Post Traumatic Stress Disorder:
History, Treatments and the Future of PTSD
Michelle Pryce
Abnormal Psychology
Dr. M. Hanna
December 1, 2009
Post Traumatic Stress Disorder
I.
Introduction
a. Description of the overarching category that PTSD belongs
b. In-depth description of PTSD
i. Similar disorders
ii. What is not PTSD
II.
History of PTSD
a. When was it first diagnosed
b. Historical varieties of PTSD
c. Events that have caused PTSD in different groups of people
III.
Components of the Disorder
A. Biological
B. Psychological
C. Social
IV.
Common treatment approaches to PTSD
a. Pharmacological
b. Non-pharmacological
V.
What is not known about PTSD
Although the name is relatively new, Post Traumatic Stress Disorder (PTSD) has
been around for centuries. It is classified as a type of anxiety disorder, and specifically as
a stress disorder. Anxiety disorders are maladaptive responses to stressors. Anxiety
disorders feature physical, biological, behavioral, and cognitive symptoms. Some of the
symptoms commonly associated with anxiety disorders are: jitteriness, excessive
perspiration, light-headedness or dizziness, difficulty swallowing or breathing, irritability,
avoidant, clingy and/or dependent behavior. Additional thoughts associated with anxiety
disorders include difficulty concentrating, inability to cope with problems, nagging sense
of dread, and constant worrying about something. Although there is a biological
component to anxiety disorders, the biological component is not the cause of the anxiety
disorder, but rather a result of the behavior associated with the disorder. Even though
anxiety disorders tend to run in families, it is generally due to environmental, rather than
genetic factors. Traumatic stress disorders are not adjustment disorders. They are not
reactions to typical life stressors such as work or school problems, relationship problems,
chronic illness, or death of a loved one. Additionally, PTSD is distinguished from Acute
Stress Disorder (ASD) in the fact that ASD occurs immediately after and up to one month
following an exposure to a traumatic stressor. PTSD is a prolonged reaction to a
traumatic stressor. It can last from months to years after the initial traumatic event.
Additionally, PTSD can develop months or years after the initial traumatic event. In
order for PTSD to be diagnosed, an individual must have experienced a “traumatic
stressor in which the person experienced or witnessed an event that involved actual or
threatened death or serious injury, or a threat to the physical integrity of self or others;
and the person’s response involved intense fear, helplessness, or horror” (DSM-IV-TR,
2000, p. 467).
In some way, Sigmund Freud has influenced most areas of modern psychology,
and PTSD is no exception. In Freud’s original model of neurosis, also known as
Seduction Theory, external stressors were emphasized. Around the turn of the century,
Freud shifted his psychiatric model to stress “intrapsychic fantasy” (Wilson, 1994, p.
681) instead of external stressors. Freud’s thoughts emphasized the classification of
PTSD in the earlier editions of the DSM with its labeling as “transient reactive processes”
(Wilson, 1994, p. 681).
PTSD was first labeled as “gross stress reaction” (Andreasen, 2004, p.1321) in the
first Diagnostics Statistical Manual of Mental Disorders (DSM). Prior to this official
label, PTSD symptoms were described in literary classics such as The Red Badge of
Courage and musicals such as Oklahoma (Andreasen, 2004, p.1321). The symptoms of
PTSD, in association with combat related trauma, have been called by several different
names throughout history. In spite of its several name changes, the symptoms associated
with military combat related trauma have remained the same, and primarily include
irritability, inability to forget, and increased mental arousal. Following the United
States’ Civil War, PTSD was called ‘soldier’s heart’. After World War I, it was called
‘combat fatigue’ or ‘shell shock’, due to the use of exploding shells. Immediately
following World War II, it was referred to as ‘battle fatigue’, ‘combat neurosis’, and
‘operational fatigue’ (Grinage, 2003, p. 2401). After the Korean War, PTSD was called
‘gross stress reaction’, and after the Vietnam War, it was called post-Vietnam syndrome.
It was first called post traumatic stress disorder in 1980 in the DSM-III.
Although Gross Stress Reaction appeared in the DSM-I, it was eliminated in the
DSM-II (Andreasen, 2004, p.1321). However, the DSM-II did mention a “transient
situational disturbance” (Wilson, 1994, p. 688). However, research about traumatized
soldiers and civilians continued and the DSM-III named two forms of PTSD—Acute
PTSD and Delayed PTSD (Andreasen, 2003, p. 1322). Acute PTSD was eventually
dropped from the DSM. However, the DSM-IV included a new disorder, Acute Stress
Disorder, which was essentially the same as Acute PTSD (Andreasen, 2003, p. 1322).
ASD and PTSD are both in the current DSM-IV-TR with the onset of stress reaction to a
stressor being the main distinguishing characteristic between the two disorders.
Currently nearly 8 million Americans have some degree of PTSD, and it is
estimated that nearly 8% of Americans will experience symptoms consistent with PTSD
at some point in their lives (Pariser, 2003). This number includes veterans of all military
engagements, survivors of personal assault and rape, as well as survivors of the 1995
Oklahoma City bombing, and the 2001 World Trade Center terrorist attacks. Survivors
of natural disasters such as 2005 Hurricanes Katrina and Rita are also included in this
figure. Children and adolescents are particularly prone to developing PTSD as up to 40%
of children who experience a traumatic event develop PTSD (Pariser, 2003). In addition
to surviving a natural disaster or violence, witnessing the death of a parent or close family
member also contributes to children developing PTSD (Pariser, 2003).
The exact causes of why one person may develop PTSD when confronted with a
traumatic stressor and one does not is not known, but there are several theories that are
being investigated. One such theory is the linkage between migraine and tension
headaches and the development of PTSD. One study cites that 43% of patients with
chronic migraine headaches had symptoms of PTSD (Afari, 1268). Additional limited
research has shown that stress and headache may be linked by “physiologic dysregulation
in multiple systems including the hypothalamic-pituitary-adreanal axis (HPA) and
autonomic nervous sysem. In a recent study surveying Operation Enduring
Freedom/Operation Iraqi Freedom veterans, nearly “60% of participants with chronic
headache met the criteria for being diagnosed with PTSD” (Afari, 2009, p. 1271)
suggesting the possibility that chronic headaches and stress disorder are linked by at least
one of the biochemical pathways.
Another study investigated the possibility of decreased locus coeruleus (LC)
neuron count in brain tissue. The brains of seven male veterans were examined postmortem using neuromorphometry. The number of neurons in the right LC was counted.
Three of the veterans had probable war-related PTSD, three had no psychiatric history,
and one had alcohol dependence. All three veterans with war-related PTSD had
“substantially lower LC neuronal counts compared to the four comparison subjects”
(Bracha, 2005, p. 503).
These results have been compared with other neuronal counts
and it seems as no other illness (psychiatric or somatic) presents with decreased right LC
neuron counts. Although the study was small (n=7), it seems to indicate that some
neurologic change occurs in the brains of people who suffer from PTSD (Bracha, 2005,
p. 506-7).
Another study has shown that “among the various 5-HT receptor subtypes,
alterations in the central 5-HT2A receptor signaling are particularly relevant to the
pathophysiology of stress-related psychiatric syndromes” (Ursano, 2009, p. 4).
Additionally, PET scans of the brain show a decrease in “5-HT2A receptor expression in
the hippocampus, amygdala, and hypothalamus” (Ursano, 2009, p. 5) during periods of
“inescapable stress” (Ursano, 2009, p. 5).
PTSD rarely occurs on its own. It is usually seen with one or more of the
following psychiatric disorders: “depression, social phobia, panic disorder, substanceabuse disorder, and other mood and anxiety disorders” (Feczer, 2009, p. 279).
Additionally, many who eventually develop PTSD have a history of trauma. Among
military veterans the prevalence of PTSD has been estimated “as high as 17%” with the
number increasing to “as high as 52% in veterans who have been previously diagnosed
with at least one mental disorder” (Corso, 2009, p. 119). As such, these other conditions
must be treated, either concurrently or sequentially if PTSD treatment is to be successful.
In some situations, PTSD may be the secondary diagnosis discovered only after initial
treatments fail to respond to therapy. In active duty military personnel only about “10%
of males and 26% of females report mental health symptoms and seek treatment” (Corso,
2009, p.120) for their mental health symptoms, and PTSD is rarely the initial diagnosis
due to the fact that PTSD status can “negatively affect their career” (Corso, 2009, p. 120).
In the case of at least one female veteran, PTSD was not considered as a diagnosis until
“much later in the psychiatric evaluation” when symptoms had stabilized, but the patient
still suffered from combat related rememberings (Feczer, 2009, p. 286).
Several classed of drugs are used in the treatment of PTSD. Some of the classes
include antidepressants, anticonvulsants, antipsychotics, and antiolytics. Other classes of
drugs are used as off-label therapy. These drugs include alpha-2 adrenergics, alpha-1
blockers, antimanics, and benzodiazepines (Coupland, 2009, p. E5). Currently, only two
antidepressants, Paxil and Zoloft, are approved by the FDA for the treatment of PTSD
(McAllister, 2009, p. 1350) Several groups, including the APA, have supported the use
of other SSRIs in the management of PTSD, but the FDA has yet to approve any other
antidepressant for treatment of PTSD (McAllister, 2009, p. 1350). Anticonvulsants are
also used in the treatment of PTSD based on the hypothesis that “re-experiencing
symptoms are caused by mechanisms analogous to models of seizure genesis”
(McAllister, 2009, p. 1352). Glutamine and GABA, both neurotransmitters, appear to
play a role in PTSD and as such, some of the newer anticonvulsants act on the glutamate
and GABA receptor systems (McAllister, 2009, p. 1352).
Antipsychotics are used in conjunction with antidepressants in the management of
PTSD mainly in the management of impulse control and disordered sleep problems
(McAllister, 2009, p. 1353). Since antipsychotics can have severe side effects, these
medications should be assessed for their continued need (McAllister, 2009, p. 1353).
While benzodiazepines are common used in the management of anxiety disorders, they
have not been especially useful in preventing the development of PTSD, nor “the
management of fully developed PTSD” (McAllister, 2009, p. 1355).
Other drug classes are also being investigated for potential usefulness in treating
PTSD. Only small scale clinical trials have been held, and these drugs have not yet been
approved for use by the FDA. These drugs include D-Cycloserine, an antibiotic
developed for use in tuberculosis. D-Cycloserine has “NMDA partial agonist properties”
and interest in its use is due to a “presumed effect on learning and fear extinction through
its modulation of NMDA receptors” (McAllister, 2009, p. 1356). In a small study
(n=11), patients with PTSD showed “modest improvement in the numbing and avoidance
symptom clusters and cognitive measures” (McAllister, 2009, p. 1356). Adrenergic
drugs such as propranolol (beta-2 blocker), prazosin (alpha-1 antagonist), and clonidine
(alpha-2 agonist) have also been used. Since both acute and chronic stress has an effect
on neuron firing, stress has the potential to “increase the efficiency of emotional memory
and fear conditioning through stimulation of beta and alpha-1 adrenergic receptors”
(McAllister, 2009, p. 1356). By mitigating the firing of presynaptic neurons, it is thought
that it can help to control the “pathological remembering” (McAllister, 2009, p. 1356)
that is a key feature of PTSD. Additionally, activation of alpha-2 receptors in the
amygdala helps to reduce the release of catecholamines possibly “dampening fear
condition response and consolidation of emotional memory (McAllister, 2009, p. 1356).
One study has found that beta blockers “reduce the consolidation of traumatic memories”
and alpha-1 antagonists “reduce nightmares associated with PTSD (McAllister, 2009, p.
1357). Another small study showed that patients with combat-related PTSD “showed a
significant improvement in PTSD symptoms” (Ursano, 2009, p. 4) when treated with the
5-HT2A antagonist nefazodone. Additional experiments with animal models seem to
indicate that a 5-HT2A has “prophylactic efficacy in preventing stress-related induced
potentiation of the startle response” (Ursano, 2009, p. 4) Future treatments may include
drugs that block the release of corticotrophin releasing factor thus preventing the stress
response from occurring.
Cognitive behavioral therapy (CBT), exposure therapy (flooding), group therapy,
family therapy, and eye movement desensitization and reprocessing (EMDR) are also use
in conjunction with medication when treating PTSD. With CBT, sufferers are taught to
correct the behaviors and thoughts associated with PTSD. Techniques generally include
relaxation techniques, effective communication skills, coping with anger, and if
necessary, eliminating substance dependence and managing anger. Depression is also
treated if it is also recognized as a problem.
Despite other therapies claiming to have a higher success rate, cognitive behavior
therapy remains the gold standard for treating patients with PTSD. One study suggests
that CBT has success rates ranging from “21 to 46 percent” (Grinage, 2003, p. 2405)
while another study claimed success rate of “32 to 53 percent” (Grinage, 2003, p. 2406).
Approximately, “14 percent of patient with PTSD discontinue therapy” (Grinage, 2003,
p. 2406); the highest attrition rates are attributed to exposure therapy.
Exposure therapy, also known as flooding, involves exposing the patient to
images, places, or thoughts for increasing amounts of time in a safe environment until the
patient no longer registers a stress response. Exposure therapy is opposite of the natural
human response to avoid situations that are uncomfortable and cause a stress response. It
is thought that through repeated exposure to previously traumatic situations, a patient will
be able to resume functioning at the same level prior to the traumatic event. One
drawback of exposure therapy is that it has the highest attrition rate (“up to 50 percent”)
(Grinage, 2003, p. 2406) of all of the therapies, probably due to the uncomfortable
feelings brought up prior to reaching the no response stage.
Group and family therapy are therapies that involve people other than the patient
in the healing process. Group therapy involves one therapist working with several people
who have experienced similar situations and are facing similar symptoms. It is based on
the principle that others can serve to reduce isolation and be empathetic to a particular
situation.
Family therapy involves treating the entire family. Patient with PTSD may not
know how to relate to close relatives and/or friends after the traumatic experience so it
provides assistance for relatives to learn how to cope and manage the person after a
traumatic experience has occurred.
EMDR is a cost-effective way of treating some patients that suffer from PTSD. It
is currently recommend by several insurance companies and organizations including the
“American Psychiatric Association and the Department of Veteran Affairs and
Department of Defense” (Salvatore, 2009, p. 153). Studies available comparing EMDR
to other treatment including cognitive therapy and treatment with Prozac indicates that
“the effectiveness of EMDR equals or exceeds other PTSD treatments, and is generally
faster (Salvatore, 2009, p. 153). Another study, conducted by the Veteran Affairs,
demonstrated “that EMDR successfully relieves phantom limb pain (Salvatore, 2009, p.
153), and a separate study of veterans with PTSD claimed that “12 sessions of EMDR
relieved the symptoms in 77% of veterans” (Salvatore, 2009, p. 154).
One of the stated advantages of using EMDR is that patients with PTSD do not
have to talk about the experiences that caused the symptoms of PTSD—in fact, “talking
too much actually gets in the way and takes the patient out of the healing process”
(Salvatore, 2009, p. 154). Another advantage of EMDR is that different types of
clinicians can be trained in its protocols. In addition to psychiatrists and medical doctors,
social workers and case managers can be taught how to effectively use EMDR for the
treatment of non-combat related trauma. According to at least one practitioner of EMDR,
EMDR “could save them (veterans) and their families from years of suffering. We could
save taxpayers hundreds of millions of dollars in disability payment and medicals costs,
which could accrue for the next 60 or more years” (Salvatore, 2009, p. 154).
The amount of research, both clinical and basic science, being conducted on
PTSD is increasing almost daily. Animal studies involving the stress response are being
applied to PTSD, and clinical information from PTSD patients is being used to conduct
more scientific research. Post-mortem brain tissue analysis is being conducted at some
research intuitions in order to look at mitochondrial genes. Scientists know that
“mitochondrial dysfunctions are increasingly recognized as key components in stressrelated mental disorders” (Ursano, 2009, p. 6-7). Unfortunately, the coming years will
give scientists and clinicians plenty of opportunity to study PTSD. First of all, there is an
increasing veteran population. Females and National Guard members are serving in the
military in higher numbers. The tour of duty duration has increased both in length and
number. It is now common for units to be deployed on more than one occasion.
Additionally, medically technology has advanced to the point where more soldiers are
surviving previously catastrophic injuries. Terrorist attacks, both foreign and domestic,
have become increasingly more frequent, and there is currently less stigma associated
with PTSD than there has been in previous years.
Testing similar to cardiac stress tests is currently being developed with the hope
that it can be applied to people at risk for developing PTSD.
Some of the hopes are that
“a definition of ‘normal’ functioning during stress” could be developed and baseline for
“cognitive psychological and physical responses” could be established.
There are still several avenues for exploration in treating PTSD.
Pharmacological research is continuing and new drugs are being tested constantly. Basic
science research continues on animal model to establish a definitive pathophysiology for
PTSD. Clinical observations are being made constantly, and treatment approaches are
being modified based on what is effective and what is not. PTSD can be a debilitative
disorder, but it doesn’t have to be. Education of patients, clinicians, and the general
population can help to reduce the stigma associated with seeking help for PTSD, and with
the right combination of therapies, PTSD can be successfully treated in the majority of
cases.
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Feczer, D., & Bjorklund, P. (2009). Forever Changed: Posttraumatic Stress Disorder
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