Posttraumatic Stress Disorder
Shifting Toward a Developmental Framework
Victor G. Carrion, MD*, Hilit Kletter, PhD
Childhood exposure to trauma is a common phenomenon, with 25% of young
people experiencing a traumatic event such as physical abuse; sexual abuse;
witnessing violence, war, and terrorism; natural disasters; illness; or injury by the
time they reach age 16 years.1Internal (eg, genetics and individual traits) and
environmental (eg, home, school, community) factors interact to determine the
outcome that trauma will have on a child. Many young people demonstrate
resilience, the ability to adapt and cope despite adversity, and continue to develop
normally.2Some will be susceptible to develop mood and/or anxiety disorders.3
Yet others are at risk to develop posttraumatic stress disorder (PTSD), which can
The authors have nothing to disclose.
Department of Psychiatry and Behavioral Sciences, Division of Child and Adolescent Psychiatry,
Stanford School of Medicine, Stanford University, 401 Quarry Road, Stanford, CA 94305, USA
* Corresponding author.
E-mail address: email@example.com
Child Adolesc Psychiatric Clin N Am 21 (2012) 573–591
1056-4993/12/$ – see front matter © 2012 Elsevier Inc. All rights reserved.
• Pediatric posttraumatic stress disorder • Childhood trauma
• Childhood development • Neurobiology • Interventions
• It has been proposed that posttraumatic stress disorder (PTSD) should be conceptualized
as a dimensional and continuous, rather than a categorical, clinical entity in youth.
• As a result of young children’s limitations in their verbal capacity, they may use other
means to express themselves such as being fussy or having temper tantrums, types of
behavior often overlooked as symptoms of PTSD.
• Chronic periods of stress may impair the hypothalamic–pituitary–adrenal (HPA) axis
resulting in dysregulation of cortisol secretion, which has been suggested as a marker for
PTSD; though neuroendocrine studies have yielded mixed results regarding the relation-
ship of cortisol and pediatric PTSD, the majority of studies report high levels of cortisol to
be indicative of PTSD.
• Psychotherapeutic interventions have the potential to modulate negative effects of PTSD
by providing new experiences that repair brain function and promote the growth of neural
have a negative impact on biological, cognitive, emotional, behavioral, and social
domains of the child.4Although trauma exposure is associated with the develop-
ment of different conditions, this article focuses specifically on PTSD because it is
the disorder (or injury) with the most widely studied outcome across populations
and trauma types.
CLASSIFICATION OF PTSD
It has long been established that PTSD occurs in adults; however, it was not until
the publication of the DSM-III-R that it was recognized that young people
experience similar symptoms.5The diagnosis of PTSD is based on six major
criteria, two of which define the trauma (criterion A). The DSM-IV-TR provides the
1. The person experienced, witnessed, or was confronted with an event or events
that involved actual or threatened death or serious injury, or a threat to the physical
integrity of self or others.
2. The person’s response involved intense fear, helplessness, or horror.6
In children, the latter may be expressed as disorganized or agitated behavior.
Symptoms of PTSD are divided into three clusters:
1. Reexperiencing of the traumatic event (criterion B), which includes flashbacks,
nightmares, exaggerated startle response, and intrusive recollections.
2. Avoidance of trauma with regard to relevant stimuli and numbing of general
responsiveness (criterion C), which includes feeling detached or estranged from
others and deriving markedly less pleasure from activities that previously were
3. Hyperarousal (criterion D), which includes irritability, hypervigilance, and difficul-
ties in sleep and concentration.
Symptoms must persist for at least 1 month (criterion E) and cause significant distress
or impairment in functioning (criterion F).
Proposed changes to the PTSD diagnosis for DSM-V take into account develop-
mental variations in symptom manifestation, including a separate subtype for children
younger than age 6 years.7Additional changes include clarification of what consti-
tutes a traumatic event, elimination of criterion A2, division of cluster C avoidance and
numbing into two separate criteria, and elimination of the acute versus chronic
designation. In addition, cluster D (numbing) has new symptoms emphasizing the role
of self or other blaming and persistently negative emotional states and cluster E
(hyperarousal) has an added symptom of reckless or self-destructive behavior.
Table 1 shows the current DSM-IV criteria and highlights the proposed DSM-V
There are instances in which PTSD symptoms may differ in young people. For
example, children may engage in repetitive play and experience frightening dreams
without specific content.8Many children develop fears associated with certain
aspects of a trauma that may develop into phobias.9Increased irritability and anger
may lead to aggressive behavior in such cases.9Children with PTSD often experience
guilt over what they should or could have done in a particular situation.10A number
of cognitive problems have also been observed in traumatized youth. Children with
PTSD frequently report difficulties in concentration, especially with regard to
schoolwork.11They may develop memory problems, both in learning new material and
in remembering previously acquired skills.11
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Proposed changes in the diagnostic criteria of PTSD in the DSM-V
A. The person has been exposed to a
traumatic event in which both of the
following were present:
1. The person experienced, witnessed,
or was confronted with an event or
events that involved actual or
threatened death or serious injury,
or a threat to the physical integrity
of self or others.
2. The person’s response involved
intense fear, helplessness, or horror.
Note: In children, this may be
expressed instead by disorganized or
DSM-V Proposed Changes
A. The person was exposed to one or more of the
following event(s): death or threatened death,
actual or threatened serious injury, or actual
or threatened sexual violation, in one or more
of the following ways:
1. Experiencing the event(s) him/herself
2. Witnessing, in person, the event(s) as they
occurred to others
3. Learning that the event(s) occurred to a
close relative or close friend; in such cases,
the actual or threatened death must have
been violent or accidental
4. Experiencing repeated or extreme exposure
to aversive details of the event(s) (eg, first
responders collecting body parts; police
officers repeatedly exposed to details of
child abuse); this does not apply to exposure
through electronic media, television, movies,
or pictures, unless this exposure is work
Criterion A2 eliminated.
B. Intrusion symptoms that are associated with
the traumatic event(s) (that began after the
traumatic event[s]), as evidenced by one or
more of the following:
1. Spontaneous or cued recurrent, involuntary,
and intrusive distressing memories of the
traumatic event(s). Note: In children,
repetitive play may occur in which themes or
aspects of the traumatic event(s) are
2. Recurrent distressing dreams in which the
content and/or affect of the dream is related
to the event(s). Note: In children, there may
be frightening dreams without recognizable
3. Dissociative reactions (eg, flashbacks) in
which the individual feels or acts as if the
traumatic event(s) were recurring (Such
reactions may occur on a continuum, with
the most extreme expression being a
complete loss of awareness of present
surroundings.) Note: In children, trauma-
specific reenactment may occur in play.
4. Intense or prolonged psychological distress
at exposure to internal or external cues that
symbolize or resemble an aspect of the
5. Marked physiological reactions to reminders
of the traumatic event(s).
B. The traumatic event is persistently
reexperienced in one (or more) of the
1. Recurrent and intrusive distressing
recollections of the event, including
images, thoughts, or perceptions.
Note: In young children, repetitive
play may occur in which themes or
aspects of the trauma are expressed.
2. Recurrent distressing dreams of the
event. Note: In children, there may
be frightening dreams without
3. Acting or feeling as if the traumatic
event were recurring (includes a
sense of reliving the experience,
illusions, hallucinations, and
dissociative flashback episodes,
including those that occur on
awakening or when intoxicated).
Note: In young children, trauma-
specific reenactment may occur.
4. Intense psychological distress at
exposure to internal or external cues
that symbolize or resemble an
aspect of the traumatic event.
5. Physiological reactivity on exposure
to internal or external cues that
symbolize or resemble an aspect of
the traumatic event.
(continued on next page)
C. Persistent avoidance of stimuli
associated with the trauma and
numbing of general responsiveness
(not present before the trauma), as
indicated by three (or more) of the
1. Efforts to avoid thoughts, feelings,
or conversations associated with the
2. Efforts to avoid activities, places, or
people that arouse recollections of
3. Inability to recall an important
aspect of the trauma.
4. Markedly diminished interest or
participation in significant activities
5. Feeling of detachment or
estrangement from others.
6. Restricted range of affect (eg,
unable to have loving feelings).
7. Sense of a foreshortened future (eg,
does not expect to have a career,
marriage, children, or a normal life
DSM-V Proposed Changes
2. Persistent and exaggerated negative
expectations about one’s self, others, or the
world (eg, “I am bad,” “no one can be trusted,”
“I’ve lost my soul forever,” “my whole nervous
system is permanently ruined,” “the world is
3. Persistent distorted blame of self or others
about the cause or consequences of the
4. Pervasive negative emotional state, eg, fear,
horror, anger, guilt, or shame
E. Alterations in arousal and reactivity that are
associated with the traumatic event(s) (that
began or worsened after the traumatic
event(s)), as evidenced by three or more of the
following: Note: In children, as evidenced by
two or more of the following:
1. Irritable or aggressive behavior
2. Reckless or self-destructive behavior
4. Exaggerated startle response
5. Problems with concentration
6. Sleep disturbance, eg, difficulty falling or
staying asleep, or restless sleep.
D. Persistent symptoms of increased
arousal (not present before the
trauma), as indicated by two (or more)
of the following:
1. Difficulty falling or staying asleep
2. Irritability or outbursts of anger
3. Difficulty concentrating
5. Exaggerated startle response.
From American Psychiatric Association. DSM-V Development. www.dsm5.org.
Carrion & Kletter
SINGLE-EVENT VERSUS MULTIPLE-EVENT TRAUMA
The distinction between single-event and multiple-event trauma (Table 2) has been
referred to by various designations such as acute versus chronic trauma, type I versus
type II trauma, and simple versus complex trauma.12,13
Type I Trauma
Type I trauma has been defined as a single-event trauma that usually meets the DSM
criteria for PTSD and is characterized by the classic symptom clusters of repetition,
avoidance, and increased arousal.12In addition, young people with single-event
trauma may experience symptoms of trauma including specific fears; regressive
behavior; loss and grief reactions; cognitive–perceptual distortions; changed attitudes
about the self, others, or the future; and reexperiencing of perceptual, affective,
ideational, or somatic components of the trauma. This type of trauma generally
occurs along with a background of normal development. Although impairments are
expected in such areas as academic performance, maintenance of peer and family
relationships and, at times, in daily living activities, individuals are expected to make
a full recovery in functioning.14
Type II Trauma
Type II trauma refers to multiple-event trauma and often presents with the classic
symptoms of PTSD. Repeated exposure can also lead to the development of more
severe symptoms such as massive denial, psychic numbing, self-anesthesia, and
personality problems.12In this type of trauma, the deviation from the normal trajectory
of development occurs earlier and the chronic nature inhibits the trajectory from
returning to its normal course. Herman (1992) coined the term “complex trauma” to
describe the chronic effects of type II trauma and maintains that the much more
diverse consequences of this type of trauma require a more comprehensive diagnosis
than the PTSD normally observed in single-incident trauma.13In line with this, a new
provisional diagnosis of Developmental Trauma Disorder has been proposed to better
capture the experiences of youth with complex trauma such as community violence
that is characterized by multiple events and/or prolonged exposure.15The premise of
this proposed diagnosis is that multiple trauma exposures have consistent and
predictable outcomes that impact on many domains of functioning. Specifically,
impairment occurs in seven domains: attachment, biology, affect regulation, disso-
ciation, behavioral regulation, cognition, and self-concept.16The diagnosis centers on
triggered dysregulation in response to traumatic reminders, stimulus generalization,
and behavioral attempts to avoid the reexperiencing of traumatic effects. Thus it is
suggested that treatment should target three key areas: establishing safety and
competence, dealing with traumatic reenactments, and integrating body and mind.15
Single-event versus multiple-event trauma
Acute, one-time event.
Classic symptoms of PTSD.
Chronic and/or many events.
Symptoms are more intrinsic (eg, numbing, denial,
Normal development is inhibited.Normal development is resumed.
Studies Comparing Single-Event and Multiple-Event Trauma
Several studies have compared single-event and multiple-event traumas in youth. In
a sample of sexually abused children, common type I trauma symptoms included
reexperiencing events such as nightmares, avoidant behaviors (ie, fear of certain
places and situations, withdrawal), and increased hyperarousal (ie, difficulties with
sleep and concentration, irritability).17Furthermore, it was found that those with type
II trauma experienced more anxiety and depression, and had deficits in coping
strategies related to daily and extreme stresses. They tended to have an enduring
maladaptive attributional style (ie, learned helplessness); often experienced dissocia-
tive states (ie, massive denial and numbing); and frequently had excessive, poorly
regulated responses to anger-provoking stimuli. In a sample of South African
adolescents, those exposed to multiple-event traumas experienced more PTSD
symptoms and depression than those exposed to single-event traumas.18Hagenaars
and colleagues found that individuals with multiple-event trauma experienced more
dissociation and shame compared to those with single-event trauma.19
LIMITATIONS OF THE CURRENT CLASSIFICATION OF PTSD
There has been much debate regarding whether the current diagnostic criteria, which
rely on behavioral descriptions, adequately capture the presentation of PTSD in
youth.20,21It has been proposed that PTSD should be conceptualized as a dimen-
sional and continuous, rather than a categorical, clinical entity in youth.22Develop-
mental variations may affect children’s expression of PTSD symptoms and there has
been much criticism that the current DSM criteria do not account for the develop-
mental nature of the disorder.23,24For example, young children are limited in their
verbal capacity and thus they may use other means to express themselves such as
being fussy or having temper tantrums.25,26These types of behavior are often
overlooked as symptoms of PTSD. Furthermore, relying on the current categorical
model for diagnosis of PTSD may result in neglect of individuals who fall short of
meeting the full criteria but may still be experiencing significant impairment. Several
studies have found that subthreshold PTSD is similar to full-criteria PTSD in terms of
its adverse effects.27–29This suggests that the diagnosis of PTSD in youth might be
more accurate based on the intensity of symptoms related to functional impairment
rather than number of symptoms met.
Another major limitation of behavioral descriptions is the lack of recognition that
fear networks underlying the mechanism of PTSD may perpetuate other forms of
anxiety. Young people with PTSD are at greater risk of the future development of
anxiety disorders such as obsessive–compulsive disorder, generalized anxiety dis-
order, and phobias.30Thus, the diagnostic criteria ought to consider that PTSD may
precede the development of other anxiety disorders and that there is potential for
symptom overlap. Comorbidity rates for mood and anxiety disorders are as high as
80% in posttraumatic populations,31which suggests that these comorbidities may
need to be included in the classification of PTSD.
ASSESSMENT OF PTSD
Numerous instruments exist for screening and diagnosis of childhood PTSD, as well
as evaluation of trauma exposure and associated symptoms. Although a full review of
all available measures is beyond the scope of this discussion, some of the most
widely used instruments are described.
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Clinician-Administered PTSD Scale for Children and Adolescents
The Clinician-Administered PTSD Scale for Children and Adolescents (CAPS-CA) is
considered the gold standard in childhood PTSD assessment.32The CAPS-CA is
used to assess PTSD and associated symptoms in youth ages 8 to 18. It consists of
36 questions based on a specific event that the child identifies as most distressing.
The CAPS-CA evaluates current and lifetime diagnosis; frequency and intensity of
symptoms; and functioning in social, developmental, and academic domains.
UCLA PTSD Reaction Index for DSM-IV
The UCLA PTSD Reaction Index for DSM-IV (PTSD-RI) is a self-report measure with
child (ages 7–12), adolescent (ages 13–18), and parent versions.33The PTSD-RI
contains 48 items that assess exposure to 26 types of traumatic events and evaluates
DSM-IV PTSD criteria for the event that the child identifies as the most distressing.
Youth rate symptoms on a 5-point Likert scale (0 ? “none of the time” to 4 ? “most
of the time”) and the parent version has an option of responding “don’t know” to
account for symptoms that the parent may not have observed. It also evaluates
associated symptoms of guilt and fear of recurrence of the event.
Child PTSD Interview
This is a 95-item semistructured interview that assesses DSM-IV PTSD criteria and
associated symptoms.34Questions are written at a third-grade level, though the
measure has been used with younger children.34Each symptom item is rated as
either being present or absent. There is also a parent form that assesses the same
dimensions as the child form.
Children’s PTSD Inventory
The Children’s PTSD Inventory (CPTSDI) is a clinician-administered measure for
children ages 6 to 18 based on the DSM-IV criteria for PTSD.35The child is first
screened for exposure to various traumatic events by being asked if he or she ever
experienced it or felt upset for not being able to stop it from happening. If an event
meets the screening criteria, then symptoms are assessed in reference to the event.
In addition to a PTSD total score, the CPTSDI also yields scores on five subscales:
Situational Reactivity, Reexperiencing, Avoidance and Numbing, Increased Arousal,
and Significant Impairment.
Child PTSD Symptom Scale
The Child PTSD Symptom Scale (CPSS) is a 26-item self-report that assesses PTSD
and symptom severity in youth ages 8 to 18.36Items are rated on a 4-point Likert
scale (0 ? “not at all” to 3 ? “5 or more times a week”). Functional impairment is also
assessed (0 ? “absent” and 1 ? “present”) but is not based on DSM-IV criteria. The
measure provides total scores for symptom severity and severity of impairment, as
well as scores for PTSD symptom clusters.
Trauma Symptom Checklist for Children
The Trauma Symptom Checklist for Children (TSCC) is a brief self-report for children
ages 8 to 16 that screens for trauma exposure and posttraumatic stress but is not
intended to be diagnostic.37It consists of two validity scales (over- and under-
reporting) and six clinical scales (anxiety, depression, posttraumatic stress, sexual
concerns, dissociation, and anger). Children are presented with thoughts, feelings,
and behaviors related to traumatic events and are asked to mark how often they
happened on a 4-point Likert scale (0 ? “never” to 3 ? “almost all the time”).
Childhood Trauma Questionnaire
The Childhood Trauma Questionnaire (CTQ) is a 28-item, self-report that screens for
a history of abuse and neglect in children over the age of 12.38It assesses exposure
to five types of trauma: emotional, physical, and sexual abuse, and emotional and
physical neglect. In addition, it contains a three-item minimization/denial scale for
THE ROLE OF NEUROBIOLOGY IN UNDERSTANDING PTSD
The Role of Cortisol
The endocrine system, crucial to growth and development, is influenced by the
hypothalamic–pituitary–adrenal (HPA) axis that secretes the hormone cortisol during
times of stress to mobilize an individual into action.39Chronic periods of stress,
however, may impair the HPA axis, resulting in dysregulation of cortisol secretion,
which has been suggested as a marker for PTSD.39Neuroendocrine studies have
yielded mixed results regarding the relationship of cortisol and pediatric PTSD. The
majority of studies report high levels of cortisol to be indicative of PTSD.40–46On the
other hand, lower cortisol levels have been associated with PTSD in youth exposed
to an earthquake, sexually abused girls, and youth bereaved by the September 11,
2001 terrorist attacks.47–49Attempts have been made to clarify these inconsistencies.
In a sample of youth exposed to interpersonal violence, a higher level of salivary
cortisol was positively associated with PTSD among individuals with recent traumas
(previous year), but in individuals with distal traumas (more than a year prior to
assessment) the association was the opposite; the more PTSD symptoms the lower
the levels of cortisol.50These findings highlight the importance of “time since trauma”
when evaluating cortisol levels in PTSD. In addition, Pervandiou and colleagues found
that, after a motor vehicle accident, children with PTSD initially had elevated evening
salivary cortisol, but that levels normalized in the 6 months after the trauma.51Thus,
the amount of time that has elapsed since the trauma may be a significant factor in the
relationship between cortisol and PTSD.
It has also been suggested that significant variations exist in patterns of cortisol
regulation among traumatized youth. For example, a study examining different trauma
types found that high morning and afternoon cortisol levels were typical of youth with
both physical and sexual abuse.52However, those with only physical abuse had lower
levels of cortisol in the morning, with a smaller decrease in levels from morning to
afternoon. In another study of youth exposed to interpersonal trauma, individuals with
posttraumatic symptoms had sharper morning declines and higher evening cortisol
levels than nontraumatized youth.53
It therefore appears that traumatized young people may display greater fluctuations
in cortisol levels throughout the day. In conclusion, it appears that what were thought
inconsistencies in the neuroendocrine literature might not be so, as the latest
evidence suggests that cortisol levels in traumatized youth may be dependent upon
trauma type and duration.
The Role of Neuroimaging
Neuroimaging (structural magnetic resonance imaging [MRI], functional MRI [fMRI],
and magnetic resonance spectroscopy [MRS]) studies indicate that abnormalities in
brain structure and function are also linked to the pathophysiology of PTSD. Three
Carrion & Kletter
brain regions that are particularly vulnerable to the effects of childhood trauma are the
amygdala, prefrontal cortex, and hippocampus (Fig. 1).
The amygdala, which is part of the limbic system, is responsible for the processing of
emotions and facilitates consolidation of emotional memories.54It plays an important role
in assessing threatening stimuli.55Potentially dangerous stimuli are first processed in the
thalamus and either directly or indirectly reach the amygdala where an emotional
response will be developed with or without cognitive input. Pediatric neuroimaging
studies suggest that there are no amygdala volume differences between traumatized
youth with PTSD and healthy controls.56–58Although one study found a 5.1% reduction
in amygdala volume of maltreated youth compared to healthy controls, when the results
were corrected for total brain gray matter, no significant differences remained.59
Numerous functional imaging studies, utilizing threatening words or faces, have
identified hyper-responsiveness of the amygdala in traumatized adults.60A similar
result was found in one study of trauma0tized youth. In youth exposed to interper-
sonal trauma, individuals with posttraumatic stress symptoms had increased
amygdala activation in response to threatening facial expressions when compared
with healthy controls.61In this study, 23 medication-naive youth with PTSD symp-
toms and 23 age- and gender-matched healthy controls underwent fMRI while
viewing fearful, angry, sad, happy, and neutral expressions. The PTSD group had
greater activation in the early part of the epoch, including greater early phase
amygdala activation to angry faces compared to the controls.
Fig. 1. The amygdala, PFC, and hippocampus. (Retrieved from www.sfn.org. Reprinted with
permission from the Society for Neuroscience.)
The prefrontal cortex
The prefrontal cortex (PFC) is the anterior part of the frontal lobes involved in
executive function. Executive function involves operations related to attention regu-
lation, memory processing, and response inhibition.62
The majority of the pediatric PTSD structural neuroimaging studies indicate abnormal-
ities of the PFC. Maltreated youth failed to show the typical frontal lobe asymmetry
(right ? left) seen in controls, mainly due to larger left frontal lobe volume.59A follow-up
study on a similar sample found reduced white matter volume in the PFC although this
was no longer significant after adjustment for intracranial volume.58In a study examining
left inferior prefrontal gray volumes.63In addition, elevated pre-bedtime cortisol levels
were associated with reduced left ventral PFC gray volume. The results suggest a
potential link between cortisol dysregulation and PFC volume. One study found no PFC
differences between traumatized youth and healthy controls.56
Within the PFC lies the medial prefrontal cortex (mPFC) which, through its connection
with the amygdala, is involved in emotional regulation and the processing of fear.54
Impairments in this region have also been implicated in pediatric PTSD. De Bellis and
colleagues used single-voxel proton MRS (proton MRS) to measure the relative concen-
tration of N-acetylaspartate and creatine, markers of neural integrity, in the anterior
cingulate, a specific area within the mPFC.64The lower concentration of N-acetylaspar-
tate compared to creatine suggests abnormal neuronal metabolism. In an fMRI task
showed relatively decreased activation of the middle frontal cortex, but increased
traumatized youth with PTSD are not engaging core areas of the PFC to the same extent
as healthy individuals.
The hippocampus is a structure in the limbic system responsible for consolidation of
memory.66Although adult trauma studies have consistently found reduced hippocampal
volumes, findings from a meta-analytic study indicate that hippocampal volumes fail to
differ in maltreated children relative to controls based on both cross-sectional child
studies and one longitudinal study.67More recent longitudinal studies, however, have
found differences in the hippocampus of traumatized youths. Carrion and colleagues
found that severity of PTSD and cortisol levels, independently, predicted reductions in
hippocampal volume over a 12- to 18-month interval.66During a memory retrieval task,
youth with PTSD showed reduced activation of the right hippocampus compared to
nontraumatized controls.68Severity of avoidance and emotional numbing symptoms
correlated with reduced left hippocampal activation during retrieval in the PTSD group.
The inconsistencies found in hippocampal volume between traumatized adults and
traumatized youth may be due to developmental processes. A study of rats exposed to
early stress and sacrificed at different ages showed that differences in the hippocampus
emerged only after young adulthood.69Thus, trauma-induced glucocorticoid exposure
may damage the hippocampus, but it is possible that decreased hippocampal volume
occurs only in later development after chronic trauma exposure.
Neurobiological Studies Supplement Behavioral Studies
language for PTSD, the aforementioned neurobiological studies may be used to supple-
ment these descriptions to further enhance our understanding of the clinical profile of
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PTSD. By facilitating the identification of biological risk factors and markers associated
with childhood PTSD symptoms, these studies may aid in early detection of individuals
susceptible to the disorder. In addition, such studies may help to clarify individual
symptom presentations and identify markers associated with resiliency. The core areas
targeted in current interventions match the impairments found in these studies. Thus,
outcomes from these studies may inform treatment development and implementation.
Furthermore, biological markers may assist in tailoring individualized treatments.
Throughout childhood, brain development occurs during specific stages, termed critical
periods, in which a specific brain structure is receptive to input from environmental stimuli
and forms rapidly.70Experience shapes the extensive formation and organization of
neural connections. Failure to form connections results in selective elimination or
“pruning” of unused neurons.71As discussed, childhood trauma has been linked with
alterations in the neurobiological systems involved in brain development and function.72
Impairments in these systems have been associated with PTSD; however, the brain has
the ability to generate new neurons and repair connections in response to novel
experiences, thus reversing the negative effects of trauma.73The brain is at its most
malleable during childhood, so early intervention can be critical. It has been suggested
that the use of evidence-based psychotherapy to treat trauma symptoms may improve
brain function by promoting cortical neurogenesis.74
Adult studies have proven the utility of psychotherapy in improving brain function for a
variety of disorders. For example, in a sample of adults with PTSD secondary to a motor
vehicle accident, cognitive behavioral therapy (CBT) compared to a waitlist control group
was effective in reducing right hemisphere activation, which is associated with avoidance
symptoms.75Another study found that before treatment, depressed individuals had
reduced activation of the dorsolateral PFC, parietal cortex, and striatum but that group
CBT helped restore activation of these regions to the same level as healthy controls.76
Similar studies devoted to youth are now emerging that examine this same interface.77
For example, a family-based intervention consisting of 22 weekly group sessions and 10
biweekly home visits was successful in altering cortisol levels in preschoolers at risk for
conduct problems, compared to healthy controls.78
The most widely used treatment for single-event trauma has been CBT.79Many
variations of trauma-specific CBT interventions exist. However, all share components
summarized by the acronym PRACTICE80:
Relaxation and coping skills
Affective expression and modulation
In vivo exposure to trauma reminders
Conjoint child–parent sessions
Enhancing safety and future development
The majority of these treatments have been implemented as school-based group
• The Multi-Modal Trauma Treatment Protocol (MMTT), an intervention utiliz-
ing developmentally sensitive methods, has been successfully implemented in
both school and community mental health settings.81,82
• The Cognitive Behavioral Intervention for Trauma in Schools (CBITS) is a
10-session treatment that has been shown to improve psychosocial functions in
youth exposed to violence.83
• Several studies of earthquake survivors, victims of the Bosnian war, and victims
of community violence, respectively, have found that trauma/grief focused
therapy resulted in significant reduction of PTSD symptoms.84–86
• Eye movement desensitization and reprocessing (EMDR) has also been
used for the treatment of single-trauma treatment. EMDR is believed to work by
helping to reprocess traumatic memories through forming associations with
positive information stored in other memory networks.87A randomized, con-
trolled trial of EMDR in youth exposed to a natural disaster resulted in a
decrease in trauma related memories and their associated symptoms.87Other
modalities that have been employed in single-trauma intervention include play
therapy and mind–body skills.88,89
Just as with single-trauma treatment, CBT-based approaches are the most common
for multiple-trauma treatment (Table 3).
• Trauma-focused cognitive behavioral therapy (TF-CBT) combines both
individual and parent-child sessions, and consists of the PRACTICE compo-
nents described previously.80TF-CBT has proven efficacious in numerous
randomized controlled trials for reduction of PTSD, depression, and other
emotional and behavioral difficulties for both single-event and multiple-event
Single-trauma versus multiple-trauma interventions
behavioral therapy (TF-CBT)
Multi-Modal Trauma Treatment
Intervention for Trauma in
Trauma/grief focused therapy
Eye movement desensitization
and reprocessing (EMDR)
Trauma systems therapy (TST)
Child–parent psychotherapy (CPP)
Parent–child interaction therapy (PCIT)
Intergenerational Trauma Treatment Model
Cue-centered treatment (CCT)
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traumas.90–92Trauma-focused CBT has also been proven to be superior to
child-centered therapy in reducing PTSD symptoms, especially hyperarousal
and avoidance in youth exposed to intimate partner violence.93
• Trauma systems therapy (TST) is an individual treatment addressing trauma-
related symptoms and the environmental factors perpetuating them.94TST has
demonstrated improvements in PTSD symptoms, environmental stability, and
Other treatments for multiple-trauma include parent–child therapies based on psy-
• Child–parent psychotherapy (CPP) is a dyadic treatment in which play and
other expressive methods are used to repair attachment and regulate traumatic
• Parent–child interaction therapy (PCIT) has also been found to improve
social, emotional, and behavioral functioning through play therapy and live
coaching aimed at improving attachment.96
• The Intergenerational Trauma Treatment Model (ITTM), an intervention
aimed at monitoring dysfunctional family patterns and altering them, has
resulted in improvements in social functioning in traumatized children.97
A manual-based hybrid treatment protocol, The Stanford Cue-Centered Therapy
(CCT), combines elements of CBT, psychodynamic, expressive, and family therapies
and augments these with education in classical conditioning and trauma-related
reminders (cues), focusing on how these are linked to current behaviors, emotions,
thoughts, and physiological reactions.98CCT emphasizes the importance of collab-
oration between the therapist, child, and caregiver to increase a sense of efficacy and
empowerment through knowledge. CCT is divided into four parts:
1. Psychoeducation and coping strategies
2. Incorporating traumas into life narratives involving expression of emotions, filling of
memory gaps, identification of cues, correction of cognitive distortions, and
integration of the traumas into the greater context of the child’s life
3. Gradual exposure to cues while replacing maladaptive behaviors with adaptive
4. Consolidation of learned skills.
The AACAP 2010 practice parameters consider trauma-focused therapies to be the
first line of treatment for youth with PTSD.99The parameters state that these therapies
ought to directly address the traumatic experience, include caregivers in the therapy
process as agents of change, and focus not only on symptom improvement but also
on enhancing functioning, resiliency, and developmental trajectories. The parameters
state that, while studies on the efficacy of PTSD interventions are limited, CBT
treatments and especially TF-CBT are the most widely researched and accepted. In
addition, psychodynamic and family therapies are also suitable.100Psychotherapy is
considered the first choice of treatment for childhood PTSD, however psychotropic
medications such as selective serotonin reuptake inhibitors (SSRIs) may be warranted
in situations of severe symptoms, comorbidity, or when psychotherapy is not
effective. A review of all psychotropic medication that may be effective in treating
childhood PTSD is beyond the scope of this article; however, Wilkinson and Carrion
provide such a review.100
IMPLICATIONS FOR RESEARCH AND CLINICAL PRACTICE
There is a growing consensus that the current diagnostic model for PTSD is neither
sensitive enough nor sufficient for traumatized youth. Research from multiple disci-
plines suggests a distinction between the manifestations of PTSD in children
compared to adults. This research also hints at the crucial role for the accumulation
of stressors throughout life in shaping PTSD. The duration of this process of stress
accumulation, referred to as “allostatic load,” may be more critical than chronological
age of the individual for physiologic effects and symptom development. For example,
an adult with no previous trauma history may present with a characteristically “young”
response (ie, dissociation, high levels of diurnal cortisol, and no markers of stress on
brain structures) whereas a child with chronic trauma may demonstrate more typical
DSM symptoms, low levels of diurnal cortisol, and insidious effects of cortisol in key
brain regions. The posttraumatic period is a dynamic process, exacerbated by the
presence of traumamimetic cues and worsening when inadequate or no intervention
is available. Vietnam combat veterans who developed PTSD have significantly more
history of child maltreatment compared to veterans with no PTSD.101While PTSD was
not manifested after child maltreatment, this previous history may have started a
process that facilitated the development of the disorder after subsequent trauma.
Advancements in the field of neurobiology have aided assessment and treatment
by identifying neurobiological risk factors and biomarkers for PTSD. Cortisol abnor-
malities have been associated with PTSD and appear to be affected by the type and
duration of trauma. Impairments in certain brain regions, especially the amygdala,
PFC, and hippocampus are also prominent in traumatized youth. Psychotherapeutic
interventions have the potential to modulate these negative effects by providing new
experiences that repair brain function and promote the growth of neural connections.
Current evidence-based treatments employ such methods as emotional and behav-
ioral regulation, cognitive processing, coping strategies, and exposure to traumatic
reminders to target the areas identified from neurobiological studies. Future treatment
outcome studies should integrate neuroscience with psychotherapy. Such studies will
help identify which components of treatment are the most crucial for specific
populations. These studies will also inform treatment outcome.
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