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Analysis of Post Traumatic Stress Disorder - Research Paper Example

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The paper "Analysis of Post Traumatic Stress Disorder" discusses that PTSD develops when an individual either experiences, witnesses or confronts with an event that is either serious injury like accident, death or in the form of any threat to physical integrity…
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Analysis of Post Traumatic Stress Disorder
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Post Traumatic Stress Disorder Introduction Post traumatic stress disorder or PTSD is a very common mental health condition that occurs as a consequence of exposure to severe form of trauma (Gore and Lucas, 2010). It can occur to any individual irrespective of sex, age, race, country, culture and profession (Gore and Lucas, 2010). The condition is the abnormal end result of an overwhelming and powerful incident that is stressful. It leads to several changes in an individual and contributes to various personality changes and illnesses and if ignored may end with suicide. The condition occurs when individuals are able to work through their normal reactions during stress and thus are unable to recover from terrible experience. It is very important to identify and manage PTSD as early as possible because; research has shown that appropriate identification and treatment in early stages prevents progression of the diseases and helps the person revert to normalcy (Gore and Lucas, 2010). In this essay, the causes, pathogenesis, diagnosis, clinical presentation, management and ethical considerations of PTSD will be discussed with reference to suitable literature. Description of the disorder and historical aspects PTSD was formerly considered as a response reaction to stress or situation. However, it is now considered as a psychiatric disorder and is classified under the Diagnostic and Statistical Manual of Mental Disorders since 1980. It is currently defined as "a pathological anxiety that usually occurs after an individual experiences or witnesses severe trauma that constitutes a threat to the physical integrity or life of the individual or of another person" (Gore and Lucas, 2010). Following the trauma, the individual initially develops intense fear, feelings of horror and helplessness. After the initial phase, the person enters a phase in which he re-experiences the event persistently, because of which he suffers from avoidance, numbness and hyperarousal. leading to significant distress and impairment of functions of the individuals (Gore and Lucas, 2010). In order to be diagnosed as PTSD, these symptoms must be present atleast for a period of one month after the traumatic incident (Gore and Lucas, 2010). Some of the traumatic incidents which may trigger PTSD are war, road traffic accidents, personal violences, natural calamities, death of a beloved one and diagnosis of life threatening condition like cancer. In children, PTSD can occur due to any form of abuse including sexual abuse (Gore and Lucas, 2010). When the symptoms of PTSD last for less than 3 months, it is known as acute PTSD; if they last more than 3 months, it is considered to be chronic PTSD and if the symptoms appear after 6 months of the traumatic event, it is known as delayed onset PTSD (Gore and Lucas, 2010). Recently, researchers have identified 2 types of PTSD: the dissociative PTSD and non-dissociative PTSD. In the former type, affect is overmodulated and their is dysregulation of emotion. This occurs mainly due to inhibition of the limbic region by prefrontal area. In the non-dissociative form, affect and emotions are intact (Gore and Lucas, 2010). The worldwide incidence of PTSD is unknown. However, it is estimated that the lifetime prevalence of this condition is 8-10 percent and is associated with significant morbidity and disability. The incidence is more among females than in males. Severity of trauma has a direct relationship to the risk of PTSD (Gore and Lucas, 2010). Presence of PTSD increases the risk of homicide, suicide and impulsiveness. These symptoms are seen more in those who are victims of sexual abuse (Gore and Lucas, 2010). Pathophysiology The main site of pathogenesis in PTSD is amygdala. It has been proposed that exposure to trauma can cause fear conditioning and activation of amygdala and various other related structures like parabrachial nucleaus, periaqueductal gray, hypothalamus and locus ceruleus. Activation of these regions, along with endocrine activation and neurotransmitter activity lead to PTSD symptoms. Usually, in normal persons, orbitoprefrontal cortex and hippocampus, cause inhibition and modulation of the activation of amygdala and related areas. However, in PTSD patients, this modulation and inhibition activity is less effective, mostly due to atrophy of the nuclei following stress. This ultimately causes symptoms (Gore and Lucas, 2010). According to the neuroendocrinology theory, overactive adrenaline response following a traumatic event causes certain typical deep neurological patterns in brain. These patterns can remain for a long time much after the traumatic event, making the individual hyperresponsive during situations which are fearful. The biochemical and neuroendocrinological changes in PTSD are different from those in depression or other psychotic diseases. One typical endocrine related change is that, individuals with PTSD respond strongly to dexamethasone suppression test when compared to those with clinical depression. Also, the secretion of cortisol, which is usually increased in stress is much low in PTSD, but the levels of catecholamines are very high. Thus the norepinephrine: cortisol ratio is much high in PTSD patients than others. In a normative stress response, both the cortisol and catecholamine response is much higher. Some research has shown that the catecholamine levels in brain per se are low and the levels of corticotrophin releasing factor are high. All these amount to the fact that in PTSD, the hypothalamic-pituitary-adrenal axis is abnormal (Yehuda et al, 2004). When a patient with PTSD is challenged with dexamethasone, cortisol suppression is strong. Some researchers attribute the development of PTSD to long term exposure to high levels of noradrenaline and low cortisol levels. Such a response is seen in learning animals and it has been thought that PTSD mainly occurs due to maladaptive pathway of learning towards response to fear through a HPA axis that is hyperreactive, hypersensitive and also hyperresponsive (Yehuda, 2002). Some researchers are of the opinion that PTSD may be hereditary an this assumption is mainly based on certain twin studies. According to a study by True et al (1993), the researchers found that when twins were exposed to war in Vietnam and developed PTSD, the opposite twin also developed the disease when he or she was a monozygotic twin rather than a dizygotic twin. Binder et al (2008) identified some single-nucleotide polymorphisms in the FK506 binding protein 5 in childhood trauma related PTSD. All these amount to the fact that PTSD is probably hereditary. Clinical presentation and diagnosis PTSD can occur subclinically and general physicians may fail to recognize these symptoms. There are 6 criteria to be met for a patient to be diagnosed with PTSD. First of all, the patient must either experience, witness or confront with a traumatic event like death, serious injury or threat to physical integrity like accident. This must be followed by development of symptoms like horror, severe fear or helplessness. In children, these typical symptoms may not be present and they may manifest as behavioral problems and agitation. The next criteria is that the person re-experiences the traumatic event by one or several ways like dreams, thoughts about the injury, images of the injury, hallucinations, illusions, intense psychological distress or flash back episodes. In children, re-experiencing occurs through repetitive play. The third criteria are avoidance of various stimuli associated with the trauma like avoidance of feelings, thoughts, conversation, people, activities and places related to the traumatic event. The patients may even fail to recall the event aspects and feel detached from others. Their affect range can get narrowed and they may show lack of interest in various important activities. The fourth criteria is presence of hyperarousal and other symptoms like sleep disturbances, hypervigilance, irritable mood, decreased concentration, startle response that is exaggerated and outbursts of anger. The fifth criteria is that the symptoms must last for atleast a month. If the symptoms last less than one moth, the diagnosis is acute stress disorder. The sixth criteria is that the patient suffers from significant distress an the functions of the individuals are impaired (Gore and Lucas, 2010). While the above criteria can be used to diagnose PTSD in adolescents and adults, in children some variations in presentation can occur. For example, in children less than 5 years of age, PTSD can manifest as severe separation anxiety, excessive crying, screaming and whimpering, facial expressions of extreme fright, severe clinging and trembling. They may also develop regressive behaviours. Children of this age group are affected strongly by the reactions of their parents to traumatic event. Children between 6- 11 years may manifest with disruptive behaviours, withdrawal symptoms and inattentiveness. Other symptoms include sleep disturbances, regressive behaviours, irrational fears, anger outbursts, refusal to go to school, excessive fighting, irritability, guilty feelings, anxiety, depression and numbness (Gore and Lucas, 2010). Physical examination of patients with PTSD may not reveal any significant findings. Those with physical traumatic injury like accident or physical abuse may have some wounds or bruises. In chronic PTSD, somatic complaints like head ache may be there, but with normal physical findings. Other findings include, poor general appearance, poor personal hygiene, altered behaviour, extreme startle reaction, poor memory, poor concentration, poor impulse, altered speech flow and rate and changed mood and affect (Gore and Lucas, 2010). Causes PTSD develops when an individual either experiences, witnesses or confronts with an event that is either serious injury like accident, death or in the form of any threat to physical integrity. The risk of PTSD depends directly on the severity of trauma and the intensity of symptoms in the acute phase. Other factors which contribute to the disease are genetic vulnerability, adversities in childhood, previous exposure to trauma, preexisting mental problems like depression and anxiety, family history of psychiatric illness, sex of the individual and several posttrauma factors like social support (Gore and Lucas, 2010). Those employed in emergency services like military operations, police services, fire services, accident and calamity rescue services and emergency health services, are at increased risk of development of PTSD because of the nature of their job. This could be due their own living environment, their protective gear, their officers and leaders, current management styles, co-workers, and the stress of leaving their families and loved ones alone during natural and man-made disasters. Many of them are required to withstand horrendous physical and psychological assaults as they perform their duty. They have to work in the midst of civil unrest, urban terrorism, structural collapse, earthquakes, and hurricanes. They need to be action oriented and need to be in control (Wagner et al, 1998). Differential diagnoses PTSD must be differentiated from other conditions like acute stress disorder, malingering, adjustment disorder, mood disorders, iatrogenic psychotic disorders and substance-induced disorders (Gore and Lucas, 2010). Laboratory findings PTSD is mainly a diagnosis based on clinical symptoms. There is no laboratory test that can be used to establish the diagnosis. Research has shown that certain hormonal changes are evident in this disorder like decrease in cortisol levels, increase in a adrenaline and noradrenaline levels and abnormal hypothalamic-pituitary-adrenal axis. Magnetic resonance imaging may show atrophy of hippocampus. Monitoring of heart rate, activity of sweat glands and electromyography may be useful to ascertain increased arousal (Gore and Lucas, 2010). Treatment Early assessment, diagnosis and management of the disease can revert many symptoms of PTSD and prevent progression of disabilities and distress. Treatment includes a combination of pharmacologic and nonpharmacologic therapies. In many people, comorbid conditions may be present and they must be identified and treated for successful outcomes. Non-pharmacological treatments include cognitive behavioural therapies or CBT, art therapy, management of anxiety, play therapy, eye movement desensitization and reprocessing or EMDR and relaxation techniques. According to a recent meta-analysis study (in Gore and Lucas, 2010), cognitive behavioral therapies and EMDR are the first line treatments. In young people, like children and adolescents, the main treatment is psychotherapy. In those with sexual or physical abuse, psychodynamic-oriented psychotherapy is preferable. In veterans, flooding is a useful treatment (Gore and Lucas, 2010). There is enough evidence to show that CBT ameliorates symptoms in PTSD. According to a study by Hembree and Foa (2000; cited in Grinage, 2003), 21- 46 percent of patients with PTSD attained relied of symptoms when CBT sessions were provided during 9 sessions over 6-week period. In yet another study by the same authors (cited in Grinage, 2003), 10 sessions of therapy spanned over 16 weeks decreased symptoms in 32- 53 percent patients. CBT is a type of psychotherapy that mainly influences cognitive thoughts, behaviours and emotions that are not only problematic, but also dysfunctional, through an approach that is systematic and also 'goal-oriented. CBT is effective in many anxiety conditions including PTSD. CBT is actually a combination of cognitive and behavioural therapy. The main objective of cognitive therapy is to identify beliefs, thoughts, behaviours and assumptions related to inaccurate, dysfunctional, unhelpful and debilitating emotions and monitor them. The therapy replaces or transcends these emotions with more useful and realistic emotions. Emotional dysfunction is basically maintained by self-focused attention that is inflexible, metacognitive beliefs and perseverative thinking. Cognitive therapy corrects this dysregulation through identification and modification of these aspects. In behaviour therapy, the main focus is on modification of behaviour. This is done by teaching the patient various relaxation skills, self-monitoring skills and techniques to extinguish certain fears. Specific components of CBT which are specifically useful in CBT patients are exposure therapy, cognition therapy and also stress inoculation training. These therapies basically focus on the strategies that patients adopt to confront fear, thus helping the patient develop anxiety management. Most trainers use a combination of various therapies in CBT. Though other treatments, other than CBT have been found useful in PTSD, lack of proper substantial demonstration has made CBT the primary mode of treatment (Grinage, 2003). One of the major problems related to success in CBT is compliance to treatment. Studies have shown that 14 percent of the patients discontinue CBT in between (Grinage, 2003). More than 50 percent drop outs occur in exposure therapy indicating difficulties in re-experiencing events of trauma. Drop out rate can be decreased by providing empathic support to the patient and also by listening to the client (Grinage, 2003). PTSD can have devastating consequences on social, financial, economic and cultural life of the patient and even family members can be affected. Hence group therapy may be useful in which even family members can get involved (Grinage, 2003). Pharmacological management Several large prospective and randomized controlled trials have been conducted to in regard to pharmacological management of PTSD. Drugs approved for use in PTSD include parxetine and sertraline. Trials have shown that both drugs are equally effective in the treatment of PTSD. According to a study by Marshall et al (2001; cited in Grinage, 2003 ), "of the patients who received 20 mg or 40 mg of paroxetine, 62 percent and 54 percent, respectively, responded positively compared with 37 percent of patients who received placebo." In the study by Davidson et al (2001; cited in Grinage, 2003) "patients who received a mean daily dosage of 146 mg of sertraline had a 60 percent positive response rate compared with a 38 percent positive response rate in patients receiving placebo." In some patients with associated psychotic symptoms, anti-psychotic medication msy need to be administered. Infact, 10 percent of patients with PTSD need antipsychotic medication like risperidone to decrease nightmares and flashbacks. other drugs useful in PTSD are clozapine, olanzipine, tricyclic antidepressants, monoamine oxidase inhibitors and mood stabilisers like valproate, lamotrigine and carbamazepine. Some research has shown that administration of propranolol in the initial acute phase following stress can have a preventive effect on the development of PTSD subsequently (Grinage, 2003). Ethical considerations There are several gaps in the understanding of PTSD and ethical and legal considerations are important because of the congressional and public interest in PTSD. The interest in this topic is more increased because many veterans suffer from this disorder and repeated deployments have caused an exacerbation of this problem. Another important aspect PTSD is that many sufferers are reluctant to seek medical help (Grifford, 2008). According to the Ethical Practices in Research, " Veterans with a diagnosis of PTSD should be afforded special consideration consistent with current regulation and policy if and when an IRB determines that these veterans have impaired decision-making capacity, an increased susceptibility to undue influence or coercion, or an increased susceptibility to the risks associated with a particular research study" (Berkowitz et al, 2009). Conclusion PTSD is a mental condition that occurs as a consequence of exposure to severe traumatic incident. It is often unrecognized and under diagnosed. Even those who are diagnosed may be reluctant to seek medical help. The condition mainly occurs due to maladaptation to stress either due to inappropriate response by the HPA axis or due to neuroanatomical changes secondary to persistent elevation of catecholamine levels, or due to genetic predisposition. The diagnosis is mainly established by clinical examination. Treatment can be pharmacological or nonpharmacological. CBT is the most useful nonpharmcological approach. Drugs approved for use in PTSD include parxetine and sertraline. Early identification of the disorder and institution of timely management prevents development of disabilities and complications and helps the individual revert back to normalcy. References Berkowitz, K., Hans, S., Olsen, D., et al. (2009). Ethical Considerations in the Report of a Work Group on Post Traumatic Stress Disorder (PTSD) and Vulnerable Populations in Research. Ethical Practices in Research. Retrieved on Dec 4th, 2010 from http://webcache.googleusercontent.com/search?q=cache:iiL-BD01C30J:www.ethics.va.gov/docs/net/NET_Topic_20090225_exec_summary.doc+PTSD+ethical+consideration&cd=5&hl=en&ct=clnk&gl=in Binder, E.B., Bradley, R.G., Liu, W., et al. (2008). Association of FKBP5 polymorphisms and childhood abuse with risk of posttraumatic stress disorder symptoms in adults. JAMA, 299 (11), 1291–305. Gore, T.A., and Lucas, J.Z. (2010). Posttraumatic Stress Disorder. Emedicine from WebMD. Retrieved on Dec 4th, 2010 from http://emedicine.medscape.com/article/288154-overview Gifford, R.K. (2008). Key Ethical Considerations in PTSD and TBI Research. Uniformed Services University. Retrieved on Dec 4th, 2010 from http://www.dtic.mil/biosys/docs/hu-key_ethical_considerations_ptsd_tbi-2008.pdf Grinage, B.D. (2003). Diagnosis and Management of Post-traumatic Stress Disorder. American Family Physician, 68(12), 2401-2409. Retrieved on Dec 4th, 2010 from http://www.aafp.org/afp/2003/1215/p2401.html, True, W.R., Rice, J., Eisen, S.A., et al. (1993). A twin study of genetic and environmental contributions to liability for posttraumatic stress symptoms. Arch. Gen. Psychiatry, 50 (4), 257–64. Yehuda, R. (2002). Clinical relevance of biologic findings in PTSD. Psychiatr Q, 73 (2): 123–33. Yehuda, R., Halligan, S.L., Golier, J.A., Grossman, R., Bierer, L.M. (2004). Effects of trauma exposure on the cortisol response to dexamethasone administration in PTSD and major depressive disorder. Psychoneuroendocrinology, 29 (3), 389–404. Read More
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