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PTSD in DSM 5

DSM-5 Criteria for PTSD


In 2013, the American Psychiatric Association revised the PTSD diagnostic
criteria in the fifth edition of its Diagnostic and Statistical Manual of Mental
Disorders (DSM-5) (1). The diagnostic criteria are specified below.
Note that DSM-5 introduced a preschool subtype of PTSD for children ages six years and
younger. The criteria below are specific to adults, adolescents, and children older
than six years.
Diagnostic criteria for PTSD include a history of exposure to a traumatic event
that meets specific stipulations and symptoms from each of four symptom
clusters: intrusion, avoidance, negative alterations in cognitions and mood, and
alterations in arousal and reactivity. The sixth criterion concerns duration of
symptoms; the seventh assesses functioning; and, the eighth criterion clarifies
symptoms as not attributable to a substance or co-occurring medical condition.
Two specifications are noted including delayed expression and a dissociative subtype
of PTSD, the latter of which is new to DSM-5. In both specifications, the full
diagnostic criteria for PTSD must be met for application to be warranted.

Criterion A: stressor
The person was exposed to: death, threatened death, actual or threatened
serious injury, or actual or threatened sexual violence, as follows: (one required)
1.

Direct exposure.

2.

Witnessing, in person.

3.

Indirectly, by learning that a close relative or close friend was exposed to trauma. If the event
involved actual or threatened death, it must have been violent or accidental.

4.

Repeated or extreme indirect exposure to aversive details of the event(s), usually in the course of
professional duties (e.g., first responders, collecting body parts; professionals repeatedly exposed
to details of child abuse). This does not include indirect non-professional exposure through
electronic media, television, movies, or pictures.

Criterion B: intrusion symptoms

The traumatic event is persistently re-experienced in the following way(s): (one


required)
1.

Recurrent, involuntary, and intrusive memories. Note: Children older than six may express this
symptom in repetitive play.

2.

Traumatic nightmares. Note: Children may have frightening dreams without content related to the
trauma(s).

3.

Dissociative reactions (e.g., flashbacks) which may occur on a continuum from brief episodes to
complete loss of consciousness. Note: Children may reenact the event in play.

4.

Intense or prolonged distress after exposure to traumatic reminders.

5.

Marked physiologic reactivity after exposure to trauma-related stimuli.

Criterion C: avoidance
Persistent effortful avoidance of distressing trauma-related stimuli after the event:
(one required)
1.

Trauma-related thoughts or feelings.

2.

Trauma-related external reminders (e.g., people, places, conversations, activities, objects, or


situations).

Criterion D: negative alterations in cognitions and mood


Negative alterations in cognitions and mood that began or worsened after the
traumatic event: (two required)
1.

Inability to recall key features of the traumatic event (usually dissociative amnesia; not due to
head injury, alcohol, or drugs).

2.

Persistent (and often distorted) negative beliefs and expectations about oneself or the world (e.g.,
"I am bad," "The world is completely dangerous").

3.

Persistent distorted blame of self or others for causing the traumatic event or for resulting
consequences.

4.

Persistent negative trauma-related emotions (e.g., fear, horror, anger, guilt, or shame).

5.

Markedly diminished interest in (pre-traumatic) significant activities.

6.

Feeling alienated from others (e.g., detachment or estrangement).

7.

Constricted affect: persistent inability to experience positive emotions.

Criterion E: alterations in arousal and reactivity


Trauma-related alterations in arousal and reactivity that began or worsened after
the traumatic event: (two required)
1.

Irritable or aggressive behavior

2.

Self-destructive or reckless behavior

3.

Hypervigilance

4.

Exaggerated startle response

5.

Problems in concentration

6.

Sleep disturbance

Criterion F: duration
Persistence of symptoms (in Criteria B, C, D, and E) for more than one month.

Criterion G: functional significance


Significant symptom-related distress or functional impairment (e.g., social,
occupational).

Criterion H: exclusion
Disturbance is not due to medication, substance use, or other illness.
Specify if:

With dissociative symptoms.

In addition to meeting criteria for diagnosis, an individual experiences high levels


of either of the following in reaction to trauma-related stimuli:
1.

Depersonalization: experience of being an outside observer of or detached from oneself (e.g.,


feeling as if "this is not happening to me" or one were in a dream).

2.

Derealization: experience of unreality, distance, or distortion (e.g., "things are not real").

Specify if:

With delayed expression.

Full diagnosis is not met until at least six months after the trauma(s), although
onset of symptoms may occur immediately.

References
1.

American Psychiatric Association. (2013) Diagnostic and statistical manual of mental disorders,
(5th ed.). Washington, DC: Author.

Dissociative Subtype of PTSD

Ruth Lanius, MD, PhD, Mark Miller, PhD, Erika Wolf, PhD, Bethany Brand, PhD,
Paul Frewen, PhD, Eric Vermetten, MD, PhD, & David Spiegel, MD
The role of dissociation as the most direct defense against overwhelming
traumatic experience was first documented in the seminal work of Pierre Janet.
Recent research evaluating the relationship between Posttraumatic Stress
Disorder (PTSD) and dissociation has suggested that there is a dissociative
subtype of PTSD, defined primarily by symptoms of derealization (i.e., feeling as
if the world is not real) and depersonalization (i.e., feeling as if oneself is not
real). Confrontation with overwhelming experience from which actual escape is
not possible, such as childhood abuse, torture, as well as war trauma challenges
the individual to find an escape from the external environment as well as their
internal distress and arousal when no escape is possible. States of
depersonalization and derealization provide striking examples of how
consciousness can be altered to accommodate overwhelming experience that
allows the person to continue functioning under fierce conditions.

An out-of-body or depersonalization experience during which individuals often see themselves


observing their own body from above has the capacity to create the perception that this is not
happening to me and is typically accompanied by an attenuation of the emotional experience.

Similarly, states of derealization during which individuals experience that things are not real; it is
just a dream create the perception that this is not really happening to me and are often associated
with the experience of decreased emotional intensity.

The addition of a dissociative subtype to the PTSD diagnosis is expected to


further advance research examining the etiology, epidemiology, neurobiology,
and treatment response of this subtype and facilitate the search for biomarkers of
PTSD.

Rationale
The recognition of a dissociative subtype of PTSD as part of the DSM-5 PTSD
diagnosis was based on three converging lines of research: (1) symptom
assessments, (2) treatment outcomes, and (3) psychobiological studies. Even
though dissociative symptoms such as flashbacks and psychogenic amnesia are
included as part of the core PTSD symptoms, evidence suggests that a subgroup
of PTSD patients exhibits additional symptoms of dissociation, including
depersonalization and derealization, thus warranting a subtype of PTSD
specifically focusing on these two symptoms. Recognizing a dissociative subtype

of PTSD has the potential to improve the assessment and treatment outcome of
PTSD.

Evidence
The addition of a dissociative subtype of PTSD in the upcoming DSM-5 was
based on three lines of evidence:
1.

Several studies using latent class, taxometric, epidemiological, and confirmatory factor analyses
conducted on PTSD symptom endorsements collected from Veteran and civilian PTSD samples
indicated that a subgroup of individuals (roughly 15 - 30%) suffering from PTSD reported symptoms
of depersonalization and derealization (1-3). Individuals with the dissociative subtype were more
likely: to be male, have experienced repeated traumatization and early adverse experiences, have
comorbid psychiatric disorders, and evidenced greater suicidality and functional impairment (4). The
subtype also replicated cross-culturally.

2.

Neurobiological evidence suggests depersonalization and derealization responses in PTSD are


distinct from re-experiencing/hyperarousal reactivity. Individuals who re-experienced their traumatic
memory and showed concomitant psychophysiological hyperarousal exhibited reduced activation in
the medial prefrontal- and the rostral anterior cingulate cortex and increased amygdala reactivity.
Reliving responses are, therefore, thought to be mediated by failure of prefrontal inhibition or topdown control of limbic regions. In contrast, the group who exhibited symptoms of depersonalization
and derealization showed increased activation in the rostral anterior cingulate cortex and the medial
prefrontal cortex. Depersonalization/derealization responses are suggested to be mediated by
midline prefrontal inhibition of the limbic regions (5,6).

3.

Early evidence suggests that symptoms of depersonalization and derealization in PTSD are
relevant to treatment decisions in PTSD (reviewed in Lanius et al., 2012;5). Individuals with PTSD
who exhibited symptoms of depersonalization and derealization tended to respond better to
treatments that included cognitive restructuring and skills training in affective and interpersonal
regulation in addition to exposure-based therapies (7,8). Additional research is needed to more fully
evaluate the effects of depersonalization and derealization on treatment response.

Assessment
The Clinician-Administered PTSD Scale (CAPS) includes items assessing
depersonalization ("Have there been times when you felt as if you were outside
of your body, watching yourself as if you were another person?") and
derealization ("Have there been times when things going on around you seemed
unreal or very strange and unfamiliar?"). In addition, there are several self-report
rating scales that assess dissociative symptomatology. These include the

Dissociative Experiences Scale, the Multiscale Dissociation Inventory, the


Traumatic Dissociation Scale, and the Stanford Acute Stress Reaction
Questionnaire. Additional interviews and scales specific to the dissociative
subtype are currently under development.

Associated features and risks of the dissociative subtype


As compared to individuals with PTSD alone, patients with a diagnosis of the
dissociative subtype of PTSD showed:

Repeated traumatization and early adverse experience prior to onset of PTSD

Increased psychiatric comorbidity, in particular specific phobia and borderline and avoidant
personality disorders among women, but not men

Increased functional impairment

Increased suicidality (including suicidal ideation, plans, and attempts)

Treatment concerns
Treatment studies specifically designed to examine clinical outcomes of
psychological and pharmacological treatment of PTSD in those with versus
without the dissociative subtype are needed. However, we do know that
individuals with dissociative PTSD may require treatments designed to directly
reduce depersonalization and derealization. For such individuals, exposure
treatment can lead to further dissociation and inhibition of affective response,
rather than the goal of cognitive behavioural/exposure therapy, which is
desensitization and cognitive restructuring.
There is preliminary evidence that relative to exposure-based therapies alone,
individuals with PTSD who exhibited symptoms of depersonalization and
derealization responded better to treatments that also included cognitive
restructuring and skills training in affective and interpersonal regulation (5,7,8).
Author Note: Dr. Ruth Lanius is a Professor of Psychiatry at Western University of
Canada; Drs. Mark Miller and Erika Wolf are Psychologists at the National Center
for PTSD at VA Boston Healthcare System; Dr. Bethany Brand is a Professor of
Psychology at Towson University; Dr. Paul Frewen is an Assistant Professor of
Psychiatry at Western University of Canada; Dr. Eric Vermetten is the Head of
Research Military Mental Health, Department of Psychiatry, University Medical
Center and Rudolf Magnus Institute of Neuroscience in Utrecht; Dr. David
Spiegel is Professor of Psychiatry at Stanford University.

References

1.

Steuwe, C., Lanius, R. A., & Frewen, P. A. (2012). The role of dissociation in civilian posttraumatic
stress disorder: Evidence for a dissociative subtype by latent class and confirmatory factor
analysis. Depression and Anxiety, 29,689-700. doi: 10.1002/da.21944

2.

Wolf, E. J., Lunney, C. A., Miller, M. W., Resick, P. A., Friedman, M. J., & Schnurr, P. P. (2012).
The dissociative subtype of PTSD: A replication and extension. Depression and Anxiety, 29, 679688. doi: 10.1002/da.21946

3.

Wolf, E. J., Miller, M. W., Reardon, A. F., Ryabchenko, K. A., Castillo, D., & Freund, R. (2012). A
latent class analysis of dissociation and posttraumatic stress disorder: Evidence for a dissociative
subtype. [Research Support, N.I.H., Extramural Research Support, U.S. Gov't, NonP.H.S.]. Archives of General Psychiatry, 69, 698-705. doi: 10.1001/archgenpsychiatry.2011.1574

4.

Stein, D. J., Koenen, K. C., Friedman, M. J., Hill, E., McLaughlin, K. A., Petukhova, M., Ruscio, A.
M., Shahly, C., Spiegel, D., Borges, G., Bunting, B., Calsa-de-Almeida, J. M., de Girolamo, G.,
Demyttenaere, K., Florescu, S., Haro, J. M., Karam, E. G., Kovess-Masfety, V., Lee, S., Matshinger,
H., Mladenova, M., Posada-Villa, J., Tachimori, H., Viana, M. C., & Kessler, R. C.
(2013). Dissociation in posttraumatic stress disorder: Evidence from the world mental health
surveys., 73, 302-312. doi: 10.1016/j.biopsych.2012.08.022

5.

Lanius, R. A., Brand, B., Vermetten, E., Frewen, P. A., & Spiegel, D. (2012). The dissociative
subtype of posttraumatic stress disorder: rationale, clinical and neurobiological evidence, and
implications. Depression and Anxiety, 29, 1-8. doi: 10.1002/da.21889

6.

Lanius, R. A., Vermetten, E., Loewenstein, R. J., Brand, B., Schmahl, C., Bremner, J. D., &
Spiegel, D. (2010). Emotion modulation in PTSD: Clinical and neurobiological evidence for a
dissociative subtype. American Journal of Psychiatry, 167, 640-647. doi:
10.1176/appi.ajp.2009.09081168

7.

Cloitre, M., Petkova, E., Wang, J., & Lu Lassell, F. (2012). An examination of the influence of a
sequential treatment on the course and impact of dissociation among women with PTSD related to
childhood abuse.Depression and Anxiety, 29, 709-717. doi: 10.1002/da.21920

8.

Resick, P. A., Suvak, M. K., Johnides, B. D., Mitchell, K. S., & Iverson, K. M. (2012). The impact of
dissociation on PTSD treatment with cognitive processing therapy. Depression and Anxiety,
29, 718-730. doi: 10.1002/da.21938

PTSD for Children 6 Years and Younger

Michael Scheeringa, MD
A challenge for the Diagnostic and Statistical Manual (DSM) taxonomy has
always been to consider developmental differences in the expressions of
disorders in different age groups. Research has suggested that individuals of
different ages may express features of the same criteria somewhat differently.
Furthermore, there may be sufficient differences in the expressions of some
disorders to justify an age-related subtype of the disorder. This is important to
consider particularly in Posttraumatic Stress Disorder (PTSD) because, although
PTSD has been widely reported in children and adolescents, the DSM-IV criteria
were developed before substantial numbers of studies had been conducted on
young children (1).
The Fifth Edition of the DSM (DSM-5) includes a new developmental subtype of
PTSD called Posttraumatic Stress Disorder in preschool children. As the first
developmental subtype of an existing disorder, this represents a significant step
for the DSM taxonomy. Since an alternative diagnostic set of criteria was initially
proposed by Michael Scheeringa and Charles Zeanah (2), the criteria have been
refined empirically (3,4), and endorsed by a task force of experts on early
childhood mental health (5). While the bulk of the empirical research that
supports this disorder was conducted on three- to six-year-old preschool
children, the studies often included one- to two-year-old toddlers. These studies
showed that when a developmentally-sensitive set of criteria were used
approximately three to eight times more children qualified for the diagnosis
compared to the DSM-IV (3,6).

What types of trauma do young children experience?


Young children are exposed to many types of traumatic experiences, placing
them at risk for PTSD. These include:

Abuse (7)

Witnessing interpersonal violence (8)

Motor vehicle accidents (9)

Experiences of natural disasters (10)

Conditions of war (11)

Dog bites

Invasive medical procedures (12)

How is the diagnosis different in preschool PTSD?


Because young children have emerging abstract cognitive and verbal expression
capacities, research has shown that the criteria need to be more behaviorally
anchored and developmentally sensitive to detect PTSD in preschool children
(2,13).
Immediate reaction to traumatic event criterion
The criterion that the children's reactions at the time of the traumatic events
showed extreme distress has been deleted. If children were too young to
verbalize their acute reactions to traumatic experiences, and there were no
adults present to witness their reactions, there was no feasible way to know
about these reactions. This criterion, which has been shown to lack predictive
validity for both adult (14) and preschool populations (6), has also been deleted
for the regular PTSD criteria in DSM-5.
Intrusion symptoms
The change to the re-experiencing symptoms is a relatively minor change in
wording to increase face validity and, thereby, lower the symptom detection
threshold. The old symptom of "recurrent and intrusive distressing recollections
of the event ..." required three conditions: (1) recurrent, (2) intrusive, and (3)
distressing. Research showed empirically that preschool children do not always
manifest overt distress with their intrusive, unwanted thoughts. Some children
were neutral or "over bright" (2,13). While distressed reactions are common,
parents also commonly reported no affect or what appeared to be excitement (6).
Furthermore, there were no differences in PTSD severity for those with overtly
distressing recollections compared to those who showed other emotions with
their recollections.
Avoidance symptoms and negative alterations in cognitions and mood
Because many of the avoidance and negative cognition symptoms are highly
internalized phenomena, the most significant changes in the criteria for preschool
children are in this section.

The major change was to require only one symptom in either the avoidance
symptoms or negative alterations in cognitions and mood, instead of the DSM-IV
threshold of three symptoms. The number of these symptoms that are possible to
detect is simply fewer compared to adults. The symptoms of "loss of interests,"
"restricted range of affect," "detachment from loved ones," and "avoidance of
thoughts or feelings related to the trauma" manifest in young children but are
consistently ranked as some of the least frequent among the PTSD symptoms
(15). The symptoms of "sense of a foreshortened future" and "inability to recall an
important aspect of the event" were deleted because of the developmental
challenges in manifesting and/or detecting them.
The wording of two symptoms was modified to enhance face validity and
symptom detection. Diminished interest in significant activities may manifest as
constricted play. Feelings of detachment or estrangement may be manifest more
behaviorally as social withdrawal.
Increased arousal symptoms
Being the most behavioral and observable types of symptoms, few changes
seem to be needed for these problems. The symptoms "irritability or outbursts of
anger" was modified to include "extreme temper tantrums" to enhance face
validity.

Validation of preschool PTSD


Evidence supports the criterion, convergent, discriminant, and predictive
validities of the preschool PTSD criteria (reviewed in Scheeringa et al., 2011;6).
Perhaps most convincingly, even when the threshold for the avoidance and
numbing criterion was lowered from three symptoms to one symptom, the
diagnosed cases were still highly symptomatic, with means of 6 to 10 symptoms
across studies. Marked functional impairment across a range of domains has
also been documented. Prospective longitudinal studies have also documented
the longer-term stability of diagnoses and impairment over time (9,16,17).

Assessment and treatment for preschool PTSD

Standardized screening and assessment instruments have been developed for


caregivers of this age group, with both self-administered checklists and
diagnostic interviews (reviewed in 18).
Evidence-based treatments for PTSD, such as cognitive behavioral therapy, are
effective (7,19,20). A long-term, relationally-based treatment has shown
effectiveness following interpersonal violence (8). Play therapy, eye movement
desensitization and reprocessing (EMDR), and other modalities may be effective
if the traumatic memories can be engaged in developmentally-appropriate
methods.
Author Note:

Dr. Michael Scheeringa is the Remigio Gonzalez, MD Professor of


Child Psychiatry, Tulane University School of Medicine, New Orleans, LA.

References
1.

Kilpatrick, D., Resnick, H., Freedy, J., Pelcovitz, D., Resick, P., Roth, S., & van der Kolk, B.
(1998). Posttraumatic Stress Disorder Field Trial: Evaluation of the PTSD construct - criteria A
through E. In T. Widiger, A. Frances, H. Pincus, R. Ross, M. First, W. Davis & M. Kline (Eds.), DSMIV Sourcebook(Vol. 4, pp. 803-844). Washington, DC: American Psychiatric Association.

2.

Scheeringa, M. S., Zeanah, C. H., Drell, M. J., & Larrieu, J. A. (1995). Two approaches to the
diagnosis of posttraumatic stress disorder in infancy and early childhood. Journal of the American
Academy of Child and Adolescent Psychiatry, 34 (2), 191-200. doi: 10.1097/00004583-19950200000014

3.

Scheeringa, M. S., Myers, L., Putnam, F. W., & Zeanah, C. H. (2012). Diagnosing PTSD in early
childhood: an empirical assessment of four approaches. Journal of Traumatic Stress, 25 (4), 359367.

4.

Scheeringa, M. S., Zeanah, C. H., Myers, L., & Putnam, F. W. (2003). New findings on alternative
criteria for PTSD in preschool children. Journal of the American Academy of Child and Adolescent
Psychiatry, 42 (5), 561-570. doi: 10.1097/01.CHI.0000046822.95464.14.

5.

Task Force on Research Diagnostic Criteria: Infancy and Preschool. (2003). Research diagnostic
criteria for infants and preschool children: The process and empirical support. Journal of the
American Academy of Child and Adolescent Psychiatry, 42, 1504-1512.

6.

Scheeringa, M. S., Zeanah, C. H., & Cohen, J. A. (2011). PTSD in children and adolescents:
Towards an empirically based algorithm. Depression and Anxiety, 28 (9), 770-782.
10.1002/da.20736.

7.

Cohen, J., & Mannarino, A. (1996). A treatment outcome study for sexually abused preschool
children: Initial findings. Journal of the American Academy of Child and Adolescent Psychiatry,
35, 42-50.

8.

Lieberman, A., Ippen, C., & Van Horn, P. (2006). Child-parent psychotherapy: 6-month follow-up
of a randomized controlled trial. Journal of the American Academy of Child and Adolescent
Psychiatry, 45 (8), 913-918. doi: 10.1097/01.chi.0000222784.03735.92

9.

Meiser-Stedman, R., Smith, P., Glucksman, E., Yule, W., & Dalgleish, T. (2008). The
posttraumatic stress disorder diagnosis in preschool- and elementary school-age children exposed
to motor vehicle accidents.American Journal of Psychiatry, 165 (10), 1326-1337. doi:
10.1176/appi.ajp.2008.07081282

10.

Scheeringa, M. S., & Zeanah, C. H. (2008). Reconsideration of harm's way: Onsets and
comorbidity patterns in preschool children and their caregivers following Hurricane Katrina. Journal
of Clinical Child and Adolescent Psychology, 37 (3), 508-518.

11.

Laor, N., Wolmer, L., Mayes, L. C., Golomb, A., Silverberg, D. S., Weizman, R., & Cohen, D. J.
(1996). Israeli preschoolers under Scud missile attacks.Archives of General Psychiatry, 53, 416423.

12.

De Young, A. C., Kenardy, J. A., & Cobham, V. E. (2011). Diagnosis of posttraumatic stress
disorder in preschool children. Journal of Clinical Child and Adolescent Psychology, 40 (3), 375384. doi: 10.1080/15374416.2011.563474

13.

Scheeringa, M. S., Peebles, C. D., Cook, C. A., & Zeanah, C. H. (2001). Toward establishing
procedural, criterion, and discriminant validity for PTSD in early childhood. Journal of the American
Academy of Child and Adolescent Psychiatry, 40 (1), 52-60. doi: 10.1097/00004583-20010100000016

14.

Friedman, M. J., Resick, P. A., Bryant, R. A., & Brewin, C. R. (2011). Considering PTSD for DSM5. Depression and Anxiety, 28 (9), 750-769.

15.

Scheeringa, M. S. (2006). Posttraumatic stress disorder: Clinical guidelines and research


findings. In J. L. Luby (Ed.), Handbook of Preschool Mental Health: Development, Disorders, and
Treatment (pp. 165-185). New York: The Guilford Press.

16.

Ohmi, H., Kojima, S., Awai, Y., Kamata, S., Sasaki, K., Tanaka, Y., . . . Hata, A. (2002). Posttraumatic stress disorder in pre-school aged children after a gas explosion. European Journal of
Pediatrics, 161, 643-648.

17.

Scheeringa, M., Zeanah, C., Myers, L., & Putnam, F. (2005). Predictive validity in a prospective
follow-up of PTSD in preschool children. Journal of the American Academy of Child and Adolescent
Psychiatry, 44 (9), 899-906. doi: 10.1097/01.chi.0000169013.81536.71

18.

De Young, A. C., Drury, S.S., Scheeringa, M.S. (in press). Assessing trauma-related symptoms
during early childhood. In R Del Carmen-Wiggins, A Carter (Eds.), Handbook of Infant, Toddler, and
Preschool Mental Health Assessment, 2nd edition. New York, NY: Oxford University Press.

19.

Deblinger, E., Stauffer, L., & Steer, R. (2001). Comparative efficacies of supportive and cognitive
behavioral group therapies for young children who have been sexually abused and their
nonoffending mothers. Child Maltreatment, 6, 332-343.

20.

Scheeringa, M. S., Weems, C. F., Cohen, J. A., Amaya-Jackson, L., & Guthrie, D. (2011). Traumafocused cognitive-behavioral therapy for posttraumatic stress disorder in three through six year-old
children: A randomized clinical trial. Journal of Child Psychology and Psychiatry, 52 (8), 853-860.

DSM-5 Diagnostic Criteria for PTSD Released


The Diagnostic and Statistical Manual of Mental Disorders provides standard criteria and
common language for the classification of mental disorders. It is published by the
American Psychiatric Association. The fifth revision (DSM-5) was released in
May 2013. This revision includes changes to the diagnostic criteria for PTSD and
Acute Stress Disorder.
The reason the PTSD diagnostic criteria were revised is to take into account
things we have learned from scientific research and clinical experience.

What are the major revisions to the PTSD diagnosis?


Classification
PTSD (as well as Acute Stress Disorder) moved from the class of anxiety
disorders into a new class of "trauma and stressor-related disorders." All of the
conditions included in this classification require exposure to a traumatic or
stressful event as a diagnostic criterion. The rationale for the creation of this new
class is based upon clinical recognition of variable expressions of distress as a
result of traumatic experience. The necessary criteria of exposure to trauma links
the conditions included in this class; the homogeneous expression of anxiety or
fear-based symptoms, anhedonic and dysphoric symptoms, externalizing anger

or aggressive symptoms, dissociative symptoms, or some combination of those


listed differentiates the diagnoses within the class (1).
Diagnostic criteria
Overall, the symptoms of PTSD are mostly the same in DSM-5 as compared to
DSM-IV. A few key alterations include:

The three clusters of DSM-IV symptoms are divided into four clusters in DSM-5: intrusion,
avoidance, negative alterations in cognitions and mood, and alterations in arousal and reactivity.
DSM-IV Criterion C, avoidance and numbing, was separated into two criteria: Criteria C (avoidance)
and Criteria D (negative alterations in cognitions and mood). The rationale for this change was
based upon factor analytic studies, and now requires at least one avoidance symptom for PTSD
diagnosis.

Three new symptoms were added:

Criteria D (negative alterations in cognitions and mood): persistent and distorted blame of
self or others, and persistent negative emotional state

Criteria E (alterations in arousal and reactivity): reckless or destructive behavior

Other symptoms were revised to clarify symptom expression.

Criterion A2 (requiring fear, helplessness, or horror happen right after the trauma) was removed in
DSM-5. Research suggests that Criterion A2 did not improve diagnostic accuracy (2).

A clinical subtype "with dissociative symptoms" was added. The dissociative subtype is applicable
to individuals who meet the criteria for PTSD and experience additional depersonalization and
derealization symptoms (3).

Separate diagnostic criteria are included for children ages 6 years or younger(preschool subtype)
(4).

What are the implications of these revisions?


Assessment
PTSD assessment measures, such as the PC-PTSD, CAPS, and PCL, are being
revised by the National Center for PTSD to be made available upon validation of
the instruments. Please see our Assessments section for more information.

Prevalence rates
Based on initial analyses of the DSM-5 criteria, the prevalence of PTSD will be
similar to what it is currently in DSM-IV (5,6). Research also suggests that
similarly to DSM-IV, prevalence of PTSD for DSM-5 was higher among women
than men, and prevalence increased with multiple traumatic event exposure (6).
National estimates of PTSD prevalence suggest that DSM-5 rates were slightly
lower than DSM-IV (6). Discordant findings in diagnostic prevalence were
attributable to three major changes in the DSM-5 criteria for PTSD:

The revision of Criterion A1 in DSM-5 narrowed qualifying traumatic events such that the
unexpected death of family or a close friend due to natural causes is no longer included. Research
suggests this is the greatest contributor (>50%) to discrepancy for meeting DSM-IV but not DSM-5
PTSD criteria.

Splitting DSM-IV Criterion C into two criteria in DSM-5 now requires that a PTSD diagnosis must
include at least one avoidance symptom.

Criterion A2, response to traumatic event involved intense fear, hopelessness, or horror, was
removed from DSM-5.

to be informed when the new criteria and


assessment measures are officially released.
Sign up for the PTSD Monthly Update

The APA summary of changes to the PTSD diagnosis can be accessed


here: Posttraumatic Stress Disorder (PDF).*

Sources
1.

American Psychiatric Association. (2013). Diagnostic and statistical manual of mental


disorders. (5th ed.). Washington, DC: Author.

2.

Friedman, Matthew J; Resick, Patricia A; Bryant, Richard A; Brewin, Chris R (Sep 2011).
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subtype of posttraumatic stress disorder: Rationale, clinical and neurobiological evidence, and
implications. Depression and Anxiety, 29, 701-708. doi: 10.1002/da.21889

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Scheeringa, M. S., Zeanah, C. H., & Cohen, J. A. (2011). PTSD in children and adolescents:
toward an empirically based algorithm. Depression and Anxiety, 28, 770-782. doi:10.1002/da20736

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Miller, Mark W; Wolf, Erika Jane; Kilpatrick, Dean G; Resnick, Heidi S; Marx, Brian P; et al. (Sep
3, 2012). The prevalence and latent structure of proposed DSM-5 posttraumatic stress disorder
symptoms in U.S. national and veteran samples. Psychological Trauma: Theory, Research,
Practice, and Policy. http://www.ptsd.va.gov/professional/articles/article-pdf/id39382.pdf

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Kilpatrick, D., Resnick, H. S., Milanak, M. E., Miller, M. W., Keyes, K. M., & Friedman, M. J.
(2013). National Estimates of Exposure to Traumatic Events and PTSD Prevalence Using DSM-IV
and Proposed DSM-5 Criteria[Manuscript submitted for publication].

PTSD History and Overview


Matthew J. Friedman, MD, PhD

A brief history of the PTSD diagnosis


The risk of exposure to trauma has been a part of the human condition since we
evolved as a species. Attacks by saber tooth tigers or twenty-first century
terrorists have probably produced similar psychological sequelae in the survivors
of such violence. Shakespeare's Henry IV appears to meet many, if not all, of the
diagnostic criteria for Posttraumatic Stress Disorder (PTSD), as have other
heroes and heroines throughout the world's literature. The history of the
development of the PTSD concept is described by Trimble (1).
In 1980, the American Psychiatric Association (APA) added PTSD to the third
edition of its Diagnostic and Statistical Manual of Mental Disorders (DSM-III)
nosologic classification scheme (2). Although controversial when first introduced,
the PTSD diagnosis has filled an important gap in psychiatric theory and practice.
From an historical perspective, the significant change ushered in by the PTSD
concept was the stipulation that the etiological agent was outside the individual
(i.e., a traumatic event) rather than an inherent individual weakness (i.e., a
traumatic neurosis). The key to understanding the scientific basis and clinical
expression of PTSD is the concept of "trauma."

Importance of traumatic events


In its initial DSM-III formulation, a traumatic event was conceptualized as a
catastrophic stressor that was outside the range of usual human experience. The
framers of the original PTSD diagnosis had in mind events such as war, torture,
rape, the Nazi Holocaust, the atomic bombings of Hiroshima and Nagasaki,
natural disasters (such as earthquakes, hurricanes, and volcano eruptions), and
human-made disasters (such as factory explosions, airplane crashes, and
automobile accidents). They considered traumatic events to be clearly different
from the very painful stressors that constitute the normal vicissitudes of life such
as divorce, failure, rejection, serious illness, financial reverses, and the like. (By
this logic, adverse psychological responses to such "ordinary stressors" would, in
DSM-III terms, be characterized as Adjustment Disorders rather than PTSD.)
This dichotomization between traumatic and other stressors was based on the
assumption that, although most individuals have the ability to cope with ordinary
stress, their adaptive capacities are likely to be overwhelmed when confronted by
a traumatic stressor.
PTSD is unique among psychiatric diagnoses because of the great importance
placed upon the etiological agent, the traumatic stressor. In fact, one cannot
make a PTSD diagnosis unless the patient has actually met the "stressor
criterion," which means that he or she has been exposed to an event that is
considered traumatic. Clinical experience with the PTSD diagnosis has shown,
however, that there are individual differences regarding the capacity to cope with
catastrophic stress. Therefore, while most people exposed to traumatic events do
not develop PTSD, others go on to develop the full-blown syndrome. Such
observations have prompted the recognition that trauma, like pain, is not an
external phenomenon that can be completely objectified. Like pain, the traumatic
experience is filtered through cognitive and emotional processes before it can be
appraised as an extreme threat. Because of individual differences in this
appraisal process, different people appear to have different trauma thresholds,
some more protected from and some more vulnerable to developing clinical
symptoms after exposure to extremely stressful situations. Although there is
currently a renewed interest in subjective aspects of traumatic exposure, it must
be emphasized that events such as rape, torture, genocide, and severe war zone
stress are experienced as traumatic events by nearly everyone.

Revisions to PTSD diagnostic criteria


The DSM-III diagnostic criteria for PTSD were revised in DSM-III-R (1987), DSMIV (1994), and DSM-IV-TR (2000) (2-5). A very similar syndrome is classified in
ICD-10 (The ICD-10 Classification of Mental and Behavioural Disorders: Clinical
Descriptions and Diagnostic Guidelines) (6). One important finding, which was
not apparent when PTSD was first proposed as a diagnosis in 1980, is that it is
relatively common. Recent data from the National Comorbidity Survey
Replication indicates lifetime PTSD prevalence rates are 3.6% and 9.7%
respectively among American men and women (7). Rates of PTSD are much
higher in post-conflict settings such as Algeria (37%), Cambodia (28%), Ethiopia
(16%), and Gaza (18%) (8).
DSM-IV Diagnostic criteria for PTSD included a history of exposure to a
traumatic event and symptoms from each of three symptom clusters: intrusive
recollections, avoidant/numbing symptoms, and hyper-arousal symptoms. A fifth
criterion concerned duration of symptoms; and, a sixth criterion stipulated that
PTSD symptoms must cause significant distress or functional impairment.
The latest revision, the DSM-5 (2013), has made a number of notable evidencebased revisions to PTSD diagnostic criteria, with both important conceptual and
clinical implications (9). First, because it has become apparent that PTSD is not
just a fear-based anxiety disorder (as explicated in both DSM-III and DSMIV),PTSD in DSM-5 has expanded to include anhedonic/dysphoric presentations,
which are most prominent. Such presentations are marked by negative
cognitions and mood states as well as disruptive (e.g. angry, impulsive, reckless
and self-destructive) behavioral symptoms. Furthermore, as a result of researchbased changes to the diagnosis, PTSD is no longer categorized as an Anxiety
Disorder. PTSD is now classified in a new category, Trauma- and StressorRelated Disorders, in which the onset of every disorder has been preceded by
exposure to a traumatic or otherwise adverse environmental event. Other
changes in diagnostic criteria will be described below.

DSM-5 Criteria for PTSD diagnosis


As noted above, the "A" stressor criterion specifies that a person has been exposed
to a catastrophic event involving actual or threatened death or injury, or a threat

to the physical integrity of him/herself or others (such as sexual violence).


Indirect exposure includes learning about the violent or accidental death or
perpetration of sexual violence to a loved one. Exposure through electronic
media (e.g. televised images the 9/11 attacks on the World Trade Center) is not
considered a traumatic event. On the other hand, repeated, indirect exposure
(usually as part of one's professional responsibilities) to the gruesome and
horrific consequences of a traumatic event (e.g. police personnel, body handlers,
etc.) is considered traumatic.
Before describing the B-E symptom clusters, it is important to understand that
one new feature of DSM-5 is that all of these symptoms must have had their
onset or been significantly exacerbated after exposure to the traumatic event.
The "B" or intrusive recollection criterion includes symptoms that are perhaps the most
distinctive and readily identifiable symptoms of PTSD. For individuals with PTSD,
the traumatic event remains, sometimes for decades or a lifetime, a dominating
psychological experience that retains its power to evoke panic, terror, dread,
grief, or despair. These emotions manifest during intrusive daytime images of the
event, traumatic nightmares, and vivid reenactments known as PTSD flashbacks
(which are dissociative episodes). Furthermore, trauma-related stimuli that trigger
recollections of the original event have the power to evoke mental images,
emotional responses, and physiological reactions associated with the trauma.
Researchers can use this phenomenon to reproduce PTSD symptoms in the
laboratory by exposing affected individuals to auditory or visual trauma-related
stimuli (10).
The "C" or avoidance criterion consists of behavioral strategies PTSD patients use in
an attempt to reduce the likelihood that they will expose themselves to traumarelated stimuli. PTSD patients also use these strategies in an attempt to minimize
the intensity of their psychological response if they are exposed to such stimuli.
Behavioral strategies include avoiding any thought or situation which is likely to
elicit distressing traumatic memories. In its extreme manifestation, avoidance
behavior may superficially resemble agoraphobia because the PTSD individual is
afraid to leave the house for fear of confronting reminders of the traumatic
event(s).

Symptoms included in the "D" or negative cognitions and mood criterionreflect persistent
alterations in beliefs or mood that have developed after exposure to the traumatic
event. People with PTSD often have erroneous cognitions about the causes or
consequences of the traumatic event which leads them to blame themselves or
others. A related erroneous appraisal is the common belief that one is
inadequate, weak, or permanently changed for the worse since exposure to the
traumatic event or that one's expectations about the future have been
permanently altered because of the event (e.g., "nothing good can happen to
me," "nobody can be trusted," "the world is entirely dangerous," "people will
always try to control me"). In addition to negative appraisals about past, present
and future, people with PTSD have a wide variety of negative emotional states
such as anger, guilt, or shame. Dissociative psychogenic amnesia is included in
this symptom cluster and involves cutting off the conscious experience of traumabased memories and feelings. Other symptoms include diminished interest in
significant activities and feeling detached or estranged from others. Finally,
although individuals with PTSD suffer from persistent negative emotions, they
are unable to experience positive feelings such as love, pleasure or enjoyment.
Such constricted affect makes it extremely difficult to sustain a close marital or
otherwise meaningful interpersonal relationship.
Symptoms included in the "E" or alterations in arousal or reactivity criterion most closely
resemble those seen in panic and generalized anxiety disorders. While
symptoms such as insomnia and cognitive impairment are generic anxiety
symptoms, hypervigilance and startle are more characteristic of PTSD. The
hypervigilance in PTSD may sometimes become so intense as to appear like
frank paranoia. The startle response has a unique neurobiological substrate and
may actually be the most pathognomonic PTSD symptom. DSM-IV's Criterion
D2, irritability or outbursts of anger, has been separated into emotional (e.g., D4)
and behavioral (e.g., E1) components in DSM-5. Irritable and angry outbursts
may sometimes be expressed as aggressive behavior. Finally reckless and selfdestructive behavior such as impulsive acts, unsafe sex, reckless driving and
suicidal behavior are newly included in DSM-5, as Criterion E2.
The "F" or duration criterion specifies that symptoms must persist for at least one
month before PTSD may be diagnosed.

The "G" or functional significance criterion specifies that the survivor must experience
significant social, occupational, or other distress as a result of these symptoms.
The "H" or exclusion criterion specifies that the symptoms are not due to medication,
substance use, or other illness.

Assessing PTSD
Since 1980, there has been a great deal of attention devoted to the development
of instruments for assessing PTSD. Keane and associates (10), working with
Vietnam war-zone Veterans, first developed both psychometric and
psychophysiological assessment techniques that have proven to be both valid
and reliable. Other investigators have modified such assessment instruments
and used them with natural disaster survivors, rape/incest survivors, and other
traumatized individuals. These assessment techniques have been used in the
epidemiological studies mentioned above and in other research protocols.
Neurobiology
Neurobiological research indicates that PTSD may be associated with stable
neurobiological alterations in both the central and autonomic nervous systems.
Psychophysiological alterations associated with PTSD include hyperarousal of
the sympathetic nervous system, increased sensitivity and augmentation of the
acoustic-startle eye blink reflex, and sleep abnormalities. Neuropharmacological
and neuroendocrine abnormalities have been detected in most brain
mechanisms that have evolved for coping, adaptation, and preservation of the
species. These include the noradrenergic, hypothalamic-pituitary-adrenocortical,
serotonergic, glutamatergic, thyroid, endogenous opioid, and other systems.
Structural brain imaging suggests reduced volume of the hippocampus and
anterior cingulate. Functional brain imaging suggests excessive amygdala
activity and reduced activation of the prefrontal cortex and hippocampus. This
information is reviewed extensively elsewhere (11-12).
Longitudinal expression
Longitudinal research has shown that PTSD can become a chronic psychiatric
disorder and can persist for decades and sometimes for a lifetime. Patients with

chronic PTSD often exhibit a longitudinal course marked by remissions and


relapses. There is also a delayed variant of PTSD in which individuals exposed
to a traumatic event do not exhibit the full PTSD syndrome until months or years
afterward. DSM-IV's "delayed onset" has been changed to "delayed expression"
in DSM-5 to clarify that although full diagnostic criteria may not be met until at
least 6 months after the trauma, the onset and expression of some symptoms
may be immediate. Usually, the prompting precipitant is a situation that
resembles the original trauma in a significant way (for example, a war Veteran
whose child is deployed to a war zone or a rape survivor who is sexually
harassed or assaulted years later).
Co-occurring conditions
If an individual meets diagnostic criteria for PTSD, it is likely that he or she will
meet DSM-5 criteria for one or more additional diagnoses (13). Most often, these
comorbid diagnoses include major affective disorders, dysthymia, alcohol or
substance abuse disorders, anxiety disorders, or personality disorders. There is
a legitimate question whether the high rate of diagnostic comorbidity seen with
PTSD is an artifact of our current decision-making rules for the PTSD diagnosis
since there are not exclusionary criteria in DSM-5. In any case, high rates of
comorbidity complicate treatment decisions concerning patients with PTSD since
the clinician must decide whether to treat the comorbid disorders concurrently or
sequentially.
Classification and subtypes
PTSD is no longer considered an Anxiety Disorder but has been reclassified as a
Trauma and Stressor-Related Disorder because it has a number of clinical
presentations, as discussed previously. In addition, two new subtypes have been
included in the DSM-5. The Dissociative Subtype includes individuals who meet full
PTSD criteria but also exhibit either depersonalization or derealization (e.g.
alterations in the experience of one's self and the world, respectively).ThePreschool
Subtype applies to children six years old and younger; it has fewer symptoms
(especially in the "D" cluster because it is difficult for young children to report on
their inner thoughts and feelings) and also has lower symptom thresholds to
meet full PTSD criteria.

Questions to consider
Questions that remain about the syndrome itself include: what is the clinical
course of untreated PTSD; are there other subtypes of PTSD; what is the
distinction between traumatic simple phobia and PTSD; and what is the clinical
phenomenology of prolonged and repeated trauma? With regard to the latter,
Herman (14) has argued that the current PTSD formulation fails to characterize
the major symptoms of PTSD commonly seen in victims of prolonged, repeated
interpersonal violence such as domestic or sexual abuse and political torture.
She has proposed an alternative diagnostic formulation, "complex PTSD," that
emphasizes multiple symptoms, excessive somatization, dissociation, changes in
affect, pathological changes in relationships, and pathological changes in identity.
Although this formulation is attractive to clinicians dealing with individuals who
have been repeatedly traumatized, scientific evidence in support of the complex
PTSD formulation is sparse and inconsistent. For this reason, it was not included
in the DSM-5 as subtype of PTSD. It is possible that the Dissociative Subtype,
which has firm scientific support, will prove to be the diagnostic subtype that
incorporates many or all of the symptoms first described by Herman.
PTSD has also been criticized from the perspective of cross-cultural psychology
and medical anthropology, especially with respect to refugees, asylum seekers,
and political torture victims from non-Western regions. Some clinicians and
researchers working with such survivors argue that since PTSD has usually been
diagnosed by clinicians from Western industrialized nations working with patients
from a similar background, the diagnosis does not accurately reflect the clinical
picture of traumatized individuals from non-Western traditional societies and
cultures. It is clear however, that PTSD is a valid diagnosis cross-culturally (15).
On the other hand, there is substantial cross-cultural variation and the expression
of PTSD may be different in different countries and cultural settings, even when
DSM-5 diagnostic criteria are met (16).

Treatment for PTSD


Most effective treatments for PTSD
The many therapeutic approaches offered to PTSD patients are presented in
Foa, Keane, Friedman and Cohen's (2009) comprehensive book on treatment

(17). The most successful interventions are cognitive-behavioral therapy (CBT)


and medication. Excellent results have been obtained with CBT approaches such
as prolonged exposure therapy (PE) and Cognitive Processing Therapy (CPT),
especially with female victims of childhood or adult sexual trauma, military
personnel and Veterans with war-related trauma, and survivors of serious motor
vehicle accidents. Success has also been reported with Eye Movement
Desensitization and Reprocessing (EMDR) and Stress Inoculation Therapy (SIT).
Sertraline (Zoloft) and paroxetine (Paxil) are selective serotonin reuptake
inhibitors (SSRIs) that are the first medications to have received FDA approval as
indicated treatments for PTSD. Other antidepressants are also effective and
promising results have recently been obtained with the alpha-1 adrenergic
antagonist, prazosin (18).
A frequent therapeutic option for mildly to moderately affected PTSD patients is
group therapy, although empirical support for this is sparse. In such a setting, the
PTSD patient can discuss traumatic memories, PTSD symptoms, and functional
deficits with others who have had similar experiences. This approach has been
most successful with war Veterans, rape/incest victims, and natural disaster
survivors. It is important that therapeutic goals be realistic because, in some
cases, PTSD is a chronic, complex (e.g., with many comorbid diagnoses and
symptoms), and severely debilitating psychiatric disorder that does not always
respond to current available treatments. Resick, Nishith, and Griffin (2003) have
shown however, that very good outcomes utilizing evidence-based Cognitive
Processing Therapy (CPT) can be achieved, even with such complicated patients
(19); and, more recently, group CPT has shown promising results (20-21). A
remarkable recent finding is the effectiveness of group CPT, adapted for illiteracy
and risk of ongoing violence, with sexual trauma survivors in the Democratic
Republic of Congo (22). The hope remains, however, that our growing knowledge
about PTSD will enable us to design other effective interventions for patients
afflicted with this disorder.
Rapid interventions for trauma survivors
There is great interest in rapid interventions for acutely traumatized individuals,
especially with respect to civilian disasters, military deployments, and emergency
personnel (medical personnel, police, and firefighters). This has become a major

policy and public health issue since the massive traumatization caused by the
September 11 terrorist attacks on the World Trade Center, Hurricane Katrina, the
Asian tsunami, the Haitian earthquake, the wars in Iraq and Afghanistan and
other large-scale traumatic events. Currently, there is controversy about which
interventions work best during the immediate aftermath of a trauma. Research on
critical incident stress debriefing (CISD), an intervention used widely, has brought
disappointing results with respect to its efficacy to attenuate posttraumatic
distress or to forestall the later development of PTSD. The National Center for
PTSD and the National Center for Child Traumatic Stress have developed an
alternative early intervention, Psychological First Aid that is available online, but which
has yet to be subjected to rigorous evaluation. On the other hand, brief cognitive
behavioral therapy has proved very effective in randomized clinical trials (23).

References
1.

Trimble, M.D. (1985). Post-traumatic Stress Disorder: History of a concept. In C.R. Figley
(Ed.), Trauma and its wake: The study and treatment of Post-Traumatic Stress Disorder. New York:
Brunner/Mazel. Revised from Encyclopedia of Psychology, R. Corsini, Ed. (New York: Wiley, 1984,
1994)

2.

American Psychiatric Association. (1980). Diagnostic and statistical manual of mental disorders,
(3rd ed.). Washington, DC: Author.

3.

American Psychiatric Association. (1987). Diagnostic and statistical manual of mental disorders,
(Revised 3rd ed.). Washington, DC: Author.

4.

American Psychiatric Association. (1994). Diagnostic and statistical manual of mental disorders,
(4th ed.). Washington, DC: Author.

5.

American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders,
(Revised 4th ed.). Washington, DC: Author.

6.

World Health Organization. (1992). The ICD-10 classification of mental and behavioural
disorders. Geneva, Switzerland: Author.

7.

Kessler, R.C., Chiu, W. T., Demler, O., Merikangas, K. R., Walters, E. E. (2005). Prevalence,
severity, and comorbidity of 12-month DSM-IV disorders in the National Comorbidity Survey
Replication. Archives of General Psychiatry, 62, 617-627. doi: 10.1001/archpsyc.62.6.617

8.

De Jong, J., Komproe, T.V.M., Ivan, H., von Ommeren, M., El Masri, M., Araya, M., Khaled,
N.,van de Put, W., & Somasundarem, D.J. (2001). Lifetime events and Posttraumatic Stress
Disorder in 4 postconflict settings.Journal of the American Medical Association, 286, 555-562. doi:
10.1001/jama.286.5.555

9.

American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders,
(5th ed.). Washington, DC: Author.

10.

Keane, T.M., Wolfe, J., & Taylor, K.I. (1987). Post-traumatic Stress Disorder: Evidence for
diagnostic validity and methods of psychological assessment.Journal of Clinical Psychology, 43, 3243. doi: 10.1002/1097-4679(198701)43:1<32::AID-JCLP2270430106>3.0.CO;2-X

11.

Friedman, M.J., Charney, D.S. & Deutch, A.Y. (1995) Neurobiological and clinical consequences
of stress: From normal adaptation to PTSD. Philadelphia: Lippincott-Raven.

12.

Shiromani, P. J., Keane, T. M., & LeDoux, J. E. (Eds.). (2009). Post-Traumatic Stress Disorder:
Basic science and clinical practice. New York: Humana Press.

13.

Friedman, M. J., Resick, P. A., Bryant, R. A., & Brewin, C. R. (2011).Considering PTSD for DSM5. Depression and Anxiety, 28, 750-769. doi: 10.1002/da.20767

14.

Herman, J.L. (1992). Trauma and recovery. New York: Basic Books.

15.

Hinton, D. E., & Lewis-Fernandez, R. (2011). The cross-cultural validity of Posttraumatic Stress
Disorder: Implications for DSM-5. Depression and Anxiety, 28, 783-801. doi: 10.1002/da.20753

16.

Marsella, A.J., Friedman, M.J., Gerrity, E. & Scurfield R.M. (Eds.). (1996).Ethnocultural aspects of
Post-Traumatic Stress Disorders: Issues, research and applications. Washington, DC: American
Psychological Association.

17.

Foa, E.B., Keane, T.M., Friedman, M.J., & Cohen, J.A. (Eds.). (2009).Effective treatments for
PTSD, Second Edition. New York, NY: Guilford.

18.

Raskind, M. A., Peterson, K., Williams, T., Hoff, D. J., Hart, K., Holmes, H., Homas, D., Hill, J.,
Daniels, C., Calohan, J., Millard, S. P., Rohde, K., O'Connell, J., Pritzl, D., Feiszli, K., Petrie, E. C.,
Gross, C., Mayer, C. L., Freed, M. C.., Engel, C., & Peskind, E. R. (2013). A trail of prazosin for
combat trauma PTSD with nightmares in active-duty soldiers returned from Iraq and
Afghanistan. American Journal of Psychiatry, Advance online publication. doi:
10.1176/appi.ajp.2013.12081133

19.

Resick, P. A., Nishith, P., & Griffin, M. G. (2003). How well does cognitive-behavioral therapy treat
symptoms of complex PTSD? An examination of child sexual abuse survivors within a clinical
trial. CNS Spectrums, 8, 340-355.

20.

Alvarez, J., McLean, C., Harris, A. H. S., Rosen, C. S., Ruzek, J. I., & Kimerling, R. (2011). The
comparative effectiveness of cognitive processing therapy for male Veterans treated in a VHA
Posttraumatic Stress Disorder residential rehabilitation program. Journal of Consulting and Clinical
Psychology, 79, 590-599. doi: 10.1037/a0024466

21.

Chard, K. M., Ricksecker, E. G., Healy, E. T., Karlin, B. E., & Resick, P. A. (2011). Dissemination
and experience with cognitive processing therapy.Journal of Rehabilitation Research and
Development, 49, 667-678. doi: 10.1682/JRRD.2011.10.0198

22.

Bass, J. K., Annan, J., McIvor Murray, S., Kaysen, D., Griffiths, S., Cetinoglu, T., Wachter, K.,
Murray, L. K., & Bolton, P. A. (2013). Controlled trial of psychotherapy for Congolese survivors of
sexual violence. New England Journal of Medicine, 368, 2182-219. doi:10.1056/NEJMoa1211853

23.

Bryant, R.A., Mastrodomenico, J., Felmingham, K.L., Hopwood, S., Kenny, L., Kandris, E., Cahill,
C. & Creamer, M. (2008). Treatment of acute stress disorder: A randomized controlled
trial. Archives of General Psychiatry, 65, 659-667. doi:10.1001/archpsyc.65.6.659

Complex PTSD
Many traumatic events (e.g., car accidents, natural disasters, etc.) are of timelimited duration. However, in some cases people experience chronic trauma that
continues or repeats for months or years at a time. The current PTSD diagnosis
often does not fully capture the severe psychological harm that occurs with
prolonged, repeated trauma. People who experience chronic trauma often report
additional symptoms alongside formal PTSD symptoms, such as changes in their
self-concept and the way they adapt to stressful events.
Dr. Judith Herman of Harvard University suggests that a new diagnosis, Complex
PTSD, is needed to describe the symptoms of long-term trauma (1). Another
name sometimes used to describe the cluster of symptoms referred to as
Complex PTSD is Disorders of Extreme Stress Not Otherwise Specified
(DESNOS)(2). A work group has also proposed a diagnosis of Developmental
Trauma Disorder (DTD) for children and adolescents who experience chronic
traumatic events (3).
Because results from the DSM-IV Field Trials indicated that 92% of individuals
with Complex PTSD/DESNOS also met diagnostic criteria for PTSD, Complex
PTSD was not added as a separate diagnosis classification (4). However, cases
that involve prolonged, repeated trauma may indicate a need for special
treatment considerations.

What types of trauma are associated with Complex PTSD?


During long-term traumas, the victim is generally held in a state of captivity,
physically or emotionally, according to Dr. Herman (1). In these situations the

victim is under the control of the perpetrator and unable to get away from the
danger.
Examples of such traumatic situations include:

Concentration camps

Prisoner of War camps

Prostitution brothels

Long-term domestic violence

Long-term child physical abuse

Long-term child sexual abuse

Organized child exploitation rings

What additional symptoms are seen in Complex PTSD?


An individual who experienced a prolonged period (months to years) of chronic
victimization and total control by another may also experience the following
difficulties:

Emotional Regulation. May include persistent sadness, suicidal thoughts, explosive anger, or
inhibited anger.

Consciousness. Includes forgetting traumatic events, reliving traumatic events, or having


episodes in which one feels detached from one's mental processes or body (dissociation).

Self-Perception. May include helplessness, shame, guilt, stigma, and a sense of being
completely different from other human beings.

Distorted Perceptions of the Perpetrator. Examples include attributing total power to the
perpetrator, becoming preoccupied with the relationship to the perpetrator, or preoccupied with
revenge.

Relations with Others. Examples include isolation, distrust, or a repeated search for a rescuer.

One's System of Meanings. May include a loss of sustaining faith or a sense of hopelessness
and despair.

What other difficulties are faced by those who experienced chronic


trauma?
Because people who experience chronic trauma often have additional symptoms
not included in the PTSD diagnosis, clinicians may misdiagnose PTSD or only
diagnose a personality disorder consistent with some symptoms, such as
Borderline, Dependent, or Masochistic Personality Disorder.
Care should be taken during assessment to understand whether symptoms are
characteristic of PTSD or if the survivor has co-occurring PTSD and personality

disorder. Clinicians should assess for PTSD specifically, keeping in mind that
chronic trauma survivors may experience any of the following difficulties:

Survivors may avoid thinking and talking about trauma-related topics because the feelings
associated with the trauma are often overwhelming.

Survivors may use alcohol or other substances as a way to avoid and numb feelings and
thoughts related to the trauma.

Survivors may engage in self-mutilation and other forms of self-harm.

Survivors who have been abused repeatedly are sometimes mistaken as having a "weak
character" or are unjustly blamed for the symptoms they experience as a result of victimization.

Treatment for Complex PTSD


Standard evidence-based treatments for PTSD are effective for treating PTSD
that occurs following chronic trauma. At the same time, treating Complex PTSD
often involves addressing interpersonal difficulties and the specific symptoms
mentioned above. Dr. Herman contends that recovery from Complex PTSD
requires restoration of control and power for the traumatized person. Survivors
can become empowered by healing relationships which create safety, allow for
remembrance and mourning, and promote reconnection with everyday life (1).

References
1.

Herman, J. (1997). Trauma and recovery: The aftermath of violence from domestic abuse to
political terror. New York: Basic Books.

2.

Ford, J. D. (1999). Disorders of extreme stress following war-zone military trauma: Associated
features of Posttraumatic Stress Disorder or comorbid but distinct syndromes? Journal of
Consulting and Clinical Psychology, 67, 3-12.

3.

van der Kolk, B. (2005). Developmental trauma disorder. Psychiatric Annals, 35(5), 401-408.

4.

Roth, S., Newman, E., Pelcovitz, D., van der Kolk, B., & Mandel, F. S. (1997). Complex PTSD in
victims exposed to sexual and physical abuse: Results from the DSM-IV field trial for Posttraumatic
Stress Disorder. Journal of Traumatic Stress, 10, 539-555.

Epidemiology of PTSD
Jaimie L. Gradus, DSc, MPH

What is epidemiology?
Epidemiology is the study of the distribution and determinants of disease in a
population. Numerous studies have been conducted to assess the prevalence of
PTSD across different populations. Below is a brief review of some of the major
studies that have assessed the prevalence of PTSD in nationally representative
samples as well as in samples of Veterans.

What is prevalence?
Prevalence is the proportion of people in a population that have a given disorder
at a given time. It represents the existing cases of a disorder in a population or
group. Prevalence estimates can be influenced by many factors including
disorder occurrence (if new disorder occurrences increase, prevalence will
increase) and the duration of the disorder (the longer people live with a disorder,
the higher the prevalence). These estimates can also differ by demographic
factors such as age and gender. It is important to qualify prevalence estimates
with the time at which they were measured, as prevalence estimates can shift
over time. Similarly, when interpreting prevalence estimates, it is important to
keep in mind that prevalence is dynamic - it can change over people, places, and
time.
Often prevalence is discussed in terms of lifetime prevalence. Other times,
statistics will be given on current prevalence of PTSD in a given time frame,
usually one year. At the end of this fact sheet you will find descriptions of other
terms commonly used in epidemiology.

Prevalence of PTSD
U.S. National Comorbidity Survey Replication
The National Comorbidity Survey Replication (NCS-R), conducted between
February 2001 and April 2003, comprised interviews of a nationally
representative sample of 9,282 Americans aged 18 years and older. PTSD was
assessed among 5,692 participants, using DSM-IV criteria. The NCS-R
estimated the lifetime prevalence of PTSD among adult Americans to be 6.8%
(1). Current past year PTSD prevalence was estimated at 3.5% (2).The lifetime

prevalence of PTSD among men was 3.6% and among women was 9.7%. The
twelve month prevalence was 1.8% among men and 5.2% among women (3).
These findings are very similar to those of the first National Comorbidity Survey.
The original survey was conducted in the early 1990s and comprised interviews
of a representative national sample of 8,098 Americans aged 15 to 54 years. In
this earlier sample, the estimated prevalence of lifetime PTSD was 7.8% in the
general population. Women (10.4%) were more than twice as likely as men (5%)
to have PTSD at some point in their lives (4).
PTSD among children and adolescents
To date, no population-based epidemiological study has examined the
prevalence of PTSD among children. However, studies have examined the
prevalence of PTSD among high-risk children who have experienced specific
traumatic events, such as abuse or natural disasters. Prevalence estimates from
studies of this type vary greatly; however, research indicates that children
exposed to traumatic events may have a higher prevalence of PTSD than adults
in the general population (5).
Kilpatrick and colleagues (2003) assessed the prevalence of PTSD among
adolescents based on data from the National Survey of Adolescents, which
included a household probability sample of 4,023 adolescents between the ages
of 12 and 17. Using DSM-IV criteria for PTSD, the six-month prevalence was
estimated to be 3.7% for boys and 6.3% for girls (6).
PTSD in other countries
In the late 1990s the World Health Organization (WHO) began collecting
epidemiological information on mental health disorders around the world. As of
2008, the research consortium had collected data from nearly 200,000
respondents in 27 countries (7). Published estimates are available of PTSD
lifetime prevalence in most of the first 17 countries to complete the World Mental
Health Surveys. In general, the estimates for lifetime PTSD prevalence range
from a low of 0.3% in China to 6.1% in New Zealand. However, statistics reported
from various countries are not directly comparable due to methodological
differences in survey administration and sampling strategies.

National Vietnam Veterans Readjustment Study


The National Vietnam Veterans Readjustment Study (NVVRS) , conducted
between November 1986 and February 1988, comprised interviews of 3,016
American Veterans selected to provide a representative sample of those who
served in the armed forces during the Vietnam era. The estimated lifetime
prevalence of PTSD among these Veterans was 30.9% for men and 26.9% for
women. Of Vietnam theater Veterans, 15.2% of males and 8.1% of females were
currently diagnosed with PTSD at the time the study was conducted (8).
Gulf War Veterans
Kang and others conducted a study to estimate the prevalence of PTSD in a
population-based sample of 11,441 Gulf War Veterans from 1995 to 1997. PTSD
was assessed using the PTSD Checklist (PCL;9) rather than interviews, with
those scoring 50 or higher considered to have met criteria for PTSD. The
prevalence of current PTSD in this sample of Gulf War Veterans was 12.1%.
Further, the authors estimated the prevalence of PTSD among the total Gulf War
Veteran population to be 10.1% (10).
Operation Enduring Freedom/Operation Iraqi Freedom
In 2008, the RAND Corporation, Center for Military Health Policy Research,
published a population-based study that examined the prevalence of PTSD
among previously deployed Operation Enduring Freedom and Operation Iraqi
Freedom (Afghanistan and Iraq) service members (11). PTSD was assessed
using the PCL, as in the Gulf War Veterans study. Among the 1,938 participants,
the prevalence of current PTSD was 13.8%.

Commonly-used epidemiologic terms (12)


What is cumulative incidence?
Cumulative incidence (sometimes called "risk") is the proportion of people that
develop a disorder over time among only the population at risk for that disorder. It
represents the occurrence of new cases of a disorder in a population or group.

Like prevalence, it is important to qualify cumulative incidence estimates with the


length of time over which they are measured (e.g., over five years). This is
because a large cumulative incidence (or a large amount of new disorder
occurrence) occurring over a short period of time has different intervention
implications than a large cumulative incidence occurring over a very long period
of time.
What is a cumulative incidence ratio?
A cumulative incidence ratio (sometimes called a risk ratio or a relative risk) is a
relative measure of the cumulative incidence of disorder in a group exposed to a
certain factor compared to the cumulative incidence of a disorder in a group that
is unexposed to that factor.
What is the incidence rate?
An incidence rate is the proportion of people who develop a disorder over a
period of time among the population at risk for that disorder. It represents the rate
at which new cases of a disorder are occurring in a population or group.
Incidence rates are expressed as the number of new cases of a disorder per
person-time.
What is an incidence rate ratio?
A rate ratio (sometimes called relative risk), is a relative measure of incidence rate of disorder in a group exposed to a
certain factor compared to the incidence rate of a disorder in a group that is unexposed to that factor.

What is an odds ratio?


An odds ratio (sometimes called a relative risk) is a relative measure of the odds
of a disorder in a group exposed to a certain factor compared to the odds of a
disorder in a group unexposed to that factor.

References
1.

Kessler, R.C., Berglund, P., Delmer, O., Jin, R., Merikangas, K.R., & Walters, E.E. (2005).
Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the National Comorbidity
Survey Replication. Archives of General Psychiatry, 62(6): 593-602.

2.

Kessler, R.C., Chiu, W.T., Demler, O., Merikangas, K.R., & Walters, E.E. (2005). Prevalence,
severity, and comorbidity of 12-month DSM-IV disorders in the National Comorbidity Survey
Replication. Archives of General Psychiatry, 62(6): 617-627.

3.

National Comorbidity Survey. (2005). NCS-R appendix tables: Table 1. Lifetime prevalence of
DSM-IV/WMH-CIDI disorders by sex and cohort. Table 2. Twelve-month prevalence of DSMIV/WMH-CIDI disorders by sex and cohort. Accessed
at: http://www.hcp.med.harvard.edu/ncs/publications.php

4.

Kessler, R.C., Sonnega, A., Bromet, E. Hughes, M., & Nelson, C.B. (1995). Posttraumatic stress
disorder in the National Comorbidity Survey. Archives of General Psychiatry, 52(12), 1048-1060.

5.

Gabbay, V., Oatis, M.D., Silva, R.R., & Hirsch, G. (2004). Epidemiological aspects of PTSD in
children and adolescents. In Raul R. Silva (Ed.),Posttraumatic Stress Disorder in Children and
Adolescents: Handbook (1-17). New York: Norton.

6.

Kilpatrick, D.G., Ruggiero, K.J., Acierno, R., Saunders, B.E., Resnick, H.S., & Best, C.L. (2003).
Violence and risk of PTSD, major depression, substance abuse/dependence, and comorbidity:
results from the National Survey of Adolescents. Journal of Consulting and Clinical Psychology,
71(4), 692-700.

7.

Kessler, R.C., & Ustun, T. B. (Eds.). (2008). The WHO World Mental Health Surveys: global
perspectives on the epidemiology of mental disorders. New York: Cambridge University Press, 1580.

8.

Kulka, R.A., Schlenger, W.A., Fairbanks, J.A., Hough, R.L., Jordan, B.K., Marmar, C.R., ...
Cranston, A.S. (1990). Trauma and the Vietnam War generation: Report of findings from the
National Vietnam Veterans Readjustment Study. New York: Brunner/Mazel.

9.

Weathers, F., Litz, B., Herman, D., Huska, J., & Keane, T. (October 1993). The PTSD Checklist
(PCL): Reliability, Validity, and Diagnostic Utility. Paper presented at the Annual Convention of the
International Society for Traumatic Stress Studies, San Antonio, TX.

10.

Kang, H.K., Natelson, B.H., Mahan, C.M., Lee, K.Y., & Murphy, F.M. (2003). Post-Traumatic
Stress Disorder and Chronic Fatigue Syndrome-like illness among Gulf War Veterans: A populationbased survey of 30,000 Veterans. American Journal of Epidemiology, 157(2):141-148.

11.

Tanielian, T. & Jaycox, L. (Eds.). (2008). Invisible Wounds of War: Psychological and Cognitive
Injuries, Their Consequences, and Services to Assist Recovery. Santa Monica, CA: RAND
Corporation.

12.

Rothman, K.J. (2002). Epidemiology: An introduction. Oxford: Oxford

Overview of Psychotherapy for PTSD

Hamblen, PhD, Schnurr, PhD, Rosenberg, MA, & Eftekhari, PhD


Several clinical practice guidelines offer recommendations for the treatment of
PTSD, for example see the VA/DoD PTSD Clinical Practice Guideline (2010). These
guidelines come from different federal agencies, professional organizations, and
countries (1-5). The Institute of Medicine (IOM) also published a report in 2007
evaluating the evidence on PTSD treatment (6). The guidelines unanimously
recommend cognitive behavioral therapies as the most effective treatment for
PTSD, and the majority of guidelines recommend Eye Movement Desensitization
and Reprocessing (EMDR) as well.
Cognitive behavioral treatments typically include a number of components,
including psychoeducation, anxiety management, exposure, and cognitive
restructuring. Exposure and cognitive restructuring are thought to be the most
effective components.

Exposure-based treatments
The greatest number of studies has been conducted on exposure-based
treatments, which involve having survivors repeatedly re-experience their
traumatic event. There is strong evidence for exposure therapy (7-12), and of the
various approaches, Prolonged Exposure (PE) has received the most attention.
PE (8) includes both imaginal exposure and in vivo exposure to safe situations
that have been avoided because they elicit traumatic reminders.
In a multisite randomized controlled trial of PE in female Veterans and active-duty
personnel with PTSD, those who received PE experienced greater reduction of
PTSD symptoms relative to women who received present-centered therapy and
were less likely to meet PTSD diagnostic criteria (13). Moreover, PE was more
effective than the combination of PE plus stress inoculation training (SIT), SIT
alone, or a waitlist control in female sexual assault survivors (10). In addition, PE
alone and PE plus cognitive restructuring reduced PTSD and depression relative
to a waitlist control in intention-to-treat and completer samples (11).

Cognitive approaches
Cognitive interventions also are widely supported in treatment guidelines (12, 1517). Cognitive Processing Therapy (CPT; 18), one of the most well-researched
cognitive approaches, has a primary focus on challenging and modifying
maladaptive beliefs related to the trauma, but also includes a written exposure
component.

Veterans with chronic military-related PTSD who received CPT showed better
improvements in PTSD and comorbid symptoms than the waitlist control group
(19). A dismantling study of CPT then examined the relative utility of the full
protocol compared with its components: cognitive therapy alone and written
exposure alone (20). Results indicated significant improvement in PTSD and
depression for participants in all three treatments. However, the cognitive therapy
alone resulted in faster improvement than the written exposure alone, with the
effects of the full protocol of CPT falling in-between (20). Both CPT and PE have
shown great success in outcome research; thus, one logical research question
involves whether one is more effective than the other. In a head-to-head
comparison, CPT and PE were equally effective in treating PTSD and depression
in female sexual assault survivors (7).
Ehlers and Clark have also developed a cognitive therapy for PTSD that involves
three goals: modifying excessively negative appraisals, correcting
autobiographical memory disturbances, and removing problematic behavioral
and cognitive strategies (21). Elements unique to Ehlers and Clark's cognitive
therapy include performing actions that are incompatible with the memory or
engaging in behavioral experiments. Two randomized controlled trials have
compared cognitive therapy to a waitlist, both with positive results (15, 16).

Adding components
Some investigators have added a novel component to an effective treatment in
hopes of further optimizing outcomes (22-27). Three groups of investigators
compared an enhanced treatment to a waitlist control group: Cloitre and
colleagues (23) sequenced skills training in affect and interpersonal regulation
before PE; Falsetti and colleagues (24) developed Multiple Channel Exposure
Therapy, a combination of PE, CPT, and interoceptive exposure techniques for
panic disorder; and Lindauer and colleagues (27) developed Brief Eclectic
Therapy, a combination of psychodynamic and cognitive behavioral therapy.
These studies showed that the combined treatments were effective, but not
whether the additional components enhanced the standard treatments.
Glynn and colleagues (25) compared exposure therapy alone with exposure
therapy followed by behavioral family therapy, and Arntz and colleagues (22)
compared imaginal exposure alone with imaginal exposure plus imagery
rescripting. In both studies, the combined treatment did not result in a greater
reduction of PTSD severity, which suggests that the novel component was not

necessary. However, statistical power may have been too low to compare the
active treatments adequately.

EMDR
In addition to cognitive behavioral therapies, EMDR is recommended in most
practice guidelines. Patients receiving EMDR engage in imaginal exposure to a
trauma while simultaneously performing saccadic eye movements. There is good
evidence that EMDR is more effective than waitlist and nonspecific comparison
conditions (28-30). Further, two well-controlled studies compared EMDR to PE.
One study found equivalent results (29) while the other found PE to be superior
(30). Additional research has investigated the mechanism of action in EMDR, and
there is growing evidence that the theorized eye movements are an unnecessary
component (31), suggesting that perhaps the mechanism of action is exposure.

Other approaches
Other treatments in addition to cognitive behavioral therapy and EMDR may be
effective; however, at this time we do not have enough evidence to confidently
indicate that they are effective. For example, despite the appeal of group
treatments, results of the few randomized controlled trials of group therapy have
been mixed (32-36). In addition, psychodynamic therapy, hypnotherapy, and
trauma desensitization were more effective than a waitlist control group in one
trial (40). Rogerian supportive therapy was less effective in treating symptoms of
PTSD and anxiety than cognitive behavioral therapy in one study (41).
Acceptance and Commitment Therapy (ACT), which is considered a third wave
behavioral therapy, focuses on reducing experiential avoidance and engagement
with maladaptive thoughts and encourages clients to approach activities
consistent with their personal values. Several case studies have documented
support for ACT in the treatment of PTSD (37, 38). However, no trials of ACT for
PTSD have been published to date. Finally, there is also interest in alternative
medicine treatments. For example, acupuncture was as effective as group
cognitive behavioral treatment, and both were more effective than the waitlist
condition (39).

Conclusion
Overall, cognitive behavioral therapies such as Prolonged Exposure and
Cognitive Processing Therapy, as well as Eye Movement Desensitization

Reprocessing, are considered first-line treatments for PTSD and have strong
evidence bases. Components of these treatments have been combined with
other interventions, with no support for improved benefits over the standard
treatments alone. Other interventions, such as group treatment, show promise;
however, more research is needed before drawing firm conclusions about their
effectiveness.

References
1.

Australian Centre for Posttraumatic Mental Health. (2007). Australian guidelines for the treatment
of adults with acute stress disorder and posttraumatic stress disorder. Melbourne, Victoria: Author.

2.

Foa, E. B., Keane, T.M., & Friedman, M.J. (2009). Effective treatments for PTSD: Practice
guidelines from the International Society for Traumatic Stress Studies (1-388). New York: Guilford.

3.

National Collaborating Centre for Mental Health. (2005). Post-traumatic stress disorder: The
management of PTSD in adults and children in primary and secondary care (1-167). London:
Gaskell and the British Psychological Society.

4.

Ursano, R. J., Bell, C., Eth, S., Friedman, M. J., Norwood, A. E., & Pfefferbaum, B. (2004).
Practice guideline for the treatment of patients with acute stress disorder and posttraumatic stress
disorder [Special issue].American Journal of Psychiatry, (Suppl), 161.

5.

VA/DoD Clinical Practice Guideline Working Group. (December 2003).Management of posttraumatic stress. Washington, DC: Veterans Health Administration, Department of Veterans Affairs
and Health Affairs; Department of Defense; Office of Quality and Performance, publication 10QCPG/PTSD-03.

6.

Institute of Medicine (2008). Treatment of posttraumatic stress disorder: An assessment of the


evidence. Washington, DC: The National Academies Press.

7.

Resick, P. A., Nishith, P., Weaver, T. L., Astin, M. C., & Feuer, C. A. (2002). A comparison of
cognitive-processing therapy with prolonged exposure and a waiting condition for the treatment of
chronic posttraumatic stress disorder in female rape victims. Journal of Consulting and Clinical
Psychology, 70, 867-879.

8.

Foa, E. B., & Rothbaum, B. O. (1998). Treating the trauma of rape: Cognitive behavioral therapy
for PTSD (1-266). New York: Guilford.

9.

Bryant, R. A., Moulds, M. L., Guthrie, R. M., Dang, S. T., & Nixon, R. D. V. (2003). Imaginal
exposure alone and imaginal exposure with cognitive restructuring in treatment of posttraumatic
stress disorder. Journal of Consulting and Clinical Psychology, 71, 706-712.

10.

Foa, E. B., Dancu, C.V., Hembree, E. A., Jaycox, L.H., Meadows, E. A., & Street, G.P. (1999). A
comparison of exposure therapy, stress inoculation training, and their combination for reducing

posttraumatic stress disorder in female assault victims. Journal of Consulting and Clinical
Psychology, 67, 194-200.
11.

Foa, E. B., Hembree, E. A., Cahill, S. P., Rauch, S. A. M., Riggs, D. S., & Feeny, N. C. (2005).
Randomized trial of prolonged exposure for posttraumatic stress disorder with and without cognitive
restructuring: Outcome at academic and community clinics. Journal of Consulting and Clinical
Psychology, 73, 953-964.

12.

Marks, I., Lovell, K., Noshirvani, H., Livanou, M., & Thrasher, S. (1998). Treatment of
posttraumatic stress disorder by exposure and/or cognitive restructuring. Archives of General
Psychiatry, 55, 317-324.

13.

Schnurr, P. P., Friedman, M. J., Engel, C. C., Foa, E. B., Shea, M. T., Chow, B. K., ...Bernardy, N.
(2007). Cognitive behavioral therapy for posttraumatic stress disorder in women: A randomized
controlled trial.Journal of the American Medical Association, 297, 820-830.

14.

Tarrier, N., Pilgrim, H., Sommerfield, C., Faragher, B., Reynolds, M., & Graham, E. (1999). A
randomized trial of cognitive therapy and imaginal exposure in the treatment of chronic
posttraumatic stress disorder. Journal of Consulting and Clinical Psychology, 67, 13-18.

15.

Ehlers, A., Clark, D. M., Hackmann, A., McManus F., & Fennell, M. J. V. (2005). Cognitive therapy
for post-traumatic stress disorder: Development and evaluation. Behavioral Research and Therapy,
43, 413-431.

16.

Duffy, M., Gillespie, K., & Clark, D. M. (2007). Post-traumatic stress disorder in the context of
terrorism and other civil conflict in Northern Ireland: Randomised controlled trial. British Medical
Journal, 334, 1147-1150.

17.

Mueser, K. T., Rosenberg, S. D., Xie, H., Jankowski. J. K., Bolton, E. E., & Lu, W. (2008). A
randomized controlled trial of cognitive-behavioral treatment of Posttraumatic Stress Disorder in
severe mental illness. Journal of Consulting and Clinical Psychology, 76, 259-271.

18.

Resick, P.A., & Schnicke, M. K. (1996). Cognitive processing therapy for rape victims: A treatment
manual. Newbury Park, CA: Sage Publications.

19.

Monson, C. M., Schnurr, P. P., Resick, P. A., Friedman, M. J., Young-Xu, Y., & Stevens, S. P.
(2006). Cognitive processing therapy for veterans with military-related posttraumatic stress
disorder. Journal of Consulting and Clinical Psychology, 74, 898-907.

20.

Resick, P. A., Galovski, T. E., Uhlmansiek, M. O., Scher, C. D., Clum, G. A., & Young-Xu, Y.
(2008). A randomized clinical trial to dismantle components of cognitive processing therapy for
posttraumatic stress disorder in female victims of interpersonal violence. Journal of Consulting and
Clinical Psychology, 76, 243-258.

21.

Ehlers, A., & Clark, D. M. (2000). A cognitive model of posttraumatic stress disorder. Behavioral
Research and Therapy, 38, 319-345.

22.

Arntz, A., Tiesema, M., & Kindt, M. (2007). Treatment of PTSD: A comparison of imaginal
exposure with and without imagery rescripting.Journal of Behavioral Therapy and Experimental
Psychiatry, 38, 345-370.

23.

Cloitre, M., Koenen, K. C., Cohen, L.R., & Han, H. (2002). Skills training in affective and
interpersonal regulation followed by exposure: A phase-based treatment for PTSD related to
childhood abuse. Journal of Consulting and Clinical Psychology, 70, 1067-1074.

24.

Falsetti, S.A., Resnick, H. S., & Davis, J. L. (2008). Multiple channel exposure therapy for women
with PTSD and comorbid panic attacks.Cognitive Behaviour Therapy, 37, 117-130.

25.

Glynn, S. M., Eth, S., Randolph, E.T., Foy, D. W., Urbaitis, M., & Boxer, L. (1999). A test of
behavioral family therapy to augment exposure for combat-related posttraumatic stress
disorder. Journal of Consulting and Clinical Psychology, 67, 243-251.

26.

Hogberg, G., Pagani, M., Sundin, O., Soares, J. J. F., Averg-Wistedt, A., & Tarnell, B. (2008).
Treatment with eye movement desensitization and reprocessing of chronic post-traumatic stress
disorder in public transportation workers: Outcome is stable in 35-month follow-up. Psychiatric
Research, 159, 101-108.

27.

Lindauer, R. J. L., Gersons, B. P. R., van Meijel, E. P. M., Els, P. M., Blom, K., & Carlier, I. V. E.
(2005). Effects of brief eclectic psychotherapy in patients with posttraumatic stress disorder:
Randomized clinical trial. Journal of Traumatic Stress, 18, 205-212.

28.

Chemtob, C. M., Tolin, D. F., van der Kolk, B., & Pitman, R. K. (2000). Eye movement
desensitization and reprocessing. In E. Foa, T. M. Keane, & M. J. Friedman (Eds.), Effective
treatments for PTSD (139-154). New York: Guilford.

29.

Rothbaum, B. O., Astin, M. C., & Marsteller, F. (2005). Prolonged exposure versus eye movement
desensitization and reprocessing (EMDR) for PTSD rape victims. Journal of Traumatic Stress, 18,
607-616.

30.

Taylor, S., Thordarson, D. S., Maxfield, L., Fedoroff, I.C., Lovell, K., & Ogrodniczuk, J.S. (2003).
Comparative efficacy, speed, and adverse effects of three PTSD treatments: Exposure therapy,
EMDR, and relaxation training.Journal of Consulting and Clinical Psychology, 71, 330-338.

31.

Davidson, P. R., & Parker, K. C. H. (2001). Eye movement desensitization and reprocessing
(EMDR): A meta-analysis. Journal of Consulting and Clinical Psychology, 69, 305-316.

32.

Alexander, P. C., Neimeyer, R. A., Follette, V. M., Moore, M. K., & Harter, S. L. (1989). A
comparison of group treatments of women sexually abused as children. Journal of Consulting and
Clinical Psychology, 57, 479-483.

33.

Chard, K. M. (2005). An evaluation of cognitive processing therapy for the treatment of


posttraumatic stress disorder related to childhood sexual abuse.Journal of Consulting and Clinical
Psychology, 75, 965-971.

34.

Krupnik, J. L., Green, B. L., Stockton, P., Miranda, J., Krause, E. D., & Mete, M. (2008). Group
interpersonal psychotherapy for low-income women with posttraumatic stress
disorder. Psychotherapy Research, 18, 497-507.

35.

Schnurr, P. P., Friedman, M. J., Foy, D. W., Shea, M. T., Hsieh, F. Y., & Lavori, P. W. (2003).
Randomized trial of trauma-focused group therapy for posttraumatic stress disorder: Results from a
Department of Veterans Affairs Cooperative Study. Archives of General Psychiatry, 60, 481-489.

36.

Zlotnick, C., Shea, M. T., Rosen, K. H., Simpson, E., Mulrenin, K., Begin, A., & Pearlstein, T.
(1997). An affect-management group for women with posttraumatic stress disorder and histories of
childhood sexual abuse.Journal of Traumatic Stress, 10, 425-436.

37.

Batten, S. V., & Hayes, S. C. (2005). Acceptance and commitment therapy in the treatment of
comorbid substance abuse and post-traumatic stress disorder: A case study. Clinical Case Studies,
4, 246-262.

38.

Orsillo, S. M., & Batten, S. V. (2008). Acceptance and commitment therapy in the treatment of
posttraumatic stress disorder. Behavior Modification, 29, 95-129.

39.

Hollifield, M., Sinclair-Lian, N., Warner, T. D., & Hammerschlag, R. (2007). Acupuncture for
posttraumatic stress disorder: A randomized controlled pilot trial. Journal of Nervous and Mental
Disorders, 195, 504-513.

40.

Brom, D., Kleber, R. J., & Defares, P. B. (1989). Brief psychotherapy for posttraumatic stress
disorders. Journal of Consulting and Clinical Psychology, 57, 607-612.

41.

Cottraux, J., Note, B., & Chen, Y. (2008). Randomized controlled comparison of cognitive
behavior therapy with Rogerian supportive therapy in chronic post-traumatic stress disorder: A 2year follow-up. Psychotherapy and Psychosomatics, 77, 101-110.

Clinician's Guide to Medications for PTSD


Matt Jeffreys, MD

Overview
Posttraumatic Stress Disorder (PTSD) has biological, psychological, and social
components. Medications can be used in treatment to address the biological
basis for PTSD symptoms and co-morbid Axis I diagnoses. Medications may

benefit psychological and social symptoms as well. While studies suggest that
cognitive behavioral therapies such as prolonged exposure (PE) and cognitive
processing therapy (CPT) have greater effects in improving PTSD symptoms
than medications, some people may prefer medications or may benefit from
receiving a medication in addition to psychotherapy.
Placebo-controlled double-blind randomized controlled trials are the gold
standard for pharmacotherapy. Less strongly supported evidence includes open
trials and case reports. It is important for the clinician to question the level of
evidence supporting the medications prescribed in PTSD treatment. There are a
variety of factors influencing prescribing, including marketing, patient
preferences, and clinical custom, all of which can be inconsistent with the
evidence base.
Currently, the evidence base is strongest for the selective serotonin reuptake
inhibitors (SSRIs). The only two FDA approved medications for the treatment of
PTSD are sertraline (Zoloft) and paroxetine (Paxil) (1, 2). All other medication
uses are off label, though there are differing levels of evidence supporting their
use. In addition to sertraline and paroxetine, there is strong evidence for the
SSRI fluoxetine (Prozac) and for the serotonin norepinephrine reuptake inhibitor
(SNRI) venlafaxine (Effexor) which are considered first-line treatments in the
VA/DoD Clinical Practice Guideline for PTSD. There are a number of biological
changes which have been associated with PTSD, and medications can be used
to modify the resultant PTSD symptoms. Veterans whose PTSD symptoms have
been present for many years pose a special challenge. Studies indicate they are
more refractory to the beneficial effects of medications for PTSD symptoms (3).

What core PTSD symptoms are we trying to treat?


The three main PTSD symptom clusters are listed below:

Re-experiencing. Examples include nightmares, unwanted thoughts of the traumatic events, and
flashbacks.

Avoidance. Examples include avoiding triggers for traumatic memories including places,
conversations, or other reminders. The avoidance may generalize to other previously enjoyable
activities.

Hyperarousal. Examples include sleep problems, concentration problems, irritability, increased


startle response, and hypervigilance.

What are some of the biological disturbances found in PTSD?


Some of the main biological disturbances in PTSD can be conceptualized as
dysregulation of the naturally occurring stress hormones in the body and
increased sensitivity of the stress and anxiety circuits in the brain. There is
dysregulation of adrenergic mechanisms that mediate the classical fight-flight or
freeze response. Yehuda and others have found that patients with PTSD have
hypersensitivity of the hypothalamic-pituitary-adrenal axis (HPA) as compared to
patients without PTSD (4). Patients have a much greater variation in their levels
of adrenocorticoids than patients without PTSD. Other researchers have found
differences in both brain structures and brain circuits that process threatening
input between patients with PTSD and those without.
It is not known for certain whether these changes were present before the
traumatic event and predisposed the person to developing PTSD or whether
these changes were the result of the PTSD. One way to think of this is the fear
circuitry no longer being integrated with the executive centers of the brain located
in the prefrontal cortex (5). Even minor stresses may then set off the "fight or
flight" response in patients with PTSD, which leads to increased heart rate,
sweating, rapid breathing, tremors, and other symptoms of hyperarousal listed
above.

How do medications help regulate these responses?


The medications prescribed for treating PTSD symptoms act upon
neurotransmitters related to the fear and anxiety circuitry of the brain including
serotonin, norepinephrine, GABA, and dopamine among many others. There is
great interest in developing newer, more specific agents than are currently
available to target the PTSD symptoms described earlier while also minimizing
potential side effects of medications.
Studies show that a number of medications are helpful in minimizing the three
symptom clusters of PTSD. Most of the time, medications do not entirely
eliminate symptoms but provide a symptom reduction and are best used in

conjunction with an ongoing program of trauma specific psychotherapy for


patients such as PE or CPT.

How do we measure the effects of treatment?


There are a number of self-rating scales and structured clinical interviews to
monitor the effects of treatment. Two examples include the Post-Traumatic
Stress Disorder Checklist (PCL) and the Clinician-Administered PTSD Scale
(CAPS). The PCL military or civilian version is an example of a patient self-rating
form without stressor information, while the CAPS is an example of a structured
clinical interview including stressor information.
There is literature supportive of a strong correlation between the two measures,
and the PCL has the advantage of being quick and easy to administer. Both the
PCL and the CAPS provide a quantitative measure of the patient's PTSD
symptoms and response to treatment over time. This information enhances the
clinical assessment and interview with the patient.

What is the evidence base for the specific groups of medications used
for PTSD treatment?
Selective Serotonin Reuptake Inhibitors (SSRIs)
These medications are the only FDA approved medications for PTSD. SSRIs
primarily affect the neurotransmitter serotonin which is important in regulating
mood, anxiety, appetite, and sleep and other bodily functions. This class of
medication has the strongest empirical evidence with well designed randomized
controlled trials (RCTs) and is the preferred initial class of medications used in
PTSD treatment (1, 2). Exceptions may occur for patients based upon their
individual histories of side effects, response, and comorbidities.

An example of an exception would be a PTSD patient with comorbid Bipolar Disorder. In this
patient, there is a risk of precipitating a manic episode with the SSRIs. Each patient varies in their
response and ability to tolerate a specific medication and dosage, so medications must be tailored
to individual needs.

Research has suggested that maximum benefit from SSRI treatment depends
upon adequate dosages and duration of treatment. Treatment adherence is key
to successful pharmacotherapy treatment for PTSD. Examples of the SSRIs and
some typical dosage ranges are listed below:

Sertraline (Zoloft) 50 mg to 200 mg daily

Paroxetine (Paxil) 20 to 60 mg daily

Fluoxetine (Prozac) 20 mg to 60 mg daily

Note: :

Only sertraline and paroxetine have been approved for PTSD treatment by
the FDA. All other medications described in this guide are being used "off label"
and may have empirical support but have not been through the FDA approval
process for PTSD.
Other newer antidepressants for PTSD
Antidepressants that work through other neurotransmitter combinations or
through different mechanisms for altering serotonin neurotransmission are also
helpful in PTSD. Venlafaxine acts primarily as a serotonin reuptake inhibitor at
lower dosages and as a combined serotonin and norepinephrine reuptake
inhibitor at higher dosages. It is now a recommended first-line treatment for
PTSD in the revised VA/DoD Clinical Practice Guideline for PTSD based upon
large multi-site RCTs (6).
There have been smaller RCTs with mirtazapine as well as open trials (7).
Mirtazapine may be particularly helpful for treatment of insomnia in PTSD.
Trazodone is also commonly used for insomnia in PTSD even though there is
little empirical evidence available for its use. Nefazodone is still available in a
generic form but carries a black box warning regarding liver failure, so liver
function tests need to be monitored and precautions taken as recommended in
the medication's prescribing information (8, 9).
Examples of the newer antidepressants for PTSD and some typical dosage
ranges are listed below:

Mirtazapine (Remeron) 7.5 mg to 45 mg daily

Venlafaxine (Effexor) 75 mg to 300 mg daily

Nefazodone (Serzone) 200 mg to 600 mg daily

All of the antidepressants described above are also effective in treating comorbid
Major Depressive Disorder (MDD) which often accompanies PTSD. While
bupropion is useful in treating comorbid MDD, it has not been shown effective for
PTSD in controlled trials (10). A recent trial showed superior outcomes on MDD
when mirtazapine was combined initially with antidepressants versus patients
being randomized to monotherapy with fluoxetine (11). This raises important
questions regarding costs, side effects, and patient preferences which merit
further study.
Mood stabilizers for PTSD
These medications, also known as anticonvulsants or anti-epileptic drugs, either
block glutamate or potentiate GABA or do both. Topiramate has demonstrated
promising results in randomized controlled trials with civilians and Veterans with
PTSD, but currently is listed as having no demonstrated benefit in the VA/DoD
Clinical Practice Guideline for PTSD.
There are two double-blind, placebo-controlled trials evaluating topiramate as
monotherapy in civilians with PTSD (12,13). The trial published in 2007 included
38 participants and found no significant difference in total CAPS scores between
topiramate and placebo. The 2010 trial included 38 participants and
demonstrated a significant decrease in total CAPS scores. There are also two
published double-blind, placebo-controlled trials evaluating topiramate as
adjunctive treatment for PTSD in Veterans (14,15). The trial published in 2004
included 67 participants and found a significant decrease in the total CAPS
score. The 2007 trial included 40 participants and showed no significant
decrease in total CAPS scores.
Based upon the current studies, topiramate could provide a useful option for
clinicians in treatment of PTSD symptoms in patients who fail first line
pharmacotherapy. Further studies and meta-analyses are needed regarding the
place of topiramate in PTSD treatment (16).
Otherwise, despite some promising open label studies, other RCTs have been
negative for this group of medications in treating PTSD (17). As a group, this

class of medications is helpful in the treatment of comorbid Bipolar Disorder and


PTSD. Patients who have Bipolar Disorder and PTSD often benefit from these
medications since SSRIs and other antidepressants sometimes precipitate a
manic episode. Most require some regular lab work to monitor side effects.
Neither lamotrigine nor topiramate require lab work but must be titrated slowly
according to package insert directions to avoid potentially serious side effects.
Examples are given below:

Carbamazepine (Tegretol). Requires monitoring of white blood cell counts due to risk of
agranulocytosis. Will self-induce its own metabolism and increase the metabolism of other
medications including oral contraceptives.

Divalproex (Depakote). Requires monitoring of liver function tests due to risk of hepatotoxicity
and platelet levels due to risk of thrombocytopenia. Target dosage is 10 times the patient's weight in
pounds.

Lamotrigine (Lamictal). Requires slow titration according to the package insert due to risk of
serious rash.

Topiramate (Topimax). Requires clinical monitoring for glaucoma, sedation, dizziness and
ataxia.

Atypical antipsychotics for PTSD


While originally developed for patients with a psychotic disorder, this class of
medications is being applied to patients with many other psychiatric disorders
including PTSD. They act primarily on the dopaminergic and serotonergic
systems. They can be used when a person with PTSD has a psychotic disorder.
There is some evidence that they are useful in ameliorating psychotic symptoms
in PTSD patients. The real question is whether these medications are useful in
PTSD when psychotic disorder or symptoms are not present.
Previously, a number of small single-site studies suggested that atypical
antipsychotic agents were effective adjunctive treatment for PTSD patients who
had poor responses to first-line SSRIs or SNRIs (18). A recent large-scale multisite trial of risperidone as an adjunctive agent for SSRI poor/partial responders
showed that there was no benefit (in comparison with a placebo group) for
adjunctive use of this agent. As a result the recent VA/DoD PTSD Clinical
Practice Guideline has been revised as follows:

Atypical antipsychotics are not recommended as monotherapy for PTSD.

Risperidone (Risperdal) is contraindicated for use as an adjunctive agent - potential harm (side
effects) exceeds benefits.

There is insufficient evidence to recommend any other atypical antipsychotic as an adjunctive


agent for PTSD.

Other medications for PTSD


There are a number of other medications that can be helpful for specific PTSD
symptoms or that have been used as second line agents including the following:

Prazosin (Minipress)

Tricyclic Antidepressants (such as Imipramine)

Monoamine Oxidase Inhibitors (MAOIs) (such as Phenelzine)

Prazosin has been found to be effective in RCTs in decreasing nightmares in


PTSD. It blocks the noradrenergic stimulation of the alpha 1 receptor. Its
effectiveness for PTSD symptoms other than nightmares has not been
determined at this time (19, 20).
The tricyclic antidepressants and MAOIs act on a number of neurotransmitters.
While there are RCTs supporting their use, these medications are not used as
first line agents due to their safety and side effect profiles (21, 22). The tricyclics
have quinidine like effects on the heart and can cause ventricular arrhythmias
especially in overdose.
The MAOI phenezine has been shown to be effective in PTSD. Careful
management of the MAOIs and strict dietary controls are important because they
can cause potentially fatal hypertensive reactions when taken with other
medications or certain foods rich in tyramine. MAOIs can also provoke the
potentially fatal serotonin syndrome when used concurrently with SSRIs.
Buspirone and beta blockers are sometimes used adjunctively in treatment of
hyperarousal symptoms, though there is little empirical evidence in support of
this. Buspirone acts on serotonin and might reduce anxiety in PTSD without
sedation or addiction. There are some case reports supporting its use. Beta
blockers block the effects of adrenalin (epinephrine) on organs such as the heart,
sweat glands, and muscles. There is interest in using beta blockers to prevent

PTSD, though the evidence at the current time does not support this. Beta
blockers reduce the peripheral manifestations of hyperarousal and may reduce
aggression as well. They may be used for comorbid conditions such as
performance anxiety in the context of social phobia for example.
Benzodiazepines and PTSD
Benzodiazepines act directly on the GABA system which produces a calming
effect on the nervous system. This is the only potentially addictive group of medications
discussed. Studies have not shown them to be useful in PTSD treatment as they
do not work on the core PTSD symptoms (23, 24). There are several other
concerns with the benzodiazepines including potential disinhibition, difficulty
integrating the traumatic experience, interfering with the mental processes
needed to benefit from psychotherapy, and addiction. Because of their potential
for addiction and disinhibition, they must be used with great caution in PTSD.
Examples are listed below:

Lorazepam (Ativan)

Clonazepam (Klonopin)

Alprazolam (Xanax)

Developing new medications for PTSD


The pathophysiological mechanism of PTSD in the nervous system is unknown,
but there are several interesting areas that could lead to new drug development
for the treatment or the prevention of PTSD. There are competing hypotheses
about the role of glucocorticoids following trauma and their effects on the brain. It
might be possible to intervene at some level in the hypothalamic-pituitary-adrenal
axis or at the level of the glucocorticoid receptors in the brain to modulate the
effects of stress and the development of PTSD. Neuropeptides such as
Substance P and Neuropeptide Y (NPY) have been implicated in PTSD as well
(25). Combat troops exposed to stress have been found to have lower levels of
NPY. Perhaps altering this neuromodulator could improve the resiliency of the
brain to the effects of trauma. One challenge with this new focus research is
dealing with the blood-brain barrier for introducing neuropeptides into the brain.

D-cycloserine (DCS) has been used in panic disorder, specifically phobia and
social phobia, to enhance the effects of exposure therapy (26). It is a partial
agonist of the glutamatergic N-methyl-D-aspartate (NMDA) receptor. Based upon
animal research supporting the use of DCS to facilitate extinction of conditioned
fear, it is hypothesized that use of DCS in conjunction with exposure therapy may
reduce the number of psychotherapy sessions required (27). This line of
research recognizes a paradigm shift in the use of pharmacotherapy to assist
learning during psychotherapy as opposed to directly affecting PTSD symptoms
(28).
Memantine (Namenda) is a drug of much interest in preventing
neurodegeneration by protecting against glutamatergic destruction of neurons. It
has been approved for use in certain neurodegenerative conditions such as
Alzheimer's disease. This drug could be potentially useful in preventing
hypothesized neurodegneration in the hypothalamus and memory loss in PTSD.
Current research is looking towards the possibility of one day intervening early in
the course of PTSD with a combination of psychotherapy and pharmacotherapy
that would prevent the development of the pathophysiology of PTSD in the brain.

Common barriers to effective medication treatment in PTSD


There are several common barriers to effective medication treatment for PTSD
which are listed below. These need to be addressed with patients in an ongoing
dialogue with their prescribing clinician. Side effects need to be examined and
discussed, weighing the risks and the benefits of continued medication treatment.
Patient education about the side effects, necessary dosages, duration of
treatment, and taking the medications consistently can improve adherence. A
simple intervention of setting up a pill organizer weekly can go a long way to
improve adherence.

Fear of possible medication side effects including sexual side effects

Feeling medication is a "crutch" and that taking it is a weakness

Fear of becoming addicted to medications

Taking the medication only occasionally when symptoms get severe

Not being sure how to take the medication

Keeping several pill bottles and not remembering when the last dosage was taken

Using "self medication" with alcohol or drugs with prescribed medications

A final word regarding medications and treatment for PTSD


A more comprehensive discussion of pharmacotherapy can be found online in
the VA/DoD PTSD Clinical Practice Guidelines. Based upon current knowledge, most
prescribing clinicians view pharmacotherapy as an important adjunct to the
evidenced based psychotherapies for PTSD. While there are few direct
comparisons of pharmacotherapy and psychotherapy, the greatest benefits of
treatment appear to come from evidenced based therapies such as CPT, PE, and
patients need to be informed of the risks and benefits of the differing treatment
options. When using a combined approach of medication and therapy, it is
important to keep several practices in mind.
If treatment is being provided by a therapist and a prescriber, it is important for
the clinicians to discuss treatment response and to coordinate efforts. It is
important for the prescribing clinician to have an ongoing dialogue with the
patient about their medications and side effects. It is important for the patient to
take an active role in his or her treatment rather than feeling they are a passive
recipient of medications to alleviate their symptoms. There is emerging evidence
that when given a choice, most patients will select psychotherapy treatment for
their PTSD symptoms rather than medications.

Important Considerations

Patients with PTSD or anxiety disorders may be very aware of their somatic reactions, and it is
important to start low and go slow often on dosage adjustments to improve patient adherence.

Be sure to ask female patients of childbearing age about contraception when prescribing
medication.

Be sure to ask all patients about substance abuse as well.

Once mediations are started, it is crucial that the provider remember to discontinue medications
which are not proving efficacious and to simplify the number and types of medications used
whenever possible.

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