Post Traumatic Stress Disorder
 The Biological Aspects
L. Michele Henline
Arizona School of Professional Psychology

 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

     Post traumatic stress disorder, (PTSD), is an extreme reaction to a traumatic event that lasts longer than one month, which may cause the person to keep reliving the event with nightmares, “flashbacks” or they may retreat into an emotional numbness (Baron-Faust, R. 1997). PTSD is not a disorder developed by simple conditioning.  Many people who have experienced a trauma but do not develop PTSD can become distressed when confronted with the tragedy.  Almost everyone exposed to extreme stress develops intrusive symptoms, but only some will develop avoidance and hyperarousal.  McFarlane (1988) has hypothesized that the reoccurring thoughts set up a chronically disordered pattern of arousal.  The victim is victimized by the memories of the event rather than the event itself (Van der Kolk, B., McFarlane, A., Weisaeth, L., 1996). There are two stages to PTSD; acute and chronic.
     This stage is described with anxiety and fear.  The traumatic event disorganizes the victim’s life causing an increase in anxiety and sometimes panics.  When minimal order has been restored the fear decreases, and anxiety evolves into a feeling of apprehensiveness over time.  Many times anger is present during this stage.  This can be helpful to victims by mobilizing the victim’s coping skills to assist in putting their life back together.  There usually are attempts to restore control, attachments, and some purposeful meaning in life.
     Victims tend to find comfort in others to help share the painful feelings.  This helps to provide new ways to respond to the current crisis.  If the victim is not successfully treated during the first six-months, the second phase, chronic PTSD, can occur.
     Chronic PTSD is when the person is not successfully treated during the first six months.  The person enters the numbing phase in this stage.  Symptoms may include withdrawal, isolation, numbing, and depression.  The body limits its capacity to respond physically and psychologically (Flannery, Jr., R., 1992).
     Physical symptoms can include hypervigilance, exaggerated startle response, difficulty sleeping, difficulty with concentration or memory, mood irritability, anger and depression.  Intrusive symptoms can vary from recurring, distressing thoughts, memories, dreams, nightmares, flashbacks; physical or psychological distress when triggered, grief or survivor grief.  Avodiant symptoms can be avoiding specific thoughts, feelings, activities or situations; loss of interest in significant activities, restricted range of emotions or numbness (Flannery, Jr., R. 1992; Tamminga, C., 1999; Mason, J. et al., 1990).  To understand the physical symptoms, it is necessary to understand the biological effects.

    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.

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