., Kasai, K., & Kato, N. (2007). Moral judgment in high-
functioning pervasive developmental disorders. Psychiatry
and Clinical Neurosciences, 61(4), 407–414. doi:10.1111/
j.1440-1819.2007.01678.x
Tobón, C., Ibañez, A., Velilla, L., Duque, J., Ochoa, J., Trujillo, N.,
. . . Pineda, D. (2015). Emotional processing in Colombian
ex-combatants and its relationship with empathy and
executive functions. Social Neuroscience, 10(2), 153–165.
doi:10.1080/17470919.2014.969406
Torralva, T., Gleichgerrcht, E., Ibanez, A., & Manes, F. (2016).
The frontal lobes. In M. Husain & J. Schott (Eds.), Oxford
textbook of cognitive neurology and dementia (pp. 27–38).
UK: Oxford University Press.
Torralva, T., Roca, M., Gleichgerrcht, E., Bekinschtein, T., &
Manes, F. (2009). A neuropsychological battery to detect
specific executive and social cognitive impairments in early
frontotemporal dementia. Brain, 132(5), 1299–1309.
doi:10.1093/brain/awp041
Torralva, T., Strejilevich, S., Gleichgerrcht, E., Roca, M., Martino,
D., Cetkovich, M., & Manes, F. (2012). Deficits in tasks of
executive functioning that mimic real-life scenarios in bipo-
lar disorder. Bipolar Disorders, 14(1), 118–125. doi:10.1111/
j.1399-5618.2012.00987.x
Turetsky, B. I., Kohler, C. G., Indersmitten, T., Bhati, M. T.,
Charbonnier, D., & Gur, R. C. (2007). Facial emotion recogni-
tion in schizophrenia: When and why does it go awry?
Schizophrenia Research, 94(1–3), 253–263. doi:10.1016/j.
schres.2007.05.001
Uddin, L. Q., Kinnison, J., Pessoa, L., & Anderson, M. L. (2014).
Beyond the tripartite cognition-emotion-interoception
model of the human insular cortex. Journal of Cognitive
Neuroscience, 26(1), 16–27. doi:10.1162/jocn_a_00462
Van Rheenen, T. E., & Rossell, S. L. (2013). Picture sequencing
task performance indicates theory of mind deficit in bipolar
disorder. Journal of Affective Disorders, 151(3), 1132–1134.
doi:10.1016/j.jad.2013.07.009
Van Rijn, S., Swaab, H., Aleman, A., & Kahn, R. S. (2006). X
Chromosomal effects on social cognitive processing and
emotion regulation: A study with Klinefelter men (47,XXY).
Schizophrenia Research, 84(2–3), 194–203. doi:10.1016/j.
schres.2006.02.020
Varjassyova, A., Horinek, D., Andel, R., Amlerova, J., Laczo, J.,
Sheardova, K., . . . Hort, J. (2013). Recognition of facial emo-
tional expression in amnestic mild cognitive impairment.
Journal of Alzheimer’s Disease : JAD, 33(1), 273–280.
doi:10.3233/JAD-2012-120148
Ventura, J., Wood, R. C., Jimenez, A. M., & Hellemann, G. S.
(2013). Neurocognition and symptoms identify links
between facial recognition and emotion processing in schi-
zophrenia: Meta-analytic findings. Schizophrenia Research,
151(1–3), 78–84. doi:10.1016/j.schres.2013.10.015
Verdejo-Garcia, A., Contreras-Rodriguez, O., Fonseca, F.,
Cuenca, A., Soriano-Mas, C., Rodriguez, J., . . . De La Torre,
R. (2014). Functional alteration in frontolimbic systems rele-
vant to moral judgment in cocaine-dependent subjects.
Addiction Biology, 19(2), 272–281. doi:10.1111/j.1369-
1600.2012.00472.x
Wang, S. M., Kim, Y., Yeon, B., Lee, H. K., Kweon, Y. S., Lee, C. T.,
& Lee, K. U. (2013). Symptom severity of panic disorder
associated with impairment in emotion processing of
threat-related facial expressions. Psychiatry and Clinical
Neurosciences, 67(4), 245–252. doi:10.1111/pcn.12039
Watermeyer, T. J., Brown, R. G., Sidle, K. C., Oliver, D. J., Allen,
C., Karlsson, J., . . . Goldstein, L. H. (2015). Executive dysfunc-
tion predicts social cognition impairment in amyotrophic
lateral sclerosis. Journal of Neurology, 10, 10.
Werner, K. H., Roberts, N. A., Rosen, H. J., Dean, D. L., Kramer, J.
H., Weiner, M. W., . . . Levenson, R. W. (2007). Emotional
reactivity and emotion recognition in frontotemporal
lobar degeneration. Neurology, 69(2), 148–155.
doi:10.1212/01.wnl.0000265589.32060.d3
Whitton, A. E., Henry, J. D., & Grisham, J. R. (2014). Moral
rigidity in obsessive-compulsive disorder: Do abnormalities
in inhibitory control, cognitive flexibility and disgust play a
role? Journal of Behavior Therapy and Experimental
Psychiatry, 45(1), 152–159. doi:10.1016/j.jbtep.2013.10.001
Wilson, R. S., Krueger, K. R., Arnold, S. E., Schneider, J. A., Kelly,
J. F., Barnes, L. L., . . . Bennett, D. A. (2007). Loneliness and
risk of Alzheimer disease. Archives of General Psychiatry, 64
(2), 234–240. doi:10.1001/archpsyc.64.2.234
Wojakiewicz, A., Januel, D., Braha, S., Prkachin, K., Danziger, N.,
Bouhassira, D. (2013). Alteration of pain recognition in
schizophrenia. European Journal of Pain, 17(9), 1385–1392.
doi:10.1002/j.1532-2149.2013.00310.x

Woolley, J. D., Khan, B. K., Murthy, N. K., Miller, B. L., & Rankin,
K. P. (2011). The diagnostic challenge of psychiatric symp-
toms in neurodegenerative disease: Rates of and risk fac-
tors for prior psychiatric diagnosis in patients with early
neurodegenerative disease. The Journal of Clinical
Psychiatry, 72(2), 126–133. doi:10.4088/JCP.10m06382oli
Yeh, Z. T., & Tsai, C. F. (2014). Impairment on theory of mind
and empathy in patients with stroke. Psychiatry and Clinical
Neurosciences, 68(8), 612–20. doi:10.1111/pcn.12173
Yirmiya, N., Erel, O., Shaked, M., & Solomonica-Levi, D. (1998).
Meta-analyses comparing theory of mind abilities of indivi-
duals with autism, individuals with mental retardation, and
normally developing individuals. Psychological Bulletin, 124
(3), 283–307.
Yang, E., Tadin, D., Glasse,r D. M., Wook Hong, S., Blake, R., &
Park, S. (2013). Visual context processing in bipolar disor-
der: A comparison with schizophrenia. Frontiers in
Psychology, 4, 569. doi:10.3389/fpsyg.2013.00569
Yoris, A., Esteves, S., Couto, B., Melloni, M., Kichic, R.,
Cetkovich, M., . . . Sedeño, L. (2015). The roles of
SOCIAL NEUROSCIENCE 39
interoceptive sensitivity and metacognitive interoception
in panic. Behavioral and Brain Functions : BBF, 11, 14.
doi:10.1186/s12993-015-0058-8
York, G. K., & Steinberg, D. A. (2001). The sacred disease of
Cambyses II. Archives of Neurology, 58(10), 1702–1704.
Young, L., Bechara, A., Tranel, D., Damasio, H., Hauser, M., &
Damasio, A. (2010). Damage to ventromedial prefrontal
cortex impairs judgment of harmful intent. Neuron, 65(6),
845–851. doi:10.1016/j.neuron.2010.03.003
Yuvaraj, R., Murugappan, M., Norlinah, M. I., Sundaraj, K., &
Khairiyah, M. (2013). Review of emotion recognition in
stroke patients. Dementia and Geriatric Cognitive Disorders,
36(3–4), 179–196. doi:10.1159/000353440
Zalla, T., Barlassina, L., Buon, M., & Leboyer, M. (2011). Moral
judgment in adults with autism spectrum disorders.
Cognition, 121(1), 115–126. doi:10.1016/j.cognition.2011.06.004
Ze, O., Thoma, P., & Suchan, B. (2014). Cognitive and affective
empathy in younger and older individuals. Aging &
Mental Health, 18(7), 929–935. doi:10.1080/
13607863.2014.899973