Abstract
Post traumatic stress disorder has two stages; acute and chronic.
In the chronic stage there are many physical, biological, and neurological
changes that need to be recognized and treated. There may also be
a correlation between certain personality traits in victims and the development
of PTSD after a traumatic event. Two studies will be examined, one
correlating responses with personality traits and the other examining important
information on the central nervous system.
Post Traumatic Stress Disorder
Biological Effects
People are effected biologically in different
ways. The brainstem / hypothalamus, the limbic system, and the neocortex
control many regulatory functions, such as, rest, sleeping, activity, feeding
and the reproductive cycle. They also monitor and assess what is
new, dangerous, or gratifying. The limbic system maintains and guides
the emotions and behavior necessary for self-preservation and survival.
Signals are sent continuously to the thalamus from the sensory organs.
They are distributed to the cortex, to the basal ganglia, and to the limbic
system. (Van der Kolk, B., McFarlane, A., Weisaeth, L., 1996).
People with PTSD cannot integrate the memories
of the trauma properly. Memory is affected when endogenous stress
hormones are released during extreme stress. Amnesia seen in PTSD
is likely to be caused by excessive norepinephrine (NE) or vasopression
release at the time of the trauma. Memories of the trauma can also
be triggered by physiological arousal. They tend to relive the past and
misinterpret innocuous stimuli as potential threats. They are also
more sensitive to sounds. Neutralizing stimuli in the environment
to attend to relevant tasks is very difficult. Instead they tend
to shut down in order to compensate. This leads to decreased involvement
in ordinary, everyday life (Van der Kolk, B., McFarlane, A., Weisaeth,
L., 1996).
PTSD has been associated with a number
of biological changes in the body, which have been examined in numerous
studies. One study measured the electodermal responses of veterans
to olfactory stimulants. This study concluded that dysfunctional cerebral
laternalisation may be responsible for some of the PTSD symptoms, such
as hypervigilance, intrusive images, and psychological numbing. PTSD
changes and chronic stress have been compared due to similarities or possible
correlation (Brende, 1982). The increase in glucocorticoid release from
the adrenal glands may lead to loss of hippocampal granule cells and the
production of complex biphasic responses which either enhances or decreases
the hippocampal function (Ver Ellen, P., & Van Kammen, D., 1990).
The hippocampal plays a critical part in learning and memory. Impairments
in these areas may appear under extreme stress. The temporal lobe,
amygdala, and hippocampus effect the deficits between learning and memory
(Bemner, J., Southwick, S., Charney, D., 1991). Information is processed
by all areas of the sensory association cortex and from the motor association
cortex of the frontal lobe. The amygdala also sends information concerning
odors and dangerous stimuli to the hippocampal complex (Carlson, N., 1999;
Bremner, J., Southwick, S., Charney, D., 1991). Hippocampus anatomically
adjacent to the amygdala records in memory the spatial and temporal dimensions
of experience. It functions in the categorization and storage of
incoming stimuli in memory. The hippocampus is very important for
short-term memory (Ver Ellen, P., & Van Kammen, D., 1990). Therefore
a decrease would lower these senses and an increase would keep the person
on alert most of the time.
Chronic physiological arousal with failure
to regulate autonomic reactions to internal and external stimuli, affect
people’s ability to utilize emotions as signals. Emotions are used
to alert people to pay attention to their surroundings and take adaptive
measures. The emotional response stops when the expectation of what
is supposed to happen is happening causing the person to take action or
change their expectations to adapt to the situation. People, who
suffer with PTSD display action following the emotional arousal that is
often interrupted or disconnected from each other. The arousal is
not used as a cue to pay attention to incoming information. Instead,
they immediately go from stimulus to response without first figuring out
what is going on. They are more likely to respond with fight – or
– flight reactions. This may cause them to freeze, or overreact and
intimidate others in response to minor provocations. This may create
extreme feelings of anger and helplessness similar as those felt during
the trauma, and like the other traumatic memories, these feelings are often
avoided (Van der Kolk, B., McFarlane, A., Weisaeth, L., 1996).
Many studies have confirmed people with
PTSD suffer from increased physiological arousal in response to sounds,
images, and thoughts related to specific traumatic incident. Their
response shows significant increases in heart rate, skin conductance, and
blood pressure (Van der Kolk, B., McFarlane, A., Weisaeth, L., 1996).
Research
One study (Metzer et al., 1999) researched
women with PTSD and their reactions to startling tones. The women
were subjected to startling tones while autonomic and eyeblink reactivity
was recorded. The purpose of this study was to determine if the responses
to startling stimuli represented enduring biological traits that persisted
through treatment and recovery. The sample consisted of 57 women
with histories of childhood sexual abuse. The subjects were recruited
from local clinics, therapists, self-help groups, and advertisements to
participate in the study. All of the women were 18 years and older
and were screened for axis I mental disorders using the Structured Clinical
Interview for DSM-III-R (SCID; Spitzer, Williams, Gibbon & First, 1989).
Women that fell into the categories of having an organic mental disorder,
schizophrenia, or current mania were excluded. These women were classified
into three different groups, lifetime PTSD (21), past PTSD but not current
(23) and never having PTSD (13). Thirty-nine of these women had comorbid
disorders. Sixteen were currently taking psychotropic medication
(Metzger et al., 1999).
The instruments used for this research
included the Mississippi Scale (Keane, Saddell, & Taylor, 1989), Impact
of Event Scale (Horowitz, Wilner, & Alvarez, 1979; Zilber, Weiss, &
Horowitz, 1982), State-Trait Anxiety Inventory (STAI; Spielberger, Gorsuch,
& Lushene, 1990), and the Beck Depression Inventory (BDI; Beck, Rush,
Shaw, & Emery, 1979). Fifty-two women took the Clinician-Administered
PTSD Scale: Current and Lifetime Diagnosis Version (CAPS; Blake et al.,
1995). The other women were studied before the test was available
(Metzger et al., 1999).
This study found that women with current
PTSD with childhood sexual abuse produced a much larger accelerated heart
rate response and slower absolute habituation of skin conduction responses
to startling tones compared to the women with similar histories but without
PTSD. There were no changes in the results after adjusting medications
and changing the tones. The women with lifetime PTSD but not current
also showed and increase in autonomic reactivity, greater skin conduction
responses, and slower absolute habituation which suggest that this may
be a preexisting trait or became trait like and persists despite the decrease
in symptoms of PTSD (Metzger et al., 1999).
The study also demonstrated that with the startling stimuli, the
participants with PTSD had greater heart rates, which may represent the
defensive mechanism found in hypervigilance. Similar responses were
found in Vietnam combat veterans with PTSD. This study did not find
any difference in eyeblink responses between women with PTSD and those
without (Metzger et al., 1999).
Another study conducted by Grillon
& Morgan III, researched Gulf War Veterans with PTSD and their startle
response. This study was done to provide important information on
the central nervous system abnormalities in this disorder. Twenty-seven
men were used for the study. The study consisted of thirteen men
with PTSD but without medication and 14 without PTSD. All of the
men were from the same unit in the war. All of them witnessed SCUD
missile attacks and bodies violently dismembered burned or disfigured.
Two men were dismissed due to no eyeblink response and another showed for
the first session but did not return. It is important to note that
this third person scored high on the startle response and did indeed have
PTSD. Only one of the men had a history of alcohol dependency and
the others had no comorbid disorders at the time of testing (Grillon, C.,
& Morgan III, C., 1999).
All of the men were free from
drug use during the time of the testing, as determined by urinary toxicology
screens. The men had hearing within normal limits and the age did
not differ significantly between he two groups (Grillon, C., Morgan III,
C., 1999). Each participant was exposed to a differential conditioning
procedure, which was performed over two sessions separated by four to five
days. The number of conditioned stimuli presented during the post-conditioning
phase was the only varying factor within the two sessions. Each session
consisted of five separate phases, which include startle habituation 1,
startle habituation 2, preconditioning, conditioning, and post-conditioning.
The shock electrodes were not attached during the startle habituation 1
phase; however, five blocks of two startle probes were delivered.
Two habituation phases were incorporated in order to reduce the initial
startle reactivity and assess the effects of placing the shock electrodes.
The study concluded with the findings that
the conditioned startle responses during the initial acquisition session
stayed the same for those with PTSD but exhibited increased startle from
session 1 to session 2. Stimulus generalization, contextual fear,
and sensitization may all play a part in these findings (Grillon, C., &
Morgan III, C., 1999).
Neurological Aspects
PTSD patients also appear to have high
serum levels of both free tyrosine and total thyroxin. Thyrotoxicosis
is often produced following extremely stressful events, such as earthquakes,
fire or combat, but it is only produced in a few of those exposed, as with
PTSD. Thyroxine increases the rate of metabolism if there are insufficient
carbohydrates and fats available. Thyroxine causes rapid degradation
of protein for energy. Studies have also revealed that high thyroxin
levels can be produced by a number of stressful psychological stimuli.
The biological and hormonal changes, which occur in PTSD, are extensive
and research indicates that significant disturbances of several areas of
the brain can eventually result from the numerous alterations of the hormonal
system. People without PTSD do not show the same biological alterations
as those with PTSD. Prior and subsequent stressors, or risk factors added
to the trauma may contribute to the neuroendocrine alterations in PTSD
(Yehuda, R., 1998; Van der Kolk, B., McFarlane, A., Weisaeth, L., 1996).
There are biological correlates, which
include the cardiovascular reactivity, autonomic hyperarousal, disturbed
sleep physiology, adregic dyregulation, enhanced thyroid function, and
altered HPA activity. The psychological correlates include depression,
hostility, and poor coping. The behavioral components include poor
health habits, such as, smoking, drinking and substance abuse (Schnurr,
P., 1996).
The intense bio-chemical changes that occur
in the victim at the time of the traumatic event may lead to permanent
changes in the victim’s nervous system. Without treatment and recovery,
this can become a chronic medical illness or have negative effects on learning,
habituation, and stimulus discrimination (Flannery, Jr., R., 1992; Bremner,
J., Southwick, S., Charney, D., 1991; Van der Kiolk, B., McFarlane, A.,
Weisaeth, L., 1996). The limbic system maintains and guides the emotions
and behaviors necessary for self-preservation and survival. Signals are
sent continuously to the thalamus from the sensory organs. They are
distributed to the cortex, to the basal ganglia, and to the limbic system.
(Carlson, N., 1999).
Psychological trauma alters some of the
neurotransmitters in the victim’s body and in the victim’s mind.
Information does not flow smoothly causing the victim not to function well
in the traumatic crisis. There are five neurotransmitters that are
altered at this time. Epinephrine, cortisol, norepinephrine, serotonin,
and endorphins. Epinephrine is a by-product of the adrenal gland,
which enables the body to cope with the stress of the traumatic event.
Heart rate, breathing, muscles, blood sugar for energy are all regulated
to prepare the victim for the current crisis. Cortisol is released
by the adrenal gland when the victim feels threatened. It provides
a source of energy by releasing blood sugar into the bloodstream and helps
to repair body tissue if injured (Flannery, Jr., R., 1992).
Norepinephrine is also a by-product of
adrenaline and is transmitted through the bloodstream to the brain.
It acts as the main facilitator in the brain to enhance alertness and efficient
problem solving. It is released in the hypothalamus locus coeruleus
and other brain areas during extreme stress. With repeated exposure
to extreme stress, a depletion of NE in the hypothalamus and hippocampus
eventually may occur (Flannery, Jr., R., 1992; Carlson, N., 1999).
Serotonin helps modulate NE responsiveness
and arousal. The inability to modulate arousal is due to lack of
serotonin. Increased arousals in response to new stimuli, handling,
or pain are also linked to low serotonin levels. Other serotonin
functions correlate with hostility, impulsivity, and self-directed aggression
in patients with depression and with Borderline Personality Disorder. Serotonin
is a transmitter produced in the brain. Endorphins when actively circulating
and an adequate supply of serotonin produce calmness, relaxation and contentment.
When there is a deficiency, there is an increase in irritability, anger,
sadness and depression. These neurotransmitters are centrally involved
in the various symptoms of PTSD. The brain structures involved in
memory are primarily involved in the neurobiological response to inescapable
stress (Flannery, Jr., R., 1992; Carlson, N., 1999; Van der Kolk, B., McFarlane,
A., Weisaeth, L., 1996).
Serotonin Reuptake Inhibitors (SSRI’s) are effective in treating
both obsessive thinking in people with Obsessive Compulsive Disorder and
involuntary preoccupation with traumatic memories in people with PTSD.
SSRI’s may also help the behavioral inhibition system related to various
problems in behavior seen in PTSD such as, impulsivity, aggressive outbursts,
compulsive reenactment of trauma related behavior patterns, and the inability
to learn from past mistakes (Van der Kolk, B., McFarlane, A., Weisaeth,
L., 1996).
Reexposure to a stimulus resembling the original trauma can cause
an endogenous opioid response indirectly measured as naloxone-reversible
analgesia when exposed to a similar traumatic stressor. This has
been correlated with a secretion of endogenous opioids equivalent to 8
mg of morphine. This may account for emotional responses being blunted
during the traumatic stimulus. These opioids which inhibit pain and
reduce panic, are released after prolonged exposure to sever stress (Van
der Kolk, B., McFarlane, A., Weisaeth, L., 1996).
Recent clinical studies have shown evidence
of long-term changes in specific brain systems when exposed to extreme
stress. This type of stress can effect or produce deficits of memory,
learned helplessness, and conditional fear responses to stressors, associated
with long-term changes in multiple neurobiological systems. This
type of stress also results in the acquisition of specific behaviors and
the alteration of multiple brain systems. Noradrenergic brain systems
react in fear response and alarm states. This increases heart rate,
blood pressure, and alerting behaviors. These are essential for the
response to life-threatening situations mediated by noradrenergic brain
systems (Bremner, J., Southwick, S., Charney, D., 1991).
The amygdala evaluates emotional meaning
of incoming stimuli by processing the fear perception, especially the negative
fear perception. This transmits the information to the central gray
matter, the lateral hypothalamus, the paraventricular nucleus, the locus
coeruleus, and the ventral tegmental area. The locus coeruleus, found
in the pons, is the noradrenergic neurons in the brain. This area
has projections to brain structures involved in learning and memory, hypothalamus,
nucleua accumbens, and prefrontal cortex (Tamminga, C., 1999; Van der Kolk,
B., McFarlane, A., Weisaeth, L., 1996; Bremner, J., Southwick, S., Charney,
D., 1991).
Endogenous, stress-response neurohormones
are released with extreme stress. Catecholamines are some that are
released which includes; epinephrine, norepinephrine, serotonin, and hormones
of the hypothalamic-pituitary-adrenal (HPA) axis and endogenous opiods.
These hormones help the organism mobilize the energy required to deal with
stress by increasing glucose release, which enhance the immune function.
In normal stressful situations, hormonal responses are rapid and pronounced,
but in chronic and persistent stress the effectiveness of the stress response
is inhibited and desensitization is induced (Flannery, Jr., R., 1992; Bremner,
J., Southwick, S., Charney, D., 1991).
Preexisting personality factors can
also play a role in developing PTSD. Mikulincer and Solomon (1988)
produced a study showing Israeli soldiers who tended to brood about their
feelings suffered a combat stress reaction during the 1982 war in Lebanon,
which developed into PTSD. Another study by the National Vietnam
Veterans Readjustment Study discovered four factors likely to increase
developing PTSD from combat stress. One was being raised with financial
difficulties, a drug abuse or dependency history, and history of behavioral
problems as a child (Carlson, N., 1999). Other studies suggest severe
family stress during childhood increase the risk to develop PTSD during
the traumatic event. There is still not enough evidence to determine
who will develop PTSD and who will not (Flannery, Jr., R., 1992).
Conclusion
In both studies discussed, there are limitations
on the research. The studies did not state ethnic, or substance abuse backgrounds
of the participants. Nor did it state the socioeconomic background
of the participants. These factors are important to take into consideration
due to the fact that these groups may respond differently to stress and
trauma.
Both studies limited their research to
people that met certain criterion that is critical for an accurate outcome.
The methods used were consistent with all participants with the exception
of the CAPS, used in the first study, which was only administered to 52
out of the 57 women studied. On going research is still necessary
to pinpoint specifics of PTSD.
PTSD manifests itself through biological,
physical and mental symptoms. Without treatment, the biochemical
changes may lead to permanent changes in the nervous system, become a chronic
illness or both. Studies have also explored the possibility that
personality traits play a part in developing PTSD when exposed to trauma.
Unfortunately there is not enough data to promote this theory. By identifying
specific neurobiological abnormalities, researchers can develop new psychopharmacological
and psychotherapeutic treatment for PTSD.
For references - Please e-mail me.
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