The information that follows is part of
an outline for a talk delivered by Dr. Lilly at Grand Rounds
for Maine Medical Center. It represents a review
of some of the available empirical literature on treatment
for PTSD. While we believe that an individual
practitioner's evaluation and judgment is essential in
shaping treatment, we hope that the following information
will be helpful.
RESEARCH-BASED
TREATMENT FOR
POSTTRAUMATIC
STRESS DISORDER (PTSD)
Summary:
Early referral for
treatment improves outcome rates.
While exposure to a traumatic incident does not
result in PTSD for most people, screening and education
regarding early intervention may be a good idea.
Severity of initial
symptoms, peritraumatic dissociation, elevated heart rate,
and type of trauma (e.g., sexual assault, MVA) may offer
particular indications that early referral is a good idea.
-Preliminary findings are that the early intervention (48hrs – 2 weeks) of choice may be a modification of
Foa’s protocol for Prolonged Exposure (initial findings: 90-92% of treated group was PTSD-free, vs. 26-
30% of control group, which was either untreated or got supportive counseling). This treatment also
markedly reduced incidence of depression.
If PTSD symptoms haven’t
resolved by 3-6 months, they are unlikely to spontaneously
remit and treatment is indicated:
-Psychosocial treatment of
choice is Foa’s protocol for Prolonged Exposure
(generally, 75% of participants
have >70% reduction in symptoms; low relapse
rate). Stress Inoculation Training may provide a
good
second alternative.
-It appears that medication
of choice is Zoloft (53-63% of participants have >30%
reduction in symptoms;
relapse rate may be high once medication is
discontinued)
For people with pervasive
dysfunction and/or high comorbidity or risk, Prolonged
Exposure may not be appropriate.
Treatment including multiple modalities such as
medication, psychotherapy, family therapy, and
rehabilitation therapy may be preferable.
INCIDENCE AND
PREVALENCE
In
a given year, more than 10 million people (about 4% of the
U.S. population) experience PTSD symptoms severe enough to disrupt their daily functioning.
q
PTSD
affects from 9-15% of the general population (lifetime)
and close to 50% of women who have been raped (Foa &
Rothbaum, 1998)
q
Lifetime
prevalence rates are twice as high for women as for men (Foa
et al., 2000).
Citing
the 1996 U.S. National Comorbidity Study, McFarlane (1997)
notes that:
q
The
most common causes of PTSD for women are rape and sexual
molestation (48.4% of rape survivors developed PTSD)
o
Sexual assault leads to the highest rates of PTSD
q
The
most common causes of PTSD for men are combat and witnessing
death or severe injury (10.7% of men who witnessed serious
death or injury developed PTSD)
q
60.3%
of men and 50.3% of women have experienced other traumas
sufficient to meet Criterion A-1 of the diagnosis (see p.3)
q
Motor
vehicle accidents result in the most adverse combination of
frequency and impact.
Risk
factors for PTSD (Halligan et al., 2000)
q
Peritraumatic dissociation is one of the best
predictors of PTSD
at six months, explaining 30% of variance
q
Prior
exposure to trauma or chronic stress, especially if
experienced at a young age
q
History
of prior assault
q
Social
factors such as family instability may increase risk, and
social support may decrease risk
q
Lower
levels of education and income
q
Being
widowed or divorced
q
Poor
coping skills, possible related to prior substance abuse,
anxiety, or depression (although note that this finding has
been contested in other research)
q
Low
intellectual functioning
q
Higher
heart rate following trauma
q
Low
cortisol
Comorbidity:
q
U.S.
epidemiological findings indicate that 80% of people with
lifetime PTSD suffer from lifetime depression, another
anxiety disorder, or chemical abuse/dependency (Foa et
al., 2000)
q
Lifetime
prevalence rates of alcohol abuse/dependence among men
and women with PTSD are about 52% and 28% respectively, and
current prevalence rates for drug abuse/dependence are 35%
and 27% respectively (Foa et al., 2000)
q
Trauma
survivors report more medical symptoms, use more medical
services, have more medical illnesses detected during
physical examinations, and display higher mortality (Foa
et al., 2000).
o
Those
with PTSD are more likely to have significant health
problems such as hypertension, bronchial asthma, peptic
ulcer, and GI problems.
They also have increased rates of surgery and doctor
visits
q
work,
marital, and family problems more common (Foa & Rothbaum,
1998)
POSTTRAUMATIC
STRESS DISORDER (PTSD)
AS
A DIAGNOTIC ENTITY
The three clusters of Sx (re-experiencing, numbing/avoidance, and arousal) that are currently used were derived by clinical observation rather than research (Foa & Rothbaum, 1998).
Subsequent factor analytic research has found that numbing and avoidance actually belong to different clusters (Foa et al., 1995).
q
Foa
& Rothbaum (1998) indicate that this distinction is not
just a matter of statistical niceties.
They suggest that effortful avoidance and numbing
are two separate mechanisms (strategic versus more
biological) (Foa & Rothbaum, 1998)
q
Factors
of increased irritability and anger belong with numbing
(Foa & Rothbaum, 1998)
o
Prominent
anger correlates with poorer treatment outcome in the
available research, and theorists have suggested that anger
may be used to inhibit or avoid symptoms of anxiety and thus
prevent habituation upon exposure to a feared stimulus
(Riggs et al., 1995)
Some of the DSM symptoms of PTSD appear to be particularly useful in distinguishing it from other disorders:
q
flashbacks and nightmares are unique to PTSD
(McFarlane, 1998b)
q
very
few people without PTSD endorse numbing symptoms (Foa
& Rothbaum, 1998)
Although
the DSM indicates that “delayed onset” should be noted,
research so far has found that there is not much
empirical support for “delayed onset” categorization
of PTSD. What
reports there are of delayed onset PTSD in published studies
have been anecdotal and retrospective (Foa & Rothbaum,
1998).
LONGITUDINAL
COURSE OF PTSD
Immediately
following a trauma (within a day or so) 95% of people met
PTSD Sx criteria (except duration; Foa & Rothbaum,
1998). Some
studies have examined the percentage of people whose
symptoms remit following a traumatic event.
Rothbaum et al. (1992) examined women who survived a
sexual assault and found that a gradually decreasing
percentage of them continued to keep a PTSD diagnosis as
time passed:
2 weeks: 94% meet criteria (excluding duration criteria)
1 month: 65%
2 months: 52.3%
3 months: 47%
6 months: 41.7%
9 months: 47.1%
q
These
statistics are similar to remission patterns for people with
non-sex assault related PTSD, although the initial rates of
PTSD are lower (initial 71% women and 50% men).
Note
that spontaneous remission rates flatten considerably at
about 3-6 months:
q
Prospective
studies suggest that by 3-4 months post trauma and
definitely by 6-8 months post trauma, the course of PTSD has
become chronic and can no longer be expected to go away
as a “normal” reaction to trauma might (Foa &
Rothbaum, 1998)
q
McFarlane
(1998): 69% of firefighters who had PTSD at 4 months
post-trauma continued to still have PTSD later
People
with more severe initial PTSD Sx were more likely to have
more persistent reactions
(Foa & Rothbaum, 1998)
The
prominence of intrusive symptoms decreases over time,
whereas avoidant symptoms increase (McFarlane, 1997)
BIOLOGICAL
THEORY & FINDINGS
q
HPA Axis Dyregulaton: Based on neurobiological
evidence that uncontrolled life-threatening trauma effects
the opiate and neuropeptidergic systems, HPA axis, and
autonomic nervous system
o
“Rather
than the classic profile of increased adrenocortical
activity and resultant dysregulation of this system
described in studies of stress and other psychiatric
disorders, trauma survivors with PTSD show evidence of a highly
sensitized HPA axis characterized by decreased basal
cortisol levels and increased negative feedback
regulation” (Yehuda 1997, p.57)
§
During
stress, neuropeptides in the brain cause the release of
corticotropin releasing factor (CRF) from the hypothalamus,
which initiates the release of adrenocoricotropic hormone
(ACTH) from the pituitary and cortisol from the adrenals.
§
Cortisol
is supposed to stop neural defensive reactions that have
been activated by stress
§
Cortisol
is usually markedly elevated in most types of stress as well
as in depression. However,
basal cortisol levels are low with PTSD
§
Glucocorticoid receptor densities are higher (upregulated)
in PTSD; chronic increases in hypothalamic CRF leads to
decreased responsivity of the pituitary to CRF
o
Animal
studies have found that stress can damage the hippocampus,
and there is some evidence that people with PTSD, overall,
tend to have reduced hippocampal volume (Pitman,
1997). Several
different explanations have been posited for this finding:
§
Repeated
exposure to high levels of cortisol that happen as a
response to exposure to stressors damages the hippocampus
§
People
with PTSD may have reduce hippocampal volume before the
trauma, and this trait serves as a vulnerability to PTSD
§
High
alcohol abuse rates in people with PTSD is common and there
is evidence suggesting that alcohol may preferentially
damage the hippocampus.
q
Kindling/Sensitization: repeated presentation of a
sub threshold stimulus can “kindle” limbic circuits,
producing a lower threshold of firing.
Sensitization is the similar concept that brief
exposure to a single or repeated stimulus may sensitize
animals to stressors of lower intensity (Foa &
Rothbaum, 1998)
q
Inescapable Shock: accompanied by initial mobilization of
catecholamines (norepinephrine and dopamine) followed by
their depletion (Foa & Rothbaum, 1998)
o
Suggested
that intrusive and avoidant symptoms correspond to
hypersensitivity to catecholamines
o
Drugs
that stimulate or down regulate the locus coeruleus (noradrenergically
rich “alarm center”) provoke or inhibit PTSD Sx in
combat vets with PTSD
o
Findings
regarding inescapable shock and opioids: “First,
inescapable shock leads to a more durable analgesia than
does escapable shock. Second, the analgesia produced by
extensive inescapable shock is mediated by opioids to a
greater extent than analgesia produced by escapable shock.
Third, inescapable shock leads to a sensitization of
the opiod system, so that it facilitates the production of
future opiod-mediated analgesia” (Foa et al., 1992).
o
Behaviorally,
also recall Seligman’s experiments with inescapable shock
resulting in “learned helplessness” and deficits in
learning active escape behaviors and enhancements in passive
avoidance
q
Conditioned
avoidance
may be mediated serotonergically by pathways arising in the
dorsal raphe and projecting to the amygdala (Foa &
Rothbaum, 1998)
BEHAVIORAL AND
COGNITIVE THEORIES
q
Mowrer’s Two Factor Theory (see Falls & Davis, 1995 for
an excellent summary)
o
Step
1: Classical Conditioning.
§
Unconditioned
stimulus (threat to life or well being) results in
unconditioned response (fear).
Intensity of UCS-UCR pairing is strong enough for
single trial learning. (Example:
car crash results in person fearing for their life)
§
Previously
neutral stimuli associated with the US become conditioned,
and evoke a conditioned emotional response (CER).
(Example:
the intersection where the crash occurred evokes fear,
hearing screeching tires evokes fear)
§
Other,
previously neutral stimuli come become associated with a CER
through generalization and second order conditioning (Example: all intersections
evoke fear; going to get in a car or thinking about driving
evokes fear)
o
Step
2: Operant Conditioning.
§
The
person learns to act in ways (conditioned response) that
help them avoid the things they have learned to fear
(conditioned stimuli).
(Example: by not getting in a
car, the person avoids the anxiety associated with going
through intersections)
§
Through
operant conditioning, the person learns increasingly
sophisticated avoidance responses.
This avoidance results in negative reinforcement
(e.g., since avoidance temporarily reduces anxiety, it is
processed as being a good thing to do and the habit of
avoidance is strengthened, as is the idea that the stimulus
being avoided is dangerous. (Example:
fear of getting in a car increases)
§
Since
the person does not get experience in learning that the CS
is not necessarily associated with UCS, s/he does not learn
that her or his conditioned responses may be excessive (Example: since the person never gets in a car, s/he
never learns through new experiences that cars are not
always dangerous)
o
Extinction/habituation
occurs when person confronts situations, thoughts, feelings,
or memories without the UCS occurring (Example: the person is confronted with a feared
stimulus, either through imaginal exposure or riding in a
car, for prolonged periods of time until their anxiety
decreases. Through
this process they are repeatedly exposed to experiences that
show that being in a car does not always mean that they are
going to be in a crash)
q
Lang’s
(1979) Bioinformational Theory of Emotion
o
Fear
is viewed as a multisystemic information and response
structure
o “Propositional representations” include information about the feared stimulus, verbal, physiological, and overt behavioral responses, and interpretive information about the meaning of the stimulus and response element
q
Emotional
Processing Theory (Foa and Kozak, 1986)
o
Integrates
learning, cognitive, and personality theories
o
Adds
to Lang the concept that it is the meaning that people
attach to information that distinguishes the fear structure
from other information structures
o
Posits
that problem is abnormal association between stimuli and
responses, and fear reduction is from dissociating those S-R
connections or increasing impact of discriminative stimuli (Foa
and Kozak, 1986)
o
“Two
conditions are required for the reduction of fear. First, fear-relevant information must be
available in a manner that will activate the fear memory. .
. Next, information made available must include elements
that are incompatible with some of those that exist in the
fear structure, so that a new memory can be formed. This new information, which is at once
cognitive and affective, has to be integrated into the
evoked information structure for an emotional change to
occur” (Foa and Kozak, 1986).
q
“Shattered Assumptions” (Janoff-Bulman,
1992)
o
Traumatic
events are so disruptive that it is difficult for people to
“assimilate” them into their existing schemata about the
world, others, and what they can expect in life.
Therefore, the traumatic experience forces them to
“accommodate” a new way of understanding the world that
no longer assumes that one is safe, etc.
o
Core
beliefs that the world is benign, the world is meaningful,
the self if worthy, and that people are trustworthy violated
CONTROLLED
RESEARCH ON TREATMENT EFFICACY:
Conclusion
of the International Society for Traumatic Stress Studies
Treatment
Guidelines Task Force:
“Comparing
the numbers and types of studies supporting each type of
treatment EX [Prolonged Exposure] has the most studies and
the greatest number of well-controlled studies to support
its use. EX
has been tested in 12 studies, all finding positive
results for this treatment with PTSD.
These are also generally methodologically
controlled studies, eight of which received the AHCPT
Level A rating, with many meeting many of the gold
standards for clinical outcome studies (Foa & Meadows,
1997); thus the strength of evidence for EX is very
conclusive. In
one study, EX was superior to SIT and SIT/PE.
Additionally, EX has been tested in a wider range
of trauma populations and more studies than any of the
other treatments. Thus,
we strongly recommend the use of some form of EX in the
treatment of PTSD unless otherwise indicated.
In conclusion, the evidence is very compelling from
many well-controlled trials with a mixed variety of trauma
survivors that EX is effective.
In fact, no other treatment modality has such
strong evidence for its efficacy. . . EX has received the
strongest evidence for PTSD; thus, it should be considered
the first line treatment unless reasons exist for ruling
it out” (Foa
et al., 2000).
Psychosocial Treatments PTSD That Have Been Studied Through Controlled Clinical Trials (Foa et al., 2000; Foa & Rothbaum, 1998) |
|
|
Prolonged
Exposure (PE - Foa) |
12
empirical studies, 8 of which were “gold
standard.” Generally, about 75% of participants
had at least a 70% reduction in symptoms within the
9-12 session protocol.
Low relapse rates, and some indications that
participants continue to improve after therapy is
over. Treatment
involves relaxation followed by structured, imaginal
reexposure and in vivo exposure exercises.
“No other treatment modality has such strong
evidence for its efficacy” (ISTSS Treatment
Guidelines Task Force).
(9-12 sessions) |
|
Stress
Inoculation Training (SIT - Meichenbaum) |
4
Studies, 2 of which were very well controlled. Support and findings similar to, but
not as strong as, those for PE, but they take a
firm second place. Treatment has several components,
including relaxation, skills training, and exposure.
(9-12 sessions) |
|
Combined
PE and SIT |
1
well-controlled study.
Findings are that a combination of SIT and
PE are as effective, but not more effective that
either component alone. |
|
Cognitive
Processing Therapy (CPT – Resick) |
1-2
studies (although more in the pipeline).
Preliminary findings have shown promise, but
more research is needed.
(9-12 sessions) |
|
Cognitive
Therapy |
2
well controlled studies demonstrating efficacy. Evidence is considered preliminary by
many researchers, however. |
|
Systematic
Desensitization (SD - Wolpe) |
6
studies that were not well controlled.
Outcomes have not given strong support to
efficacy. Generally
abandoned in favor of PE since opinion seems to be
that the intermittent relaxation element of SD
prolongs treatment but does not enhance effectiveness. (9-12 sessions) |
|
Assertiveness
Training |
One
study, not well controlled.
Not significantly different from comparison
treatments. |
|
Biofeedback
and Relaxation Training |
One
study for biofeedback and several for relaxation. Findings indicate that they are less
effective than comparison treatments. |
|
Eye
Movement Desensitization and Reprocessing (EMDR) |
Proponents
have made remarkable claims, but these claims have not
been supported by controlled research trials.
Probably more effective than placebo or
non-specific therapy, but most studies have not been
well designed (e.g., no standardized measures, not
“blind,” etc.).
Strong preliminary evidence that eye movements
are not necessary, leaving a protocol that bears some
similarity to exposure-based treatment. |
|
Unfortunately,
there are no studies that systematically examine the
value of combining psychotherapy with medication or
combinations of medications. Psychodynamic
approaches, creative therapy, and marital therapy have
not been examined using well-controlled research.
Available studies have found that they do not
appear to show efficacy in treating PTSD.
Research on psychoanalytic psychotherapy is
similar, with one study reporting iatrogenic effects. |
|
Psychosocial Interventions Initiated from 48 hrs to 2 weeks Following a Trauma |
|
|
Abbreviated
Variant of Prolonged Exposure |
2
studies available, and findings are preliminary.
However, initial findings suggest that there
may be promise: 90-92% of treated group was
PTSD-free, vs. 26-30% of control group (which was
either untreated or got supportive counseling).
Also markedly reduced incidence of depression. |
|
Critical
Incident Stress Debriefing (CISD) & variants |
Few
controlled studies.
Of available information, there is no support
that CISD prevents PTSD, and there have been some
results that point to the possibility of harm. Before considering CISD consider risks
carefully, given that there are few benefits and
preliminary data on risk of harm.
That said, even if CISD is not appropriate,
some form of early education, screening, and support
is likely to be helpful.
|
Pharmacological Treatments PTSD That Have Been Studied Through Controlled Clinical Trials (Foa et al., 2000; Foa & Rothbaum, 1998)(Please note: The following information has been taken from standard references. We are not psychiatrists, and intend only to offer a sampling of information from available published research.) |
|
SSRIs
|
Large,
double blind trials have led to recent FDA approval
for sertraline (Level A quality studies –
well controlled).
Responder rate of 53% for sertraline
(compared to 32% for placebo).
Criterion for categorizing successful response
was a 30% decrease in Sx from baseline.
(Brady et al. date?).
Davidson et al. (1997) found 43% response with
sertraline compared with 27% placebo.
Only one small, randomized clinical trial with
Fluoxetine (Van der Kolk got 25.4% reduction on CAPS
vs 12.6% placebo; for non-vets in the study, 41.1 vs
20.3% response).
SSRIs have a broad spectrum of action on
re-experiencing, avoidance/numbing, and hyperarousal
(some have found just an effect on numbing and
hyperarousal) (Friedman, 2000) |
|
MAOIs |
Fewer
trials, and those that do exist have not been
well-controlled (Level B quality study).
Some indications that they may be effective for
cluster B symptoms. |
TCAs
|
The
few available studies indicate TCAs may have a similar
spectrum of action as MAOIs, but overall appear less
effective (Level A quality study – well controlled).
Friedman’s (2000) review of available
research found possible positive results with
imipramine, mild to moderate with amitriptyline,
and negative effects with desipramine.
Positive results for early intervention using
imipramine for pediatric burn patients with ASD
(Friedman, 2000) |
Anticonvulsants
|
Tested
on open clinical trials, but no randomized control
trials. May
reduce cluster D symptoms.
Carbamazepine may reduce cluster B symptoms,
and valproate may reduce cluster C symptoms. |
Benzodiazepines
|
Friedman
(2000) states that most trials with alprazolam have
shown negative results.
Random assignment double blind cross over with
alprazolam: symptoms specific to PTSD were not altered
by alprazolam (Braun et al. 1990).
However, there are also Level B trial for
alprazolam and Level C for Clonazepam indicating that
they may reduce arousal. Indications that alprazolam use during
exposure therapy for panic disorder results in much
higher relapse rates than would be expected for
exposure therapy alone.
May have implications for PTSD. |
|
Other
Serotonergic Agents |
Preliminary
indications from open label trials that nefazodone may
reduce anger and improve sleep.
Trazodone may be helpful as an adjunct to SRIs
by reversing SRI-induced insomnia |
|
Antipsychotics |
Only
clinical anecdotes for evidence.
|
|
Regrettably,
current research has found that most forms of
pharmacotherapy for PTSD leave patients with
significant symptoms. Placebo
response rates relatively low for PTSD (20%) compared
with MDD and Panic. |
|
REFERENCES
American
Psychiatric Association (1994). Diagnostic and
Statistical Manual of Mental Disorders. (4th
ed.). Washington
D.C.: Author.
Brady,
K., Pearlstein, T., Asnis, G.M., Baker, D., Rothbaum, B.,
Sikes, C.R., Farfel, G.M. (date?). “Double blind,
placebo-controlled study of the efficacy and safety of
sertraline treatment of posttraumatic stress disorder.”
Journal of the American Medical Association.
Braun,
P., Greenberg, D., Dasberg, H., Lerer, B. (1990). “Core
symptoms of posttraumatic stress disorder unimproved by
alprazolam treatment.” Journal of Clinical Psychiatry,
51, 236-238.
Davidson,
J.R.T., Londborg, P.D., Pearlstein, T., Weisler, R., Sikes,
C., & Farfel, G.M. (1997). “Double-blind comparison of
sertraline and placebo in patients with posttraumatic stress
disorder (PTSD).” American College of
Neuropsychopharmacology Abstracts, 36th Annual
Meeting, 147.
Falls,
W.A. & David, M. (1995).
“Behavioral and physiological analysis of fear
inhibitions: Extinction and conditioned inhibition.
In (Eds. Friedman, M.J., Charney, D.S., & Deutch,
A.Y.) Neurobiolgical and Clinical Consequences of Stress:
From Normal Adaptation to PTSD.
Philadelphia: Lippincott-Raven Publishers.
Foa,
E.B., Zinbarg, R., & Rothbaum, B.O. (1992).
“Uncontrollability and unpredictability in post-traumatic
stress disorder: An animal model.
Psychological Bulletin, 112, 218-238.
Foa,
E.B., Keane, T.M., & Friedman, M.J. (2000).
“Guidelines for Treatment of PTSD.” Journal
of Traumatic Stress, 13, 539-589.
Foa,
E.B. & Kozak, M.J. (1986). “Emotional processing of
fear: Exposure to corrective information.”
Psychological Bulletin, 99, 20-35.
Foa,
E.B., Riggs, D.S., & Gershuny, B.S. (1995). “Arousal,
numbing, and intrusion: Symptom structure of PTSD following
assault.” American
Journal of Psychiatry, 152(1), 116-120.
Foa,
E.B. & Rothbaum, B.O. (1998) Treating the Trauma of
Rape: Cognitive-behavioral therapy for PTSD.
New
York: The Guilford Press.
Friedman,
M. (2000) “A guide to the literature on pharmacotherapy
for PTSD.” PTSD
Research Quarterly, 11, 1-8.
Halligan,
S.L., Yehuda, R. (2000). “Risk Factors for PTSD.” PTSD
Research Quarterly, 11, 1-8.
Janoff-Bulman,
R. (1992). Shattered Assumptions: Towards a New
Psychology of Trauma. New
York: The Free Press.
Lang,
A.J., Craske, M.G., & Bjork, R.A. (1999).
“Implications of a new theory of disuse for the treatment
of emotional disorders.” Clinical Psychology: Science &
Practice, 6, 80-94).
Lang,
P.J. (1978). “A bio-informational theory of emotional
imagery.” Presidential
address delivered to the Society for Psychophysiological
Research, 18th meeting, Madison, WI.
McFarlane, A.C. (1997). “The
prevalence and longitudinal course of PTSD.” In Yehuda, R.
& McFarlane, M.C. (Eds.) The Psychobiology of
Posttraumatic Stress Disorder. New York: The New York Academy of
Sciences.
McFarlane,
A.C. (1998a). “The
longitudinal course of posttraumatic morbidity: the range of
outcomes and their predictors.”
Journal of Nervous and Mental Disease, 176,
30-39.
McFarlane,
A.C. (1988b). “The phenomenology of posttraumatic stress
following a natural disaster.” Journal of Nervous and
Mental Disease, 176, 22-29.
Meichenbaum,
D. (1994). A
Clinical Handbook/Practical Therapist Manual for Assessing
and Treating Adults with Post-Traumatic Stress Disorder
(PTSD). Waterloo,
Ontario: Institute Press.
Mohlman,
J. & Zinbarg, R. (2000). “What kind of attention is
necessary for fear reduction?
An empirical test of the emotional processing
model.” Behavior Therapy, 31, 113-133.
Pitman,
R.K. (1997). “Overview of biological themes in PTSD.” In
Psychobiology of Posttraumatic Stress Disorder. In
Yehuda, R. & McFarlane, A.C. (Eds.) New York: The New
York Academy of Sciences.
Riggs,
D.S., Rothbaum, B.O., & Foa, E.B. (1995). “A
prospective examination of symptoms of post-traumatic stress
disorder in victims of non-sexual assault.”
Journal of Interpersonal Violence, 2, 201-214.
Rothbaum,
B.O., Foa, E.B., Riggs, D., Murdock, T., & Walsh, W.
(1992). “A prospective examination of post-traumatic
stress disorder in rape victims.”
Journal of Traumatic Stress, 5, 455-475.
Yehuda,
R. (1997). “Sensitization of the
hypothalamic-pituitary-adrenal axis in posttraumatic stress
disorder.” In Yehuda, R. & McFarlane, A.C. (Eds.) Psychobiology
of Posttraumatic Stress Disorder. New York: The New York Academy of
Sciences.