Post traumatic stress disorder (PTSD) is a mental health condition that presents in form of anxiety disorder, and it usually develops following exposure to an event or incident that is terrifying and mostly associated with an increased risk or actual occurrence of severe body harm. These events exceed the coping capabilities of the individual, resulting into psychological trauma. As a result of the trauma, the affected individual develops fear conditioning in their brain, possibly because of certain brain chemicals that are released. Some structures in the brain are also thought to undergo atrophy. The risk of developing post traumatic stress disorder is also influenced by genetics and personal characteristics, for example childhood experience, previous exposure and preexisting conditions such as depression, gender and degree of exposure to trauma (Fullerton & Ursano, 2005).
Most people who develop this condition are those who have been exposed to traumatic incidents in their childhood or adulthood, like natural disasters, manmade disasters, accidents, military combat, and violent physical abuse, as individuals or witnessing someone else undergo the incidents. About two thirds of the population worldwide becomes exposed to significant traumatic situations in the course of their lifetime. The level of exposure to or experience of a traumatic event is consistently associated with the likelihood of developing PSTD. The development of post traumatic stress disorder also shows significant correlation with poor socioeconomic settings, age, race, ethnicity, and employment status. The affected people undergo continuous frightening thoughts as they recall the terrifying experiences, often having sleep problems and feeling detached and becoming withdrawn.
The patients develop psychological problems such as neuroticism, guilt, difficulties in concentration, poor coping skills, and obsessive symptoms. The level of social support available for the people who have been exposed to traumatic events is the strongest determinant of the risk of post traumatic stress disorder (Fullerton & Ursano, 2005). Post traumatic stress disorder is classified as acute, chronic or delayed onset. Acute posttraumatic stress disorder presents with symptoms that do not persist beyond three months, while in the chronic form the symptoms last more than three months. Delayed onset post traumatic stress disorder is the one in which the symptoms start appearing about six months following exposure to the traumatic event. As compared to normal stress that is usually associated with acute reactions that rapidly return to the normal state, the biological and psychological mechanisms in post traumatic stress disorder are chronic and often become severe with time (Fullerton & Ursano, 2005).
Current treatment of post traumatic stress disorder includes exposure therapies and anxiety management trainings as the first-line treatments. Pharmacological therapies such as the use of selective serotonin reuptake inhibitors have also been designed and shown to be effective, though intensive studies are in progress to develop other form of drugs. In spite of the possible efficacy of pharmaceutical interventions, psychological treatments still remain the preferred therapeutic approaches for this disorder (Keane, Marshall & Taft, 2006). The outcome of the therapeutic interventions depends on the level of social support, and lack of symptoms such as avoidance, emotional numbing and hyperarousal. According to Keane, Marshall and Taft (2006), PSTD has been in existence for many centuries though it became recognized in the 1980.
This condition was commonly linked to warfare, until studies demonstrated the occurrence of similar symptoms in the civilian population exposed to natural disasters, mass catastrophes and tragic accidents. Prior to this, post traumatic stress disorder was identified by different names such as, “shell shock, battle fatigue, accident neurosis, and post-rape syndrome” (Keane, Marshall & Taft 2006, p.163). After the American Psychiatric Association classified post traumatic stress disorder, it was generally agreed that the condition resulted from traumatic events and not the previously perceived individual weakness. However, these traumatic events were taken to be stressors beyond the daily human experiences including war, natural calamities, manmade disasters, and rape among others.
Symptoms of PSTD
Symptoms of post traumatic stress disorder frequently alter the patient’s personal life and can affect one’s functional abilities. These symptoms mostly start immediately after the traumatic experience, but often they may appear several months or years since the exposure. These symptoms are classified into four types including reliving, avoidance, numbing and hyperarousal (Fletcher, 1996). Patients suffering from this disorder frequently relive memories of the traumatic incidents in form of flashback and nightmares. This reliving of traumatic events is often triggered by stimuli related to the event.
Avoidance of scenes related to the traumatic event is also a common symptom presenting in individuals with post traumatic stress disorder. The patients show a tendency to avoid stimuli and triggers that are associated with the traumatic memories, and may engage in activities to keep them from thinking or discussing such events. Numbness may also manifest as a way of avoiding the traumatic memories. Hyperarousal is another common symptom in PSTD patients, whereby the victims become highly alert and lookout for threats. This makes the patients to become very irritable and have difficulties in concentrating. The patients may also develop sleeping disorders, exhibit violent behavior and startled responses (Rosen, 2004).
Information processing in patients with PSTD
Various models have been developed to explain the memory and concentration problems manifested by patients affected by post traumatic stress disorder. These models relate the cognitive problems with these patients with the changes in the brain structures that function in learning and memory. The first model is described as fear structure, whereby the brain of the affected individuals become programmed to process information associated with the threatening experience and subsequent physiological, physical and behavioral responses.
Another information processing model is based on cognitive theory, with an assumption that the disorder progresses only if a person perceives the traumatic incident in a manner that makes the incident to become threatening after it has taken place. The perception of the trauma as being present results into intrusions and reliving symptoms, anxiety, and over alertness. Subsequently, the affected individual tries to decrease perceptions of the threat through behavioral and cognitive modifications, although these changes further perpetuate the symptoms (Rosen, 2004).
Prevalence of PSTD
Epidemiologic studies indicate that about 10 percent of the universal population experience PSTD at some point in their lifetime. Epidemiologic surveys also indicate that between a third and two-thirds of the world population experience or witness trauma at some point in life. The most common forms of traumatic events people get exposed to or experience in developed countries include grave harm or death, fire disasters, natural calamities, and life-threatening accidents. The most prevalent forms of trauma experienced by females are rape, sexual exploitation and abuse, physical assault, and neglect, while physical assault and military-related trauma are more prevalent in males (Fullerton & Ursano, 2005). Post traumatic stress disorder can occur at any age, and the period it takes to develop following exposure or experiencing of a traumatic event ranges from hours to years.
The prevalence of PSTD in the general population is higher in females as compared to males, with an estimated prevalence of 10 percent and 5 percent respectively. Among individuals exposed to trauma, the prevalence of post traumatic stress disorder in males is 8 percent, while in females it is about 20 percent. The prevalence differences across gender lines are thought to be related to the specific form of trauma experienced. For instance, it has been shown that females who experience physical assault or are threatened with a weapon are at a high risk of developing post traumatic stress disorder as compared to men subjected to the same trauma. Similarly, males who experience sexual abuse are at a higher risk of developing PSTD as compared to the females who also experience the same stressor. Additionally, exposure to interpersonal violence among women is positively associated with later development of post traumatic stress disorder. In general, exposure to interpersonal violence is strongly associated with the development of PSTD as compared to traumatic events that occur without a human perpetrator.
Further studies show that of the entire population that experience or witness severe trauma at some point in their life, it is less than 20 percent who develop post traumatic stress disorder, thus suggesting the existence of many risk factors (Fullerton & Ursano, 2005). The prevalence is significantly increased in countries where rates of violence, crimes and war are high, and also in parts of the world that are more prone to natural catastrophes. Younger age appears to be associated with a higher risk of developing post traumatic stress disorder (Keanne, Marshall, & Taft, 2006). Meta analysis studies have also shown that children and teenagers who get exposed to traumatic events are 1.5 times likely to develop post traumatic stress disorder than adults exposed to the same trauma.
These findings suggest that the developmental process of the disorder in young individuals varies from that of the adults. Lower education achievement is also associated with increased risk for this disorder. Other factors associated with high prevalence of post traumatic stress disorder include pre-existing psychiatric problems, juvenile delinquency, childhood adversity, personality disorders, genetic factors, severity of the trauma, and lack of social support (Schnurr, Friedman & Bernardy, 2002). Though findings on race are not consistent, a strong correlation has been shown to exist between the race of a person and the development of post traumatic disorder. Some studies have indicated that whites have a lower risk of developing post traumatic stress disorder as compared to nonwhites, even when other risk factors like exposure to traumatic events are held constant (Fullerton & Ursano, 2005).
Study findings have established that chronic PSTD is mostly associated with some psychiatric conditions and impaired psychosocial activities. Among these comorbid conditions include, “major depression, dysthemia, mania, generalized anxiety disorder, panic disorder, simple phobia, agoraphobia, alcohol abuse/dependence, drug abuse, social phobia, and conduct disorder” (Schnurr, Friedman & Bernardy 2002, p. 880). Despite these psychiatric conditions being risk factors for post traumatic stress disorder, the disorder itself can also be a predisposing factor for the psychiatric conditions.
Etiology of PSTD
The major etiologic factor in PSTD is the trauma. However, various studies have shown that not all individuals who get exposed to same traumatic events develop the disorder, thus indicating the existence of certain predisposing conditions. Recognition that trauma alone may not be the sole cause of post traumatic stress disorder and the observations that not all people who get exposed to traumatic events develop the disorder have led to identification of various aspects where individual differences may determine vulnerability. These aspects include appraisal tendencies, genetic makeup, and certain risk factors (Fullerton & Ursano, 2005). Appraisal tendencies relate to the individual perceptions of situations or events, whereby some individuals are likely to consider situation or events as threatening or horrifying as compared to other individuals. Clinical studies have shown that many individuals who experience or witness traumatic events do not develop post traumatic stress disorder.
This is attributed to the individual variations on the ability to cope with traumatic situations, thus different individuals possess differing psychological reactions to similar traumatic situations. It has, therefore, been recognized that exposure to traumatic events gets perceived through cognitive and emotional mechanisms involving appraisal (Vieweg et al., 2006). Whereas some individuals may perceive a situation or event as a huge threat, others may perceive the same situation as a challenge that demands them to evolve coping abilities. A number of risk factors that render some people more vulnerable to developing post traumatic stress disorder than others have been identified. These risk factors are classified as pre-traumatic, traumatic or post-traumatic (Vieweg et al., 2006).
Pre-traumatic factors that may predict later development of post traumatic stress disorder as identified by various studies are childhood trauma, the existence of psychiatric problems, childhood maladaptive behaviors, poor family background, introversion, gender, and existence of physical health problems among others. Studies on early periods of development show an increasing relationship between early life trauma and a greater likelihood for the development of PSTD (Keanne, Marshall & Taft, 2006; Edsall, Karnik & Steiner, 2005). This hypothesis is, however, supported by few data obtained from small samples. But still, it is well established that childhood abuse and experience of other trauma early in life are partially responsible for the manifestation of post PSTD later in life in the general adult population. In a study carried out in the USA by MaCauley et al. (1997), it was shown that a significantly high number of women with a greater disposition to develop post traumatic stress disorder had undergone early life physical assault, sexual abuse or serious neglect.
The study investigated about 2000 adult females drawn from different socioeconomic groups, and who were attending primary care internal medicine practices. McCauley and colleagues found that 22 percent of the study population experienced many physical symptoms with much higher levels of, “depression, anxiety, somatization and interpersonal sensitivity, a fivefold higher prevalence of drug abuse and a twofold higher level of alcohol abuse” (McCauley et al. 1997, p. 1367). In general, the data supports the established models of risk for the development of PSTD, whereby genetic predisposition, temperament and childhood or adulthood trauma are significant risks factors for PSTD development. Therefore, the recent trauma experienced by an individual also triggers the development of post traumatic stress disorder.
This has been shown to arise from the effects of corticotropin releasing factor (CRF), which is a hormone involved in regulating the autonomic, immune and behavioral reactions to any stress. Increased secretion of corticotropin releasing factor is associated with increased expression of psychiatric symptoms, including PSTD symptoms (Sapolsky, 1996). With regard to traumatic factors, many studies on post traumatic stress disorder have shown that there exists a direct relationship between severity of the trauma and subsequent development of the disorder. The severity of the trauma includes characteristics like the length of time the trauma took, the frequency of occurrence and the degree of harm or threat on life. Other aspects of the severity of trauma are the severity of the experience, whether somebody was harmed during the incident, whether the victim was involved directly or witnessed the trauma, and in case of sexual abuse, if the perpetrator of the atrocity was previously known to the victim.
The severity of the trauma and PSTD are very consistent in the entire population, with high severity associated with increased risk for post traumatic stress disorder or severity of its symptoms (Edsall, Karnik & Steiner, 2005). Studies have also shown that the post traumatic environment is also connected to later development of PSTD. Environments that are characterized by poor social support and disoriented social interaction patterns make people more vulnerable to develop post traumatic stress disorder (Ford, 2009). It has been shown that people who experience traumatic events such as rape victims and war veterans suffer from deleterious effects due to lack of post traumatic social support. Similarly, a number of studies have shown that post traumatic clinical interventions like debriefing are effective preventing later development of PSTD.
Pathophysiology of PSTD
Major psychobiologic processes that give human beings capabilities to effectively deal with stressful events have been shown to be impaired in individuals having PSTD. Among the affected processes include the fight and flight responses, the hypothalamic-pituitary-adrenocortical axis, the fear conditioning, appraisal and the acoustic startle reactions (Ford, 2009). The fight and flight responses are brought about by the stimulation of the sympathetic nervous system. In normal persons, the stimulation of the sympathetic nervous system by a traumatic event results into a sequence of autonomic and muscular responses, which provide the person with capabilities to cope with the possible threat. However in people who have PSTD, it has been established that sympathetic nervous system responses and adrenergic dysregulation are excessively elevated. Even minor trauma related stimuli have been observed to trigger autonomic hyperresponsiveness.
It has also been found that the amount of catecholamine in the urine of the victim is significantly increased. Other sympathetic nervous system abnormalities observed include, “down regulation of beta-2 and alpha-2 adrenergic receptors and increased reactivity to the alpha-2 antagonist yohimbine” (Ford 2009, p. 37). Increased reactivity of yohimbine is associated with triggering of panic attacks and trauma-related memories in people suffering from PSTD. The hypothalamic-pituitary-adrenocortical system also acts to enhance the ability of people to cope effectively with stress. In patients who are experiencing post traumatic stress disorder, the hypothalamic-pituitary-adrenocortical system is poorly modulated and the victims exhibit abnormal features like decreased amounts of cortisol in urine, increased amounts of lymphocyte glucocorticoid receptor and excessively inhibited dexamethasone (Sapolsky, 1996).
Another psychobiologic process that has been shown to be impaired in patients with PSTD is the acoustic startle response. In normal individuals, the acoustic startle system helps in creating awareness of any possible threat. However, in patients affected by the disorder, they exhibit a reduced latency and elevated amplitude in acoustic-startle-eyeblink reflex. Besides, the patients also show marginally reduced normal dysregulation of the startle reflex (Fullerton & Ursano, 2005). Fear conditioning mechanisms have also been shown to be impaired in patients with PSTD. In normal individuals, fear conditioning mechanisms facilitate the storage of information relating to exposure or experience of aversive and threatening events, thus providing one with capabilities to cope with similar challenges in future (Fullerton & Ursano, 2005). Studies have, however, shown that people who suffer from this disorder exhibit a characteristic progression of the fear conditioning, evoking excessive emotional responses to perceived threats (Wisco, Marx & Keanne, 2012).
Appraisal process has also been shown to be diminished in patients with posttraumatic stress disorder. Appraisal is a psychological process through which people develop capabilities to determine the nature of an event or situation, whether it is pleasant, challenging or threatening. This in turn determines the coping, adapting and survival abilities of the individual. Patients with PSTD lack these abilities and often perceive the world as unsafe, leading to development of deleterious cognitive, emotional and behavioral effects. (Wisco, Marx & Keanne, 2012) Another possible pathophysiologic mechanism involved in posttraumatic stress disorder relates to brain abnormalities in terms of structure and function (Ford, 2009). Various studies using magnetic resonance imaging techniques have demonstrated that the hippocampus volume in patients who suffer from PSTD who were previously exposed to traumatic events is significantly decreased (Fletcher, Creamer & Forbes, 2010).
These findings have been supported by animal studies, which have shown that continued stress causes hippocampus degeneration and loss of function of apical dendrite nerve cells. It has been hypothesized that this degeneration is as a result of secretion of neurotoxic amino acids by the increased quantities of glucocorticoids. Studies using positron emission tomography have also indicated some functional brain abnormalities in individuals who are affected by PSTD. These studies have suggested elevated regional cerebral circulatory around the limbic and paralimbic regions. These regions play a role in the recognition and processing of emotions and stimuli, thus signifying their possible functions in the regulation of fear conditioning and appraisal (Rosen, 2004).
Neurobiological aspects of PSTD
Traumatic events directly stimulate the catecholamine system, triggering fight and flight responses such as rates of cardiac activity, blood circulation, metabolism, and alertness. Subsequently, the hypothalamus is stimulated to release corticotropin-releasing hormone, thus activating the hypothalamic-pituitary-adrenal axis due to the resultant stimulation of the pituitary gland and subsequent release of adrenocorticotropin hormone (Fullerton & Ursano, 2005) Furthermore, cortisol is secreted by the adrenal glands, leading to increased stimulation of the sympathetic nervous system. All these responses serve to provide a person with coping and survival abilities when faced with a threatening or dangerous situation. However when the trauma experienced or witnessed is chronic, these fight and flight responses often become counterproductive. Regulation of the hypothalamic-pituitary-adrenal axis finally restores cortisol to normal levels through a negative feedback mechanism. In some instances, however, the catecholamine system and the hypothalamic-pituitary-adrenal axis may become poorly modulated, thus impeding normal trauma- and stress-related responses and leading to development of the deleterious effects of PSTD (Keanne, Marshall & Taft, 2006).
Various studies have shown that poor modulation of the hypothalamic-pituitary-adrenal axis and increased amounts of catecholamine generated by trauma adversely impair neuronal development in the brain. This occurs through different mechanisms such as increased degeneration of the nerve cells, impairment of the myelination process, reduction of the quantity and size of dendritic processes, impairment in neural pruning, suppression of the synthesis of nerve cells, and a reduction in the synthesis of neutrophic factor by the brain cells (Schnurr, Friedman, & Bernardy, 2002).
Exposure to traumatic events has also been shown to cause certain structural changes in the nervous system, including “reduced corpus callosum size, attenuated development of the left neocortex, hippocampus and amygdala, enhanced electrical irritability in limbic structures, and reduced functional activity of the cerebellar vermis” (Edsall, Karnik & Steiner 2005, p. 110). The parts of the brain that become impacted by traumatic events have been shown to exhibit postnatal development for long periods of time, possess increased levels of glucocorticoid receptors and some formation of the nerve cells in the postnatal period. The above damages to the regions of the brain may cause the affected person to develop socialization, attachment, bonding and cognitive problems.
The Catecholamine system and Trauma
Studies have shown that trauma may affect the catecholamine system, as demonstrated by the increased levels of noreadrenaline and dopamine excreted in urine in people with PSTD. It has also been shown that the concentration of the catecholamine in urine in the patients relates to the length of time one is exposed to the traumatic event, and also to the severity of the disorder cells (Schnurr, Friedman, & Bernardy, 2002).
The Hypothalamic-Pituitary-Adrenal Axis and Trauma
Investigations on the role of the hypothalamic-pituitary-adrenal axis in the development of post traumatic stress disorder have indicated that affected children have elevated basal amounts of cortisal, while the affected adults have reduced amounts. The reduced cortisol levels in adults who are suffering from chronic PSTD is thought to be caused by the down-regulation of the anterior pituitary corticotropin-releasing hormone binding sites following the increase in corticotropin-releasing hormone levels, in addition to the increased negative feedback suppression of cortisol amounts by the pituitary gland. The down regulation process is considered as an adaptation response against the chronically increased amounts of cortisol, which may cause neurotoxicity cells (Schnurr, Friedman, & Bernardy, 2002). Other studies have hypothesized the decreased baseline cortisal amounts in adults to result from adrenal insufficiency and chronically reduced secretion of cortisal from the adrenal glands.
This hypothesis is supported by findings that adults with post traumatic stress disorder show increased adrenocorticotropin hormonal response to corticotropin releasing factor than normal persons (Keanne, Marshall & Taft, 2006). The observations that the baseline cortisal amounts are increased in children who have been exposed to traumatic situations have post traumatic disorder indicates different physiological impacts compared to adults, though similar studies have yielded contrasting results indicating the cortisal levels to be increased. The variations in baseline cortisol amounts among children may be related to factors such as developmental stage of the child during the trauma experience and the period of time that has passed since the trauma occurred (Wolfgang et al., 2012).
It is generally suggested that corticotropin releasing hormone and cortisol amounts are increased acutely after exposure to trauma, while developmental effects of the traumatic experience result into reduced amounts of cortisol because of the consistently increased corticotropin releasing hormone and the raised hypothalamic-pituitary-adrenal axis negative feedback mechanism (Keanne, Marshall & Taft, 2006). Functional and structural changes in the brain due to traumatic stress A number of literatures continue to indicate that glucocorticoids have some effects on the hippocampus in individuals who are suffering from post traumatic stress disorder. Most of these studies have demonstrated a reduction of the hippocampus in adult individuals with PSTD. The atrophy of the hippocampus is also reported in various conditions characterized by excessive secretion of glucocorticoid, such as the Cushing syndrome and recurrent major depressive disorder.
Further, it has also been demonstrated that the neurotoxic effects of glucocorticoid may be due to chronically increased levels of excitatory amino acids like glutamate (Sapolsky, 1996). Studies using magnetic resonance imaging have shown that adults previously exposed to trauma and who have developed post traumatic stress disorder have significantly decreased hippocampus volumes. Hippocampal atrophy has, however, not been observed in children suffering from this disorder. Instead, these children have, “smaller intracranial, cerebral, and prefrontal cortex, prefrontal cortical white matter, right temporal lobe volumes, and smaller areas of the corpus callosum” (Edsall, Karnik & Steiner 2005, p. 114). These neurobiological observations are possibly caused by reduced cortical hemispheres communication because of memory impairment and dissociative disorders associated with PSTD (Sapolsky, 1996).
The differences in brain structure between adults and children suffering from PSTD has been hypothesized to arise from co-occurrence of other disorders such as those associated with drug and alcohol abuse in adults. It is also suggested that stress response tend to gradual, thus the neurobiological changes develop over time. Many brain structures, including the hippocampus are known to continue developing after birth. Studies have established that the hippocampus depicts increased formation of axons, dendrites, synapses and receptors, which become pruned after puberty (Vieweg et al., 2006). Generally, these studies indicate that traumatic experiences during the early years of life cause progressive developmental impacts on the brain, hence implying that the development of post traumatic stress disorder, to some extent, is determined by the stage of neural development of a person (Sapolsky, 1996).
It is also suggested that hippocampus atrophy may be a risk factor for the development of PSTD. This is based on comparison studies of twins who have post traumatic stress disorder exposed and those who did not have the disorder with other normal individuals. The study demonstrated that both the twins exposed to trauma and those not exposed had reduced hippocampi volumes as compared to the control group (Sapolsky, 1996). As regards to metabolic alterations in the brain of people with PSTD, various studies using positron emission tomography and functional magnetic resonance imaging techniques have been carried mostly in adults. These studies have indicated higher activities in the amygdale and anterior paralimbic areas, and reduced activity around the anterior cingulated and orbitofrontal sections in patients with PSTD (Havard Women’s Health Watch, 2005).
Assessment of Trauma and PSTD
Assessment of trauma is the initial phase in the diagnosis of post traumatic stress disorder. It involves assessing if a person has experienced a traumatic situation, and identifying the situations that the person has had exposure to. The event or situation has to be evaluated whether it is life threatening. This is a significant step since symptoms of the disorder like re-experiencing, avoidance, numbing, arousal, and concentration difficulties need to be examined against particular events. PSTD is assessed through a cluster of three symptoms including re-experiencing, avoidance and arousal. Appearance of the symptoms should be determined, whether they started immediately following exposure to the trauma and whether the symptoms are progressively increasing (Robertson, Humphreys & Ray, 2004).
Diagnosis of PSTD
Diagnosis of post traumatic stress disorder is based on certain set of criteria, which are six in number. The first criterion is the demonstration of the existence of a stressor. An individual must have been exposed to, experienced or threatened with a situation where death or physical harm was eminent or real. The second criterion is the existence of re-experiencing symptoms, whereby the affected individual persistently perceives imaginary threats witnessed or experienced before. This mostly occurs as flashbacks and the affected individual feels and behaves as if the trauma is repeating. Re-experiencing may also come in form of distressing memories and nightmares, particularly when the person faced with situations related to the trauma. In some cases, the patients may present with physiological or psychological stress reactions such as full-blown panic attacks.
The third criterion for diagnosis is the existence of avoidance and numbing symptoms (Robertson, Humphreys & Ray, 2004). Individuals presenting with this disorder often try to escape trauma-related thoughts and actions and regularly present with reduced capabilities to engage in pleasure activities, difficulty in recalling some dimensions of the trauma, withdrawal from social activities, and detachment. The forth criterion includes observation of symptoms related to hyperarousal and hypervigilance. In this criterion, persons affected by post traumatic stress disorder may exhibit features such as lack of concentration, irritability, and disturbed sleep patterns.
The fifth criterion is the demonstration that re-experiencing symptoms, avoidance of actions and thoughts related to trauma, withdrawal, and irritability, and lack of concentration, disturbed sleep patterns, and irritability symptoms have occurred persistently for more than one month. The last criterion is the demonstration that the combined symptoms impairs with the functional and social abilities of the affected individual, coupled with significant distress. Under this criterion, the existence of PSTD is ruled out if the patient presents with mild symptoms or when the person exhibits competent functional abilities (Wolfgang et al., 2012).
Treatment of PSTD
The major treatment intervention measures for patients who have post traumatic stress disorder are, “cognitive behavioral therapy, pharmacotherapy and individual and group dynamic therapy” (Wolfgang et al. 2012, p. 72).
This is the most effective form of treatment currently available for PSTD. The main approaches to cognitive-behavioral therapy involve exposure therapy and anxiety management interventions. Exposure therapies mostly focus on the elimination of the strong effects caused by fear conditioning in people suffering from post traumatic stress disorder. These therapeutic approaches are based on the recognition that consistent exposure to perceived threats helps in decreasing the victim’s fear response to stimuli associated with trauma. Further, exposure therapy also helps in lessening the victim’s sympathetic nervous system and adrenergic hyperactivity triggered by trauma related stimuli (Wolfgang et al., 2012). Anxiety management interventions are usually geared towards equipping the patient with skills that can help in decreasing anxiety.
These strategies, therefore, involve training the patient on areas like relaxation, social skills, stress management, and cognitive restructuring among others. Cognitive restructuring is the most preferred training since it helps patients to be able to correct the impaired appraisal mechanisms, thus lessening their tendency to perceive threats from unwarranted situations. Cognitive-behavioral therapy can be provided on individual basis or in a group. In group psychotherapy, the patients are given trainings through psychoeducation, exposure and cognitive processing (Vieweg et al., 2006).
Based on the identified neurobiological abnormalities that accompany post traumatic stress disorder, pharmacotherapeutic interventions can help in the treatment of many associated symptoms such as anxiety, depression and insomnia. Pharmacotherapy is often essential before induction of the patient to other therapeutic approaches like cognitive-behavioral therapy and psychodynamic therapy (Gibson, 2012). Many studies on the efficacy of antidepressants such as imipramine and fluoxetine have generated mixed results, often indicating that patients having severe and chronic PSTD show refractory responses towards these medications. Clinical trials on the effectiveness of anti-adrenergic drugs like propranolol and clonidine also yield promising results, indicating the possible benefits in treating this disorder (Wisco, Marx & Keanne, 2012).
This form of therapy involves encouraging the patient to make free association of ideas and feelings, while allowing the psychotherapist to make interpretations of the implications of the associations. The psychotherapist also provides recommendations depending on the comprehension of the situations and the perceived causes of the symptoms. The main objective of this form of therapy is to unravel the exact nature of the patient’s psyche so as to help in managing the psychic tension (Wisco, Marx & Keanne, 2012).This therapy approach, therefore, relies on the establishment of an interpersonal relationship between the patient and the psychotherapist.
It can be applied in various contexts such as in individual psychotherapy, group psychotherapy, and family therapy among other areas. In dealing with PSTD patients, the dynamic psychotherapy approach mostly targets the creation of a trustworthy and safe environment so as to enable the patient reveal the hidden traumatic experiences. Once the traumatic content has been obtained, focus shifts to analysis of the trauma in detail and examinations of the re-experiences together with the avoidance symptoms. Patients are finally guided to disengage from the perceived threat and make appropriate reconnections in their social life (Wisco, Marx & Keanne, 2012).
Because of the increased rates of traumatic experiences in the world nowadays, prevalence of PSTD is anticipated to increase with time. It is imperative that more research be carried out to develop appropriate prevention and early intervention measures to curb the disorder (Keanne, Marshall & Taft, 2006). These measures should be based on the already established risk factors for the disorder and should mainly target individuals exhibiting acute stress symptoms so that early cognitive-behavioral interventions are given. It is also important that further research be carried out on the neurobiological aspect of posttraumatic stress disorder, particularly in children (Rosen, 2004). These studies will provide more information regarding functional and structural alterations in the brain associated with this disorder to enable designing of appropriate diagnosis tools.
Post traumatic stress disorder is an anxiety disorder presumed to be caused by traumatic experiences. However, many individuals exposed to traumatic events do not develop the disorder. In addition, the prevalence of the disorder in people who have been traumatized is low, thus indicating the existence of other certain risk factors that predispose some individuals to develop the disorder. Intensive studies have helped in creating more understanding of the function of the risk factors in the development of the disorder, and subsequent development of treatment approaches. Despite various interventions such as CBT and pharmacotherapy aiding in management of PSTD, there is need to conduct more studies to establish measures that can be used as early interventions and proper diagnostic tools for PSTD.
Edsall, S., Karnik, N. & Steiner, H. (2005). “Childhood trauma.” In, Clinical child psychiatry, 2nd ed, Eds. Klykylo, W. and Kay, J. London: John Wiley & sons. Fletcher, K. (1996). Childhood posttraumatic stress disorder. New York, NY: Guildford Publications Inc. Fletcher, S., Creamer, M. & Forbes, D. (2010). Preventing post traumatic stress disorder: Are drugs the answer? Australian and New Zealand Journal of Psychiatry, 44, 1064-1071. Ford, J. D. (2009). Post traumatic stress disorder: Science and practice. New York, NY: Academic Press. Fullerton, C. S. & Ursano, R. J. (2005). Posttraumatic stress disorder: Acute and long-term responses to trauma and disaster. Washington DC: American Psychiatric Press. Gibson, C. (2012). Review of posttraumatic stress disorder and chronic pain: The path to integrated care. JRRD, 49(5), 753-776. Harvard Women’s Health Watch. (2005). Not getting over it: Post-traumatic stress disorder. Keanne, T. M., Marshall, A. D. & Taft, C. T. (2006). Posttraumatic stress disorder: Etiology, epidemiology, and treatment outcome. Annual Review of Clinical Psychology, 2, 161-197. McCauley, J., Kern, D. E., Kolodner, K., Dill, L., Schroeder, A. F., DeChant, H. K., rydden, J., Derogatis, L. R. & Bass, E. B. (1997). Clinical characteristics of women with a history of childhood abuse: Unhealed wounds. JAMA, 277, 1362-1368. Robertson, M., Humphreys, L. & Ray, R. (2004). Psychological treatments for posttraumatic stress disorder: Recommendations for the clinician based on a review of literature. J Psychiatr Pract, 10(2): 106-18. Rosen, G. (2004). Posttraumatic stress disorder: Issues and controversies. West Sussex: John Wiley & Sons. Sapolsky, R. M. (1996). Stress, glucocorticoids, and damage to the nervous system: The current state of confusion. Stress, 1(1), 1-19. Schnurr, P. P., Friedman, M. J. & Bernardy, N. C. (2002). Research on posttraumatic stress disorder: Epidemiology, pathophysiology, and assessment. Journal of Clinical Psychology, 58(8), 877-889. Vieweg, W. V., Julius, D. A., Fernandez, A., Beatty-Brooks, M., Hettema, J. M. & Pandurangi, A. K. (2006). Posttraumatic stress disorder: Clinical features, pathophysiology,
and treatment. Am J Med, 119(5), 383-390. Wisco, B. E., Marx, B. P. & Keane, T. M. (2012). Screening, diagnosis, and treatment of post-traumatic stress disorder. Military Medicine, 177(8), 7-13. Wolfgang, W., Falk, L., Frank, L. & Johannes, K. (2012). Psychodynamic psychotherapy for posttraumatic stress disorder related to childhood abuse- principles for a treatment manual. Bulletin of the Menninger Clinic, 76(1), 69-93.
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