C h a p t e r 9
Stress and Adaptation
217
is the removal of the necessity for the individual to
experience an intense emotional response at the time
of the exposure. This change was made because many
individuals, particularly professionals that witness
horrific events, reported feeling nothing at the time
of the event—instead their professional training
“kicked in.”
71
With PTSD, the threat results in a constellation of
symptoms that are experienced as intrusion, avoid-
ance, negative alterations in cognition and mood
associated with the event, and marked alterations
in arousal and reactivity associated with the event.
Intrusion
involves the recurrent involuntary distress-
ing memories or “flashbacks” during waking hours or
nightmares in which the past traumatic event is relived,
often in vivid and frightening detail. In children, there
may be frightening dreams without recognizable con-
tent.
Avoidance
refers to the attempt to avoid situa-
tions, including people, places, activities, and objects
that arouse distressing memories. At least one avoid-
ance symptom must be present for definitive diagnosis
of PTSD.
Negative alterations in cognition and mood
involve an inability to remember an important aspect
of the event (i.e., dissociative amnesia) that is not the
result of a head injury, alcohol, or drugs.
Marked alter-
ations in arousal and reactivity
replace the numbing
symptom in DSM-IV, and it includes inability to expe-
rience positive emotions such as love, joy, pleasure,
or satisfaction. In addition, distorted beliefs regard-
ing blame of self or others about the causes or conse-
quences of the traumatic event may occur. In addition,
irritable and angry outbursts, reckless and destructive
behavior, hypervigilance, problems with concentra-
tion, and sleep disturbances may occur. DSM-5 no
longer includes immediate fear, helplessness, or horror
following the event, as it did not improve diagnostic
accuracy. Diagnosis of PTSD requires that the dura-
tion of disturbance persists for more than a month,
causes clinically significant distress or impairment of
social or other areas of functioning, and is not attrib-
utable to the effects of medication, alcohol, or other
medical condition.
Pathophysiology.
Although the pathophysiology of
PTSD is not completely understood, there is increasing
evidence that the disorder results from an exaggerated
stress response and a failure of the stress response sys-
tem to regain homeostasis. The SNS and the HPA axis
are the major constituents of the body’s neuroendocrine
response to physical and physiological threat and stress.
Normally, the SNS response is brief, followed by an
HPA axis response that serves to reinstate homeostasis
and induces long-lasting adaptive changes that contrib-
ute to stress recovery and resilience. This is mediated by
glucocorticoids (i.e., cortisol), the product of the HPA
axis.
72
Initial research focused on an exaggerated and unre-
lenting extension of the normal sympathetic and HPA
response to the stress associated with the traumatic
event. More recent research has revealed that although
persons with PTSD have been shown to have increased
levels of the SNS activity, they have decreased cortisol
levels and an enhanced negative feedback inhibition of
cortisol release with the dexamethasone (a synthetic
glucocorticoid) suppression test.
72
Cortisol’s circadian
rhythm, which is critically influenced by corticosteroid
function, is altered with the progression of PTSD, sug-
gesting a explanation for sleep disturbances that accom-
pany the disorder.
Although neuroendocrine research suggests that
lower cortisol levels are implicated in the pathophysi-
ology of PTSD, emerging research findings suggest
this may instead reflect pretraumatic stress vulner-
ability, explaining why some people develop the dis-
order and others do not. It has been suggested that
genetic
73,74
and previous environmental/experiential
factors
65,75,76
may predispose to subsequent develop-
ment of PTSD.
In addition to the neuroendocrine changes that occur
with PTSD, neuroanatomic studies have identified alter-
ations in two brain structures (the amygdala and hip-
pocampus) that occur in persons with PTSD. Positron
emission tomography (PET) and functional magnetic
resonance imaging (MRI) have shown increased reac-
tivity of the amygdala and hippocampus and decreased
reactivity of the anterior cingulate and orbitofrontal
areas. These areas of the brain are involved in fear
responses. The hippocampus also functions in memory
processes. Differences in hippocampal function and
memory processes suggest a neuroanatomic basis for the
intrusive recollections and other cognitive problems that
characterize PTSD.
77
Diagnosis and Treatment.
Although originally con-
ceptualized as a mental disorder, PTSD is becoming
increasingly recognized as a highly comorbid condi-
tion, much like hypertension, cardiovascular disease,
chronic fatigue syndrome, fibromyalgia, and other dis-
eases. For a number of reasons, including the stigma
attached to mental illness, limited availability and high
cost of treatment, and socioeconomic issues associ-
ated with the disorder, people with PTSD frequently do
not seek specialized mental health treatment until the
disorder has been present for a considerable amount
of time.
78,79
Initial treatment of PTSD focuses on reducing or
eliminating the symptoms and signs of PTSD and any
trauma-related comorbid conditions. Next, adaptive
functioning must be improved, with an emphasis on
returning the person to a psychological state of safety
and trust. Finally, general treatment approaches focus
on limiting any generalizations of the initial trauma
and protecting the person with PTSD from subse-
quent relapse. Debriefing, or talking about the trau-
matic event at the time it happens, often is an effective
therapeutic tool. Crisis teams are often among the
first people to attend to the emotional needs of those
caught in catastrophic events. Some people may need
continued individual or group therapy. Selective sero-
tonin reuptake inhibitors (SSRIs) are considered the
first-line drug treatment for PTSD. Often concurrent
pharmacotherapy with antidepressant, antianxiety,
