Review

How understanding the neurobiology of

complex post-traumatic stress disorder can
inform clinical practice: a social cognitive
and aective neuroscience approach
Lanius RA, Bluhm RL, Frewen PA. How understanding the
neurobiology of complex post-traumatic stress disorder can inform
clinical practice: a social cognitive and aective neuroscience approach.
Objective: In this review, we examine the relevance of the social
cognitive and aective neuroscience (SCAN) paradigm for an
understanding of the psychology and neurobiology of complex post-
traumatic stress disorder (PTSD) and its eective treatment.
Method: The relevant literature pertaining to SCAN and PTSD was
reviewed.
Results: We suggest that SCAN oers a novel theoretical paradigm for
understanding psychological trauma and its numerous clinical
outcomes, most notably problems in emotional self-awareness,
emotion regulation, social emotional processing and self-referential
processing. A core set of brain regions appear to mediate these
collective psychological functions, most notably the cortical midline
structures, the amygdala, the insula, posterior parietal cortex and
temporal poles, suggesting that problems in one area (e.g. emotional
awareness) may relate to diculties in another (e.g. self-referential
processing). We further propose, drawing on clinical research, that the
experiences of individuals with PTSD related to chronic trauma often
reect impairments in multiple social cognitive and aective functions.
Conclusion: It is important that the assessment and treatment of
individuals with complex PTSD not only addresses traumatic
memories but also takes a SCAN-informed approach that focuses on
the underlying decits in emotional self-awareness, emotion
regulation, social emotional processing and self-referential processing.
R. A. Lanius
1
, R. L. Bluhm
2
,
P. A. Frewen
1,3
1
Department of Psychiatry, Schulich School of Medicine
and Dentistry, The University of Western Ontario,
London, ON, Canada,
2
Department of Philosophy and
Religious Studies, Old Dominion University, Norfolk, VA,
USA and
3
Department of Psychology, Schulich School of
Medicine and Dentistry, The University of Western
Ontario, London, ON, Canada
Key words: complex PTSD; fMRI; self-reflection;
default mode network; emotion regulation;
dissociation; medial prefrontal cortex
Ruth A. Lanius, Department of Psychiatry, London
Health Sciences Centre-University Hospital, 339
Windermere Road, London, ON N6A 5A5, Canada.
E-mail: ruth.lanius@lhsc.on.ca
Accepted for publication July 5, 2011
Summations
The social cognitive and affective neuroscience (SCAN) paradigm offers a metatheory for
understanding the psychology and neurobiology of complex post-traumatic stress disorder (PTSD)
and its effective treatment.
A SCAN approach may offer new insights into disturbances related to emotional self-awareness,
emotion regulation, social emotional processing and self-referential processing often observed in
individuals with complex PTSD.
A core set of brain regions appear to mediate these psychological functions. These include the
cortical midline structures, the amygdala, the insula, posterior parietal cortex and temporal poles.
Patients with PTSD have been shown to exhibit behavioural and neurobiological impairments
impacting emotional self-awareness, emotion regulation, social emotional processing and self-
referential processing as compared to healthy controls.
Acta Psychiatr Scand 2011: 124: 331348
All rights reserved
DOI: 10.1111/j.1600-0447.2011.01755.x
2011 John Wiley & Sons A/S
ACTA PSYCHIATRICA
SCANDINAVICA
331
Introduction
The eld of social cognitive and affective neurosci-
ence (SCAN) seeks to understand how brain
mechanisms mediate the complex social and
emotional functions of the human mind. Topics
of investigation within SCAN include the study of
motivation and emotion, self-referential process-
ing, empathy and mentalizing (theory of mind),
just to name a few. As is well known, disturbances
in these psychological functions are variably
involved in a number of complex neuropsychiatric
disorders, including autism (1, 2), attention decit
hyperactivity disorder (3), schizophrenia (4), anxiety
(5) and depression (69).
The contemporary discipline of affective neuro-
science originated from the landmark publications
of Panksepp (10) and Davidson (11). From the
beginning, the eld of aective neuroscience has
been inuenced by the basic emotion view that
there might be brain systems dedicated to mediat-
ing particular types of emotional behaviour (e.g.
fear vs. anger), systems that might be relatively
preserved across lower and higher species. Increas-
ingly, higher-order explicitly social and metacog-
nitive aspects of emotional processing and
behaviour have also been studied in humans and
their relationship to psychiatric disorders has been
of growing interest (12, 13). In contrast, social
cognitive neuroscience from the outset concerned
itself with higher-order complex social behaviours
including attitudes, empathy and theory of mind
(14). The disciplines of aective neuroscience and
social cognitive neuroscience are increasingly
united under the eld of SCAN, although for the
purposes of simplicity and clarity, in the present
review, we will discuss concepts traditionally
falling under the scope of aective neuroscience
and social cognitive neuroscience separately.
Social cognitive and aective neuroscience
provides a perspective for the understanding of
psychiatric disorders that is both scientically and
clinically valuable, as it provides a way to integrate
research in emotion and social psychology with
research in neuroscience (15). The complexity of
psychiatric disorders and the need to understand
them at multiple levels of analysis suggest that they
can be best understood via a paradigm that
integrates dierent levels. Lieberman [(15), p. 1],
as one of the cofounders of social cognitive
neuroscience, notes: A full accounting of human
biology cannot proceed without incorporating the
social and emotional factors that modulate the
functioning and health of biological systems.
In this review, we examine the relevance of the
SCAN paradigm for an understanding of the
psychology and neurobiology of complex post-
traumatic stress disorder (PTSD) and its eective
treatment. For the purposes of the present review,
complex trauma will be dened as repeated inter-
personal trauma occurring during crucial develop-
mental periods, as opposed to simple PTSD that
follows more single incident trauma events.
Researchers and clinicians who focus on complex
PTSD are becoming increasingly aware of the need
to account for physiological, developmental,
environmental and social factors, suggesting that
a SCAN approach may be particularly appropriate
for promoting our understanding of PTSD.
Aims of the study
The aims of this study are to survey the literature
illustrating how the core constructs and methods in
social cognitive and aective neuroscience have
been used towards understanding the pathophys-
iology of complex post-traumatic stress disorder
with a particular focus on emotional awareness,
emotion regulation, social emotional processing
and self-referential processing. We propose that
social cognitive and aective neuroscience oers a
novel theoretical and methodological paradigm for
understanding the psychological trauma and its
myriad clinical outcomes, most notably self- and
Considerations
It will be important that the assessment of complex PTSD includes an examination of the decits in
emotional self-awareness, emotion regulation, social emotional processing and self-referential
processing.
The treatment of individuals with complex PTSD should take a SCAN-informed approach that
directly addresses underlying impairments in emotional self-awareness, emotion regulation, social
emotional processing, and self-referential processing.
Outcome studies examining the effectiveness of treatments for complex PTSD should not only
examine outcomes for PTSD symptoms but also measure the impact of interventions on
emotional self-awareness, emotion regulation, social emotional processing and self-referential
processing.
Lanius et al.
332
aect-dysregulation commonly observed clinically
in persons who have suered chronic interpersonal
and developmental trauma.
Material and methods
Relevant empirical literature pertaining to SCAN
and PTSD was reviewed.
Results
Affective neuroscience
In this section, we will discuss two concepts
particularly relevant to understanding PTSD,
namely decits in emotional awareness and emotion
regulation.
Emotional self-awareness. Theorists have increas-
ingly pointed out the signicant role played by
emotional processing in the across-species
evolution of consciousness (16), and the brain
mechanisms underlying how humans become
subjectively aware of their emotional feelings and
behaviour is a topic of signicant interest in
aective neuroscience. Emotional awareness
refers to the capacity to be aware of and describe
emotions in oneself and others and involves the
ability to reect upon internal aective experience
(17, 18). As emotional awareness enables increased
self-reection and regulation of aective states, it is
often considered a cornerstone of emotion
regulation. A history of a secure attachment with
ones primary caregivers has been suggested to play
a key role in the development of emotional
awareness (19, 20).
The neurobiology of emotional self-awareness. Cur-
rent theoretical models propose a superiorinferior
division within the medial prefrontal cortex
underlying emotional awareness [see (2125); also
see Table 1 for a description of frequently
discussed brain regions and their functions (26
36)], and a distinction between conceptual and
embodied forms of emotional awareness has been
proposed. Conceptual emotional awareness refers
to the ability to reect on, interpret and make a
decision about an embodied sensation or emotion
[reviewed by Fogel (21)]. It is based on linguistic
forms of expression, is usually considered to be
rational, logical and explanatory and tends to
transcend the present moment. This form of
awareness is thought to be partly mediated by the
dorsomedial prefrontal cortex and its connections
with the interoceptive and body schema networks.
In contrast to conceptual awareness, embodied
emotional self-awareness is based on sensing, feel-
ing and acting, tends to be spontaneous and
creative and is usually lived in the present
moment. The ventromedial prefrontal cortex has
been hypothesized to be a key brain structure
underlying embodied emotional awareness. It is
also thought to aid in making decisions when one is
in the subjective emotional present.
The impact of early life trauma on emotional
self-awareness. Early adverse experience can signif-
icantly interfere with the development of emotional
awareness. Being trapped in a dangerous environ-
ment, such as being with a chronically physically or
sexually abusive caregiver, prevents individuals
from using their emotional responses to guide
eective actions and behaviours. For example, if a
child is in an abusive relationship with a caregiver
and has the impulse to escape, he she may quickly
learn that escape is not possible. A sense of learned
helplessness may ensue. Individuals with such
experiences therefore learn that emotional
responses to traumatic events are futile because
there is no escape from the situation and hence
become increasingly disconnected from their inner
emotional life in an attempt to disconnect them-
selves from extreme emotions that are out of their
control. It is therefore not surprising that individ-
uals with PTSD often exhibit problems being aware
of their aective states and have diculties identi-
fying and labelling these states. Studies have shown
Table 1. Summary of brain structures and related functions relevant to this review
Brain structure
Social cognitive and affective
neuroscience-related functions
Medial prefrontal
cortex (26, 27)
Self-referential, reflective awareness
Monitoring and modulation of emotions through
strong connection with emotional limbic system
Anterior cingulate
cortex (28, 31)
Integrates cognitive and emotional aspects
of experience
Emotional component
of the anterior cingulate
cortex (28, 31)
Assesses salience of emotional and motivational
information
Regulates autonomic (heart rate, blood pressure)
changes to emotional stimuli
Pain processing
Cognitive component
of the anterior cingulate
cortex (31)
Attention to error processing
Sustained attention and cognitive control
Posterior cingulate
cortex (29, 30)
Self-referential processing
Episodic memory retrieval
Amygdala (32, 33) Emotional and social processing
Fear conditioning
Modulation of memory consolidation
Insula (3436) Interoceptive awareness of bodily states
Bodily self-awareness
Regulation of sympathetic and
parasympathetic systems
Sensation of pain
Neurobiology of PTSD and clinical practice
333
that these individuals have lower scores on the
Levels of Emotional Awareness Scale (19, 37), that
they consistently exhibit higher levels of alexithy-
mia (diculties identifying and labelling emotional
states; for a meta-analysis, [see: (38, 39)]) and that
they often show intense levels of emotional numb-
ing, i.e. feeling like they cannot experience emotions
(40). Below, we describe the studies of individuals
with PTSD aimed at uncovering the underlying
neurobiological mechanisms mediating such prob-
lems, namely emotional numbing and alexithymia
(37, 4042).
The neurocircuitry underlying emotional numbing in
PTSD. Emotional numbing symptoms have long
been recognized as an important symptom cluster
in chronic PTSD (4345) and represent negative
prognostic indicators of psychological treatment
(46, 47). Our group has recently examined trait
emotional numbing symptoms as a predictor of
neural activation during script-driven imagery in
patients with PTSD related to childhood abuse of
standardized positive (receiving others aection-
praise) and negative (rejection-criticism) emotional
scenarios. Patients were instructed to imagine that
what was being described in the scripts was
actually happening in the present and to pay
attention to their emotional responses to each
script. In order to measure emotional numbing
symptoms, participants were asked to rate how
often they had felt: i) emotionally numb, as if
you cant experience emotions or feelings?; ii) like
your emotions and feelings are frozen,
sedated, or numbed out, so that you cant
physically sense them?; iii) shut down in an
emotional sense, as if your emotional feelings have
been turned o or tuned out in your body?;
and iv) cut o from your emotions and feelings,
so that you cant physically feel them, even if you
try?. Their ratings were then correlated with the
extent of brain activation during imagery of
positive (receiving others aection-praise) and
negative (rejection-criticism) scripts. In women
with PTSD related to prolonged childhood abuse,
increased emotional numbing symptoms predicted
decreased brain activation within the dorsomedial
prefrontal cortex during imagery of both positive
and negative social scripts, consistent with a role of
the dorsomedial prefrontal cortex in higher-order
reective and metacognitive aspects of emotional
functioning (see Fig. 1, left).
It is interesting to note that, within healthy
women completing the same task, the more an
individual exhibited the trait of mindful observ-
ing, referring to the intentional paying attention to
ones inner and external stimuli and experiences
[e.g. When Im walking, I deliberately notice the
sensations of my body moving; I notice changes in
my body, such as whether my breathing slows
down or speeds up (48, 49)], the more activation
was observed within the dorsomedial prefrontal
cortex (see Fig. 1, right) (50).
The development of the neural circuitry facilitat-
ing the humanability for conscious awareness of our
emotional states, includingthe dorsomedial prefron-
tal cortex, may therefore be disturbed in PTSD,
leading tothe diculties these individuals oftenhave
in reecting on, interpreting and acting in accor-
dance with emotion. Apatient suering fromPTSD
related to prolonged childhood abuse summarized
feelings of emotional numbing in the following
statement: Its like a blank, I think about my kids
andI feel nothing for them. Ill be sitting there feeling
confused and numb, and I wonder what Im
supposed to be feeling. Its like dead space...and
when that happens, I have trouble using words,
nding my words, I cant talk. The inability to
describe feelings in words also relates to the concept
of alexithymia, which will be described below.
The neurocircuitry underlying alexithymia in
PTSD. Alexithymia refers to diculties identify-
ing and labelling emotional states (51, 52). Krystal
(43, 44) described alexithymic traumatized persons
as being without emotion, robotic, and as if
living-dead. These descriptions parallel test items
from the Glover (53) Numbing Questionnaire (e.g.
Fig. 1. The role of the dorsomedial prefrontal cortex in emo-
tional numbing and mindfulness. Left panel: Emotional
numbing symptoms were associated with less response in the
dorsomedial prefrontal cortex during imagery of positive
(aliation-praise) scripts and negative (rejection-criticism)
scripts. Right panel: The more an individual exhibited trait
mindfulness (mindful observing), the more activation was
observed within the dorsomedial prefrontal cortex.
Lanius et al.
334
I act mechanically like a robot; I feel dead or shut
down; My body feels paralyzed; I feel that I am
in a fog), illustrating the conceptual overlap
between the emotional numbing and alexithymia
concepts in traumatized subjects (54). Researchers,
however, more often assess alexithymia using the
20-item Toronto Alexithymia Scale (TAS-20) (55),
which measures diculties i) identifying feelings
and distinguishing them from bodily sensations
(e.g. I am often confused about what emotion I am
feeling, I have feelings that that I cant quite
identify) and ii) diculties describing and com-
municating feelings (e.g. It is dicult for me to
nd the right words for my feelings, People tell me
to describe my feelings more). The following quote
from a traumatized client in psychotherapy with
the rst author describes the experience of alexi-
thymia and elegantly illustrates the problems
identifying and communicating feelings in words
which is often so prominent in individuals with
PTSD (42): When I get emotions and stu like that
I dont really feel them. I can say to someone I feel
sadness because tears are welling in my eyes, but
I do not know what that is really. They are just
physical symptoms. This quote also exemplies
that an individual may exhibit behavioural (e.g.
crying) and psychophysiological signs (e.g. tachy-
cardia) of emotional processing without being
subjectively aware of his her emotional state (56).
Further evidence for the latter also stems from
studies that have observed lower correspondence
between self-reported aective experience and
objectively coded facial aect in PTSD subjects
as compared to controls in response to emotionally
provocative stimuli (57, 58).
We have also reported that alexithymia symp-
toms predict brain activation during traumatic
script-driven imagery in individuals with PTSD
(42). In these studies, patients construct a narrative
of their traumatic experience including as many
sensory details as possible. These narratives are
subsequently read to patients who are instructed to
recall the traumatic memory as vividly as possible
during an fMRI scan. Associations between alex-
ithymia and neural activation were particularly
marked for regions of the embodied emo-
tional self-awareness network. Specically, during
traumatic memory recall, increasing severity of
trait alexithymia was associated with reduced
activation within the ventromedial prefrontal
cortex and the anterior insula. As described earlier,
the ventromedial prefrontal cortex may be related
to embodied emotional self-awareness that is
based on sensing, feeling and acting and may
play a role in assigning the emotional value of a
stimulus during self-referential processing. In con-
trast, the anterior insula has been proposed to be
part of the interoceptive network. Craig (35, 59)
has postulated that the anterior insula of the right
hemisphere, possibly uniquely to humans, consti-
tutes a basis for the subjective evaluation of ones
condition, that is, how you feel. It is therefore not
surprising that higher levels of alexithymia or
diculties identifying and labelling feeling states
are associated with lower brain activation of the
anterior insula.
In addition to correlations with the ventromedial
prefrontal cortex and anterior insula, increasing
severity of alexithymia was associated with reduced
brain activation in the right inferior frontal gyrus.
The right inferior frontal cortex responds to
emotion regulation tasks, and therefore, a relative
absence of response in this area as a function of
increasing levels of alexithymia is consistent with a
view of alexithymia as a disorder of aect regula-
tion (24, 52, 60). These ndings are consistent with
the notion that the more an individual is capable of
emotional self-awareness and interoceptive moni-
toring, the less likely that he or she will be
overwhelmed by intense emotional experiences
and face a loss of executive control during
reminders of past traumatic events and other
stressful life events (61).
Emotion regulation. As described previously, emo-
tional awareness has long been thought to be
crucial to the regulation of aective states and is
therefore often considered to be the cornerstone
of emotion regulation. Emerging research has
clearly shown that the aective disturbances expe-
rienced by many PTSD subjects not only involve
just fear, but also include the dysregulation of a
variety of emotional states, including fear, anger,
guilt and shame (62, 63). This point has been
acknowledged in the newly developed provisional
criteria for PTSD in the DSM-5 (http://www.
dsm5.org). The term emotion dysregulation will
be used in this review to collectively refer to
disturbances in a variety of emotional responses
and to the process by which we inuence how
much emotion we have and when we have it as
outlined by Gross (64).
Two pathways to emotion dysregulation in PTSD.
We have recently reviewed two pathways to
emotion dysregulation in PTSD (65). The rst of
these pathways involves understanding emotion
dysregulation as a result of fear conditioning
through the mechanisms of stress sensitization
and kindling. Over time, an individual who is
sensitized to subtle reminders of traumatic and
related memories may develop a general pattern of
Neurobiology of PTSD and clinical practice
335
emotion dysregulation, including anger, grief,
numbing, and dissociation, in addition to a gener-
alization of the fear response. The mechanism
underlying this process is understood as being
analogous to kindling, which involves the
emergence of generalized seizures in response to
repeated, subthreshold electrophysiological stimu-
lation. In PTSD, similarly to kindling of seizures,
the progressive augmentation and amplication of
symptoms occurs over time, possibly as a result of
the neural circuitry associated with the emotional
memory response becoming increasingly reactive
and also expanding into neighbouring neural
circuits (6668).
The second pathway emphasizes the importance
of early childhood environment (69, 70). In indi-
viduals whose environment is impoverished owing
to the unavailability of a responsive attachment
gure or to childhood maltreatment and abuse, the
emotional and arousal regulatory neural systems
may not develop appropriately. This results in
emotion dysregulation, which in turn results in an
diminished ability to regulate physiological arousal
to threatening or traumatic events. In a cycle of
positive feedback, this leads to an exacerbation of
emotion dysregulation, including the development
of PTSD after exposure to traumatic event(s) later
in life.
Emotion dysregulation in PTSD: behavioural evidence.
Recall of traumatic memories through trauma
script-driven imagery in individuals with PTSD
predominantly owing to prolonged childhood
maltreatment has been shown to elicit not only
fear and anxiety responses but also other negative
emotions, including anger, guilt, disgust and shame
(7173). Subsequent studies using standardized
stimuli conrm that emotional disturbances in
PTSD related to childhood abuse are rarely
restricted to fear. Studies have observed elevated
self-reported negative aect in response to stan-
dardized scripts, the content of which focused on
anger or safety concerns (74) or rejectionshame
(75). Furthermore, structural equation modelling
analyses in a sample of 215 maltreated and 206
non-maltreated children (aged 612 years) demon-
strated that a history of neglect, physical and
or sexual abuse, multiple maltreatment subtypes,
and earlier onset of maltreatment were directly
related to symptoms of emotion dysregulation (76).
Symptoms of emotion dysregulation are at the core
of Developmental Trauma Disorder, a diagnosis
suggested to reect complex adaptations to
prolonged psychological trauma in childhood
(77). Further support for emotion dysregulation
in PTSD comes from a recent study by Cloitre
et al. (78) who specically examined the treatment
of PTSD related to childhood abuse. Results
from this randomized controlled trial in adults
with a history of childhood trauma showed that
a phase-based emotion interpersonal regulation-
to-exposure treatment was associated with greater
benets and fewer side-eects than treatment that
excluded emotion and interpersonal training, indi-
cating the need to address emotion dysregulation
in the treatment (78).
The neural correlates underlying traumatic and non-
traumatic emotional processing and emotion regulation
in PTSD. Studies examining brain activation in
response to trauma script-driven imagery in
subjects who experienced a re-experiencing
hyperarousal response to recalling their traumatic
memory showed decreased responses in brain
regions involved in emotion and arousal regula-
tion, including the ventromedial prefrontal cortex,
rostral anterior cingulate cortex and, in some cases,
the amygdala [reviewed by Etkin and Wager (79)].
In our own studies, PTSD subjects who reported
re-experiencing their traumatic events in the
scanner described, for example, feeling that they
were being raped all over again. I could feel him
holding down my hands. Another subject stated It
felt like I was surrounded by smoke. I could smell
and see it. The latter responses were usually
associated with an increase in heart rate. However,
it is important to note that these brain activation
patterns strikingly dier from those observed in
PTSD patients who exhibited a depersonaliza-
tion derealisation response to the traumatic script.
For example, one subject stated I was outside my
body looking down at myself. It was too over-
whelming to recall the traumatic memory while
she tried to recall her traumatic memory. These
dissociative patients had higher levels of brain
activation in the rostral anterior cingulate cortex
and dorsal anterior cingulate cortex, medial
prefrontal cortex and areas in the superior and
middle temporal cortices and usually did not
exhibit a signicant increase in heart rate during
the traumatic memory recall (8083).
Neuroimaging studies in PTSD that examined
aective disturbances other than fear or that used
stimuli other than exposure to traumatic memories
also suggested the importance of the prefrontal
amygdala circuitry. Recall of non-traumatic sad
and anxious memories in PTSD was associated
with decreased activity in the rostral anterior
cingulate cortex and thalamus similar to those
observed during recall of traumatic memories (72).
Another study using negatively valenced or
aversive pictures showed that activity decreased
Lanius et al.
336
in the ventromedial prefrontal cortex response
and the amygdala in PTSD subjects as compared
to controls (84). A more recent study examined
emotion regulation more directly. Non-traumatized
healthy controls and subjects with a history of
sexual assault with and without PTSD were asked
to enhance, diminish or maintain their emotional
responses to negative pictures. Non-traumatized
controls were better able to downregulate their
emotional response to negative pictures than were
subjects with a history of sexual assault, either with
or without PTSD. Successful regulation was
associated with greater activity of prefrontal
regions in the non-traumatized group (85).
The studies described earlier indicate a role of
medial prefrontal amygdala circuitry in both fear
traumatic and other non-traumatic, negatively
valenced emotions. In general, PTSD has been
shown to be associated with two dierent types of
emotion dysregulation: i) undermodulation of
aect, such as re-experiencing traumatic events,
hyperarousal and anger symptoms mediated by
failure of prefrontal inhibition of limbic regions,
resulting in overactivation of these regions, includ-
ing the amygdala, and ii) overmodulation of aect,
often associated with a feeling of subjective distance
from emotional experience such as during acute
depersonalization, derealization and analgesia,
thought to be mediated by midline prefrontal
inhibition of the same limbic regions (86). A
recent review proposed clinical and neurobiologi-
cal evidence for a dissociative subtype of PTSD in
an attempt to classify PTSD patients who show
signicant symptoms of depersonalization, dereal-
ization and analgesia in contrast to PTSD patients
who exhibit predominantly re-experiencing and
ashback-type symptoms (86). It was suggested
that individuals with a dissociative subtype of
PTSD may be more likely to have experienced a
history of repeated interpersonal trauma occurring
during crucial developmental periods.
Social cognitive neuroscience
Within the scope of social cognitive neuroscience,
we will discuss two concepts we nd to be
especially important for an understanding of
PTSD: disturbances in social emotional processing
and self-referential processing. We also discuss the
notion of a default mode network (DMN) in the
brain and its relevance to self-referential processing
and PTSD symptomatology.
Social emotional processing. Current emotiontheory
suggests a distinction between social and non-
social emotions [reviewed by Hareli and Parkinson
(87)]. Even though it is recognized that all emo-
tional responses are potentially elicited by social
stimuli or take place within a social framework (88),
certain emotions are considered as necessarily
social [reviewed by Hareli and Parkinson (87)].
Social emotions [e.g. pride, guilt and shame; (87)]
require metacognitive processing, specically,
consideration of the self-relevance of stimuli and
the appraisal of others thoughts and emotional
states. Social emotions can be both positive and
negative in valence. Positive social encounters, for
example, can elicit admiration, appreciation,
empathy and pride (8991), whereas negative
social encounters may provoke anger, disdain,
envy, guilt or shame (87). In contrast, non-social
positive emotions may be elicited by non-social
stimuli such as taking a walk in the mountains alone.
Non-social negative emotions can be evoked
when an individual is confronted with threatening
circumstances occurring outside a social context, for
example a fear of heights or of certain animals (e.g.
spiders).
Processing of the social dimension of emotion
exerts powerful eects on brain activation [e.g. (25,
9195); reviewed by Van Overwalle (96)]. The
dorsomedial prefrontal cortex, the posterior
cingulate precuneus, the bilateral temporal poles,
the right amygdala and the bilateral temporopari-
etal junction are brain regions that have been
suggested to play a role in social cognition
[reviewed by Van Overwalle (96)]. Specically, the
dorsomedial prefrontal cortex and posterior
cingulate cortex precuneus are involved in self-
referential processing (25, 29, 97101). These areas
of the brain are also implicated, along with the
temporoparietal junction and temporal poles, in
the task of mentalizing (attending to states of
mind in oneself and others) theory of mind (the
ability to attribute mental states-beliefs, intents and
desires to oneself and others and to understand
that others have beliefs, desires and intentions that
are dierent from ones own) (27, 95, 100, 102
109). The right amygdala has also been suggested
to respond to salient emotional properties that are
specically social (93).
Social emotion processing in PTSD. In PTSD related
to prolonged childhood abuse, neural activation
patterns to positive standardized social (rejection
shame) and non-social (fearanxiety) emotional
imagery have been examined (75). PTSD sub-
jects showed altered brain responses in brain
regions involved in higher-order social cognition
(mentalizing and theory of mind), including the
dorsomedial prefrontal cortex, temporal poles and
amygdala particularly during positive social emo-
Neurobiology of PTSD and clinical practice
337
tional imagery. These results may have important
implications for key social functions in individuals
with PTSD and point to important new research
questions. For example, to what degree, do decits
in this circuitry aect the ability to engage in
psychotherapy? Can activation of the social emo-
tional system in psychotherapy lead to a reversal of
the brain activation patterns during social emo-
tional processing in PTSD (110)? To what extent,
do the neural networks underlying social emotions
need to be intact in order to use available social
support before, during and in the aftermath of
trauma? Lastly, do decits in the social emotion
neural circuitry aect the ability to parent and
thereby facilitate the intergenerational transmission
of trauma, i.e. the emergence of psychopathology as
a result of emotion processing regulation decits in
the parent(s)?
Self-referential processing. Individuals with PTSD
often exhibit disturbances in self-referential pro-
cessing [(111113); also reviewed in Ref. (114)].
Johnson et al. (115) proposed that the ability to
reect upon oneself requires a robust sense of self,
which has been described as a collection of
schemata regarding ones abilities, traits and atti-
tudes that guides our behaviors, choices and social
interactions (115). It has been well described that
psychological trauma can undermine the sense of
an adaptive and agentive self, challenging ones
sense of identity and life purpose [see (116, 117) for
reviews]. Foa et al. (112) capture these symptoms
well in the Posttraumatic Cognitions Inventory that
includes items such as I feel dead inside; I will never
be able to feel normal emotions again; I have
permanently changed for the worse; I feel like an
object, not like a person; I have no future; I dont
know myself anymore; and My life has been
destroyed by the trauma. Disturbances in self-
referential processing in PTSD are further appar-
ent through symptoms of identity disturbance (118,
119), dissociation and the related experience of a
fragmented sense of self (86, 119, 120) and symp-
toms of shame (119, 121, 122). Cloitre et al. (122)
have further suggested that shame can lead to the
experience of the self as inferior, bad, annihilated
and or identied with the perpetrator of abuse.
The neural correlates of self-referential processing in
PTSD. Neuroimaging studies suggest that self-
referential processing is partly mediated via corti-
cal midline structures, including the medial
prefrontal cortex, perigenual anterior cingulate
cortex, posterior cingulate cortex, as well as the
temporoparietal junction and temporal poles (96
101, 123). One model of self-referential processing
proposes that the dorsal medial prefrontal cortex
and the posterior cingulate cortex are involved in
self-referential processing independent of whether
the stimulus or task is emotionally relevant, while
the ventral medial prefrontal cortex may be
particularly involved in negative emotionally
relevant self-referential processing tasks (123
125). A recent meta-analysis has also suggested a
unique role of the medial prefrontal cortex in
self-referential processing, with response within
the posterior cingulate and precuneus occurring
also with familiar stimuli that are not necessarily
self-referential (126).
Our group has recently examined the neural
underpinnings of self-referential processing in
patients with PTSD as compared to healthy
controls (R.L. Bluhm, P.A. Frewen, N.C. Coup-
land, M. Densmore, A.N. Schore, T.K. Stevens,
R.W.J. Neufeld, R.A. Lanius, unpublished data).
In order to examine the brain mechanisms under-
lying self-reective functioning, participants were
asked to respond via button-press yes or no to a
series of statements regarding their own self-
characteristics (e.g. I am a good friend; I learn
new things quickly) or general facts (e.g. Paris is
the capital of France) while undergoing a fMRI
scan. Controls demonstrated signicantly greater
response within medial prefrontal cortex and
posterior cingulate cortex during this self-reective
task as compared to individuals with PTSD.
In addition, a novel cognitive paradigm akin to
mirror viewing has been developed to investigate
self-referential processing disturbances in women
with PTSD predominantly related to maltreatment
experienced during childhood (113). This study
population was selected because it is particularly
vulnerable to negative self-referential processing
following trauma, because of the relational nature
of childhood abuse [see (127) for review]. The
paradigm involved the collection of self-descrip-
tiveness ratings for negatively (e.g. abandoned,
unlovable, despicable, and broken) and positively
valenced trait words (e.g. lovable, special and
adorable) and later exposing participants to pic-
tures of themselves while such words were spoken.
Results showed that PTSD patients endorsed more
negative and fewer positive trait adjectives as self-
descriptive, which support repeated clinical obser-
vations that individuals with PTSD especially
related to childhood trauma often experience
intense negative thoughts and even self-hatred
about themselves. For example, responses from
individuals with PTSD to viewing their own face
paired with negative adjectives included I relate to
the negative side; or I noticed I was agreeing with
all the negative words; or It made me feel bad
Lanius et al.
338
about myself. Responses from individuals with
PTSD to seeing their own face paired with a
positive word included I did not believe it; or It
did not mean anything; or I questioned it. I did
not feel the condence. Brain activation patterns
demonstrated that healthy women showed an
increased response within the perigenual anterior
cingulate cortex when viewing their face and
listening to positive trait adjectives, whereas
women with PTSD did not show this eect.
Interestingly, the perigenual anterior cingulate
cortex is one of the most responsive brain regions
to emotional manipulations as assessed by neuro-
imaging (109). It has also been linked to self-
referential processing (123, 128) and is more active
during negative emotional events in healthy
individuals than in individuals with PTSD [see
(79) for review].
In contrast to healthy controls, patients with
PTSD exhibited an increased response within the
right amygdala when viewing their face and
responding with positive trait adjectives (113).
Although response within the amygdala has more
often been associated with negative emotional
processing, particularly of threat-related visual
stimuli (79), research also implicates the amygdala
in positive emotional processing [e.g. see (129) for
review]. In this study, right amygdala activation
may be a sign of relatively more positive and
healthy self-appraisal within women who, as a
group, can be characterized by severe negative
self-referential processing. It is also interesting to
note that the right amygdala has been suggested to
be involved in social emotion processing (see
earlier section), and more positive and healthy
self-appraisal may be related to better social
functioning.
The aforementioned ndings suggest alterations
in brain functioning during self-referential process-
ing tasks in PTSD. Future studies will need to
examine the relationship between the intensely
disturbed sense of self and brain activation
patterns in regions involved in self-referential
processing in PTSD and whether psychotherapeu-
tic interventions that are specically designed to
improve the capacity for introspection and self-
awareness can restore the functional abnormalities
observed in brain regions such as the medial
prefrontal cortex and the posterior cingulate
cortex (130).
The default mode network. The DMN is one of the
main intrinsic or resting state networks in the brain
and has been suggested to play an important role in
self-referential processing (131134). The DMN is
activated when individuals are engaged in stimulus-
independent thought [reviewed by Buckner et al.
(135)], and it is thought to aid in serving to
consolidate, stabilize and set the context for future
information processing (135). A recent meta-anal-
ysis demonstrated that autobiographic memory
recall, theory of mind tasks and prospec-
tion thinking about the future activate the DMN
(136, 137). This may indicate that these functions
bear a direct relationship to the connectivity of this
network.
The DMN includes several brain regions that
have been associated with self-referential process-
ing (138), including the medial prefrontal cortex,
posterior cingulate cortex in addition to midline
parietal structures, medial and lateral temporal
lobes and lateral parietal regions. The regions
comprising this network were originally thought to
be involved in the maintenance of a default mode
of brain functioning that occurred in the absence of
task-related processes as the regions of this net-
work had a high level of metabolic activity during
rest and showed consistent decreases in activity
level during the performance of cognitive tasks
(139). Later studies showed that these brain regions
exhibit positive correlations with each other (140,
141) and negatively correlate with brain areas
involved in many cognitive tasks (140, 142). These
DMN areas have anatomical connections that may
explain their functional connectivity during rest.
(143, 144).
Given that PTSD has been associated with
decits in self-referential processing, as described
earlier, and has been associated with altered
activation in areas associated with the default
network (e.g. medial prefrontal cortex, anterior
cingulate and posterior cingulate cortex) across a
variety of paradigms (71, 145150), our group
chose to embark on a study that examined the
integrity of this network in PTSD. In patients with
chronic PTSD owing to prolonged childhood
abuse, signicantly reduced resting state connec-
tivity within the DMN was demonstrated (151) (see
Fig. 2). The PTSD group showed diminished
connectivity between the posterior cingulate seed
region and the medial prefrontal cortex, right
superior frontal gyrus and left thalamus. Further-
more, the connectivity of the medial prefrontal
seed region was strictly limited to adjacent areas in
the medial prefrontal cortex. Because auto-
biographic memory recall has previously been
shown to bear a direct relationship to the connec-
tivity of the DMN (152), alterations in brain
activation in PTSD during autobiographic memory
recall as observed during the script-driven imagery
symptom provocation studies may be one under-
lying mechanism contributing to the altered DMN
Neurobiology of PTSD and clinical practice
339
connectivity observed. We have also recently
suggested that in adult patients with PTSD related
to childhood abuse, DMN connectivity resembles
that observed in children aged 79, possibly
indicating interference with the maturation process
because of the toxic eects of stress hormones on
the myelination of the corpus callosum (153).
Daniels et al. (154) also studied the ability of
patients with chronic PTSD to engage and disen-
gage from a working memory task, as decits in
working memory performance have been well
documented in PTSD (155157). It has recently
been shown that failure to suppress activity in the
DMN can result in poorer working memory
performance (158). In the light of these ndings,
it is interesting that PTSD subjects showed sus-
tained connectivity in the DMN during the work-
ing memory task. In contrast, the control group
showed signicantly stronger connectivity with
areas implicated in salience and executive control,
including the right inferior frontal gyrus and the
right inferior parietal lobule during the working
memory task as compared to the resting condition.
These diering patterns of connectivity suggest
diculties with task-induced switches, i.e. engaging
and disengaging the DMN, potentially causing the
observed reductions in working memory perfor-
mance as often seen in individuals with PTSD.
Future studies will have to investigate the causal
relationship between specic PTSD symptoms
experienced during the resting scan and connectiv-
ity of the DMN as well as to further elucidate the
mechanism underlying switching between resting
and cognitive and emotional networks (159). In
addition, the relationship between self-referential
processing and the altered sense of self in relation
to DMN connectivity will have to be explored. We
hypothesize that the negatively valenced and often
fragmented sense of self that is often experienced
by individuals with highly dissociative PTSD will
be related to the degree of anteriorposterior
integration of the DMN.
SCAN-informedtreatment applications. As described
earlier, a number of recent studies, falling under
the scope of SCAN, suggest that patients with
PTSD show problems in emotional self-awareness,
emotion regulation, social emotional processing
and self-referential processing. Interestingly, a core
set of brain regions appear to partly mediate these
collective psychological functions, most notably the
cortical midline structures, the amygdala, the insula,
posterior parietal cortex and temporal poles, sug-
gesting that problems in one area (e.g. emotional
awareness) might relate todiculties inanother (e.g.
self-referential processing). There is also evidence
that these regions are implicated in the pathophys-
iology of PTSD. In this section, we consider the
signicance of these ndings for the treatment of
PTSD.
Emotional self-awareness. Exposure-based treat-
ments of PTSD (160) involve repeated imaginal
and in vivo exposure to trauma-related stimuli.
Although these treatments have strong empirical
support, in order to be successful, it is important
for patients to be able to fully engage emotionally
with the traumatic material. During exposure
(a)
(b)
Fig. 2. (a) Default mode network (DMN) connectivity in
control (top panel) and post-traumatic stress disorder (PTSD)
subjects (bottom panel). Areas of correlation with posterior
cingulate precuneus in healthy comparison subjects (n = 15)
and in patients with PTSD (n = 17), thresholded at P < 0.05,
corrected using false discovery rate correction. (b) DMN
connectivity between group comparison. Areas in which cor-
relation with the posterior cingulate precuneus is stronger in
healthy control subjects (n = 15) than in patients with PTSD
(n = 17), thresholded at P < 0.05, corrected using false dis-
covery rate correction. Figure originally published in Bluhm
et al. (151) and reprinted with permission.
Lanius et al.
340
therapy, patients are usually asked to recall details
of their traumatic experience while describing them
in the present tense. Exposure sessions are thus
designed to overcome the avoidance of such stimuli
by providing a safe context in which patients can
fully engage with both trauma-related and correc-
tive (safety) information. In this way, exposure
treatment is designed to overcome and reduce
avoidance symptoms, enhance aect management,
diminish anxiety and fear associated with the
traumatic material and facilitate cognitive restruc-
turing of trauma-related memories. In turn, this
should bring about the reduction of re-experienc-
ing and hyperarousal symptoms and, ultimately,
lead to a signicant reduction of symptoms or
elimination of the disorder itself (161).
Teaching PTSD patients with impairments in
emotional awareness to identify their aective
feelings early on in treatment may make expo-
sure-based treatments more ecient (78, 86, 162,
163) because such therapies are dependent on a
patients judgment of their internal aect and as
well as a reliable report of their symptom presen-
tations. In addition, such treatments may be less
eective in the early stages of treatment for
patients who are unable to modulate, regulate
and engage in the intense aective experiences that
may be elicited by exposure-based therapies. Inter-
oceptive awareness training to help patients
become aware of and describe bodily sensations
and their relationship to emotions is therefore
often a crucial part of the rst stage of trauma
treatment. Such awareness can prevent individu-
als from entering severe hypo- or hyperarousal
states that can prevent emotional and cognitive
processing.
During this phase of treatment, patients have to
develop an awareness and language that helps
them identify bodily sensations and how dierent
bodily sensations relate to dierent emotional
experiences. For example, for one person, tension
in the jaw in combination with a feeling of
tightness in the throat may correlate with sadness,
while in another individual, sadness may correlate
with tightness in the stomach and a feeling of
heaviness in the chest. By developing emotional
awareness, patients can then learn to identify
precursors to extreme emotional states and learn
to intervene before these states become too intense
and overwhelming. Once a patient has mastered
these skills, they can be applied during the expo-
sure-based treatments, thereby preventing extreme
emotional states that preclude optimal emotional
engagement during exposure therapy.
Emotional interoceptive awareness training has
been incorporated into several forms of psycho-
therapy for PTSD. Dialectical Behaviour Therapy
(164, 165), skills training in aective and interper-
sonal regulation (STAIR) (122) and emotion
focused therapy (166) all include a focus on
increasing patients capacity for introspection and
self-awareness, particularly with regard to emo-
tional experiences. In addition, mindfulness-based
approaches such as those outlined by Kabat-Zinn
and Siegel (167, 168) can be helpful to increase the
capacity for emotional awareness. In particular,
teaching patients to become aware of physical
sensations through engaging in body scans at a
pace that feels safe for them can help to increase
their introspective ability. Yoga has also been
suggested to be eective in treating PTSD, partially
by increasing ones interoceptive ability (169, 170).
Emotion regulation and social emotions. In recogni-
tion of complex emotion dysregulation, social and
self-dysfunction in patients with chronic PTSD
related to childhood abuse, Cloitre et al. (162)
developed an empirically validated stage-oriented
intervention for PTSD related to childhood abuse.
STAIR is a stage-oriented treatment model that
uses skills training in emotion and self-regulation
and interpersonal eectiveness prior to engaging in
exposure-based therapy. Results published by
Cloitre et al. (78) support the suggestion that,
before beginning exposure therapy, patients need
to develop mood regulation skills, allowing them to
better identify and modify disordered attachment
schemas learned in childhood and enhancing their
competence in social interactions.
Early stages of STAIR teach patients how to
enhance their capacity to regulate dysregulated
emotional states through cognitive strategies
(attention shifting, positive self-statements, posi-
tive imagery), behavioural strategies (time out,
replacement behaviours, engaging in pleasurable
activities) and enhancing distress tolerance skills.
Enhancing emotion regulation skills prior to
engaging in exposure-based treatment may be
particularly important in individuals with emotion
regulation problems involving signicant symptoms
of emotional overmodulation, such as dissociative
(e.g. depersonalization, derealization and analgesia)
symptoms (86). Such symptoms can reduce or
prevent emotional engagement with trauma-related
information and thereby reduce treatment eective-
ness (171). Further evidence for the latter stems
froman investigation by Hagenaars et al. (172) who
reported a dierential outcome for PTSD patients
with high vs. low dissociative symptomatology.
Whereas only 10% of PTSD patients with low
dissociative symptoms still met PTSD criteria after
a trial of exposure therapy, 69% of PTSD patients
Neurobiology of PTSD and clinical practice
341
with high levels of dissociation continued to meet
PTSD criteria at follow-up. Therefore, it is crucial,
before commencing exposure-based treatments, to
assess the levels of emotional overmodulation and
provide interventions to reduce such symptomatic
responses to trauma-related stimuli (86).
Following the emotion regulation component of
STAIR, patients begin interpersonal regulation
training that involves understanding interpersonal
schemas, changing relationship patterns through
role-play using appropriate assertiveness skills and
an enhanced understanding of power balances in
relationships. In addition, providing a corrective
interpersonal experience through a therapeutic
relationship can provide a secure base (173),
thereby facilitating trust and eective communica-
tion is also an important aspect of facilitating
enhanced social competence (122, 164, 166).
In the later stages of STAIR treatment, exposure
therapy and narrative story telling is designed to
help patients reach a stage of resolution of their
feelings of shame and grief. This intervention
involves both telling the story of the trauma and
a related meaning analysis in order to help patients
understand who they have come to be as a result of
what they have experienced. This understanding
may decrease feelings of shame and loss, as well as
related experiences of the self as inferior, bad,
annihilated, fragmented and or identied with the
perpetrator (122). The resolution of the experience
of the self as an extremely negative entity will also
likely result in signicantly increased social func-
tioning. It is often the experience of the self as bad
and inferior that perpetuates individuals being in
abusive relationships as they may feel like they
deserve to be punished or treated without respect.
With regard to the latter, this part of STAIR also
involves role-play during which emotions and
actions are integrated, thus providing individuals
the experience of learning about who they can
learn to become through action.
Self-referential processing. Self-referential process-
ing is most closely related to the concept of
mentalizing attending to states of mind in oneself
and others (174), and mentalization-based treat-
ments have been shown to be eective in individ-
uals who have suered from disrupted early
attachments and childhood abuse (175). Increased
self-referential processing mentalizing has been
suggested to enhance emotion regulation skills as
well as to facilitate the process of exposure to
traumatic memories. As Jon Allen states: We work
clinically [using mentalization-based therapy] with
patients who are prone to be swept away by
emotion, carried along into impulsive action,
without any felt sense of self. We encourage such
patients to push a metaphorical pause button by
mentalizing [(174), p. 11]. Moreover, Allen has
stressed that the alternative to traumatic re-enact-
ments is mentalizing, that is developing the capac-
ity to reect on the relationship between triggering
events in the current relationship and previous
traumatic experiences. Allen has also suggested
that encouraging mentalizing while recalling vivid
traumatic memories as is done during classic
desensitization procedures allows individuals to
take a more active stance in the recall of their
traumatic memories, thereby creating an increased
mastery experience.
Self-referential processing is also a key compo-
nent of cognitive restructuring. The latter involves
identifying and modifying catastrophic and
unrealistic interpretations of ones traumatic
event and future expectations, thereby leading to
cognitive schema that will decrease the outcome of
psychopathological states with a resulting reduc-
tion in trauma-related symptomatology (176). In
fact, evidence has shown that optimal treatment
outcomes in PTSD are achieved when cognitive
restructuring is combined with exposure therapy
(176). Cognitive restructuring is also an important
component of cognitive processing therapy (177).
These ndings therefore provide further evidence
for the importance of self-reection in the treat-
ment of traumatized individuals.
Discussion
In conclusion, researchers and clinicians with an
interest in complex PTSD have become increas-
ingly aware of the potential eects of early life
trauma on neurobiology, symptomatology and
prognosis. Yet much remains to be done in
developing a concept of PTSD that can account
for the far-reaching eects of chronic traumatiza-
tion. In this review, we have examined the
relevance of the SCAN paradigm for an under-
standing of the psychology and neurobiology of
complex PTSD and its eective treatment. We have
suggested that SCAN oers a novel theoretical
paradigm for understanding psychological trauma
and its numerous clinical outcomes, most notably
problems in emotional self-awareness, emotion
regulation, social emotional processing and self-
referential processing. A core set of brain regions
appear to mediate these collective psychological
functions, most notably the cortical midline struc-
tures, the amygdala, the insula, posterior parietal
cortex and temporal poles, suggesting that prob-
lems in one area (e.g. emotional awareness) may
relate to diculties in another (e.g. self-referential
Lanius et al.
342
processing). We have further suggested, drawing
on clinical research, that the experiences of indi-
viduals with PTSD related to chronic trauma often
reect impairments in many of these abilities. It is
therefore crucial that the assessment and treatment
of individuals with chronic PTSD not only
addresses the traumatic memories but also takes
a SCAN-informed approach that focuses on the
underlying decits in emotional self-awareness,
emotion regulation, social emotional processing
and self-referential processing. Finally, treatment
outcome studies examining the eectiveness of
treatments for complex PTSD will not only need to
focus on PTSD symptoms but also ought to assess
the eect of the intervention on emotional self-
awareness, emotion regulation, social emotional
processing and self-referential processing.
Future research directions
Future studies in complex PTSD should further
evaluate social cognitive processes and their shared
and non-shared neural correlates, including empa-
thy (178, 179, 180), moral reasoning, theory of
mind and emotion comprehension in order to
broaden our understanding of the potential decits
in these functions as a result of chronic traumati-
zation. Moreover, the relationship between
declines in basic cognitive processes, including
working memory, executive functioning and
anterograde memory, on the one hand, and decits
in higher-level aective processes such as concep-
tual emotional awareness and self-referential pro-
cesses, on the other, will need to be explored. It will
also be crucial to develop a detailed understanding
of the relationship between specic stress-related
symptoms (e.g. emotional numbing) and their
precise eects on social cognition. For example,
we would hypothesize that signicant symptoms of
numbing emotional detachment would substan-
tially interfere with both the capacity for empathy
and theory of mind mentalizing. Research will also
have to address to what degree decits in the neural
circuitry underlying social cognition aect the
ability to engage in psychotherapy and to what
extent do the neural networks underlying social
emotions need to be intact in order to utilize social
support before, during and in the aftermath of
trauma. Furthermore, it will be important to
determine whether psychotherapeutic interventions
that specically target interpersonal dysfunction
and the capacity for introspection and self-aware-
ness can restore the functional abnormalities
observed in the neural circuitry underlying these
processes. In addition, the relationship between
self-referential processing and the intensely nega-
tive and fragmented sense of self often observed in
complex PTSD, on the one hand, and DMN
connectivity, on the other, deserves exploration.
Lastly, it will be important to determine whether
decits in the neural circuitry underlying self-
reection and social cognition aect the ability to
parent and thereby facilitate the intergenerational
transmission of trauma.
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