Post-Traumatic Stress Disorder

Division of Traumatic Stress Studies and Department of Psychiatry, Mount Sinai School of Medicine and Bronx Veterans Affairs Medical Center, New York 10468, USA.
New England Journal of Medicine (Impact Factor: 55.87). 02/2002; 346(2):108-14. DOI: 10.1056/NEJMra012941
Source: PubMed


Although most people will gradually recover from the psychological effects of a traumatic event, PTSD will develop in a substantial proportion. PTSD appears to represent a failure to recover from a nearly universal set of emotions and reactions and is typically manifested as distressing memories or nightmares related to the traumatic event, attempts to avoid reminders of the trauma, and a heightened state of physiological arousal. Studies of the biologic mechanisms of PTSD have delineated circumscribed alterations in brain regions, such as the amygdala and hippocampus, that are associated with fear and memory, as well as changes in hormonal, neurochemical, and physiological systems involved in coordinating the body's response to stress. The treatment of PTSD involves educating the patient about the nature of the disorder, providing a safe and supportive environment for discussing traumatic events and their impact, and relieving the distress associated with memories and reminders of the event. A variety of approaches, such as exposure therapy, cognitive therapy, and pharmacotherapy, have been found to be effective in the treatment of PTSD.

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    • "Thus, dendritic remodeling of BLA neurons seems to require an incubation period after the stressful experience before they become evident and this structural change coincides with delayed anxiety behavior. In this regard, the effect of acute CORT treatment appears to be reminiscent of PTSD, in which a single traumatic event triggers changes in behaviors including anxiety that are both delayed and prolonged [21,22] and accompanied by BLA hyperactivity [23]. "
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    ABSTRACT: Background Glucocorticoid released by stressful stimuli elicits various stress responses. Acute treatment with a single dose of corticosterone (CORT; predominant glucocorticoid of rats) alone has previously been shown to trigger anxiety behavior and robust dendritic hypertrophy of neurons in the basolateral amygdala (BLA). Neurons in the medial prefrontal cortex (mPFC) are also known to be highly sensitive to stress and regulate anxiety-like behaviors. Nevertheless, we know less about acute CORT-induced structural changes of other brain regions and their behavioral outcomes. In addition, the temporal profile of acute CORT effects remains to be examined. The current study investigates time course changes of dendritic architectures in the stress vulnerable brain areas, the BLA and mPFC, and their behavioral consequences after acute treatment with a single dose of CORT. Results Acute CORT treatment produced delayed onset of dendritic remodeling in the opposite direction in the BLA and mPFC with different time courses. Acute CORT induced dendritic hypertrophy of BLA spiny neurons, which was paralleled by heightened anxiety, both peaked 12 days after the treatment. Meanwhile, CORT-induced dendritic atrophy of mPFC pyramidal neurons peaked on day 6, concomitantly with impaired working memory. Both changed dendritic morphologies and altered behavioral outcomes were fully recovered. Conclusion Our results suggest that stress-induced heightened anxiety appears to be a functional consequence of dendritic remodeling of BLA neurons but not that of mPFC. Instead, stress-induced dendritic atrophy of mPFC neurons is relevant to working memory deficit. Therefore, structural changes in the BLA and the mPFC might be specifically associated with distinct behavioral symptoms observed in stress-related mental disorders. Remarkably, stress-induced dendritic remodeling in the BLA as well as mPFC is readily reversible. The related behavioral outcomes also follow the similar time course in a reversible manner. Therefore, further studies on the cellular mechanism for the plasticity of dendrites architecture might provide new insight into the etiological factors for stress-related mental illness such as posttraumatic stress disorder (PTSD).
    BMC Neuroscience 05/2014; 15(1):65. DOI:10.1186/1471-2202-15-65 · 2.67 Impact Factor
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    • "PTSD is a group of diseases that are observed in patients who experience a serious incident and then feel fear and anguish from repeated recollections of such incident, and waste their energy in escaping from such feelings. Accordingly, PTSD patients' social activities are severely and adversely affected28). PTSD was introduced by Da Costa9) when they described the mental anguish of people who had experienced the American Civil War. "
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    ABSTRACT: Objective Post-traumatic stress disorder (PTSD) is a group of diseases that are observed in patients who had experienced a serious trauma or accident. However, some experienced it even after only a mild traumatic brain injury (TBI), and they are easily ignored due to the relatively favorable course of mild TBI. Herein, the authors investigated the incidence of PTSD in mild TBI using brief neuropsychological screening test (PTSD checklist, PCL). Methods This study was conducted on patients with mild TBI (Glasgow coma scale ≥13) who were admitted from January 2012 to December 2012. As for PCL, it was done on patients who showed no difficulties in communication upon admission and agreed to participate in this study. By using sum of PCL, the patients were divided into high-risk group and low-risk group. PTSD was diagnosed as the three major symptoms of PTSD according to the Diagnostic and Statistical Manual of Mental Disorders, fourth-edifion. Results A total of 314 TBI patients were admitted and 71 of them met the criteria and were included in this study. The mean age was 52.9 years-old (range: 15-94). The mean PCL score was 28.8 (range: 17-68), and 10 patients were classified as high-risk group. During follow-up, 2 patients (2.7%) of high risk group, were confirmed as PTSD and there was no patient who was suspected of PTSD in the low-risk group (p=0.017). Conclusion PTSD is observed 2.8% in mild TBI. Although PTSD after mild TBI is rare, PCL could be considered as a useful tool for screening of PTSD after mild TBI.
    Journal of Korean Neurosurgical Society 04/2014; 55(4):190-4. DOI:10.3340/jkns.2014.55.4.190 · 0.64 Impact Factor
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    • "Stressful life events are often accompanied by disruptions in cognitive and emotional processes related to learning and memory. In humans, stressful experiences can induce or exacerbate the symptoms of stress-related mental illness including post-traumatic stress disorder (PTSD) and generalized anxiety disorder (Kendler et al., 1995, 1999; Kessler, 1997; Brown, 1998; Lupien and Lepage, 2001; Yehuda, 2002; O’Donnell et al., 2004; Shors, 2004; McEwen, 2005; Lupien et al., 2009). Stressful life experiences have a significant impact on mental health in women, who are twice as likely as men to suffer from these disorders (Nolen-Hoeksema and Girgus, 1994; Breslau et al., 1997; Foa and Street, 2001; Tolin and Foa, 2006; Nolen-Hoeksema, 2012). "
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    ABSTRACT: Women are nearly twice as likely as men to suffer from anxiety and post-traumatic stress disorder (PTSD), indicating that many females are especially vulnerable to stressful life experience. A profound sex difference in the response to stress is also observed in laboratory animals. Acute exposure to an uncontrollable stressful event disrupts associative learning during classical eyeblink conditioning in female rats but enhances this same type of learning process in males. These sex differences in response to stress are dependent on neuronal activity in similar but also different brain regions. Neuronal activity in the basolateral nucleus of the amygdala (BLA) is necessary in both males and females. However, neuronal activity in the medial prefrontal cortex (mPFC) during the stressor is necessary to modify learning in females but not in males. The mPFC is often divided into its prelimbic (PL) and infralimbic (IL) subregions, which differ both in structure and function. Through its connections to the BLA, we hypothesized that neuronal activity within the PL, but not IL, during the stressor is necessary to suppress learning in females. To test this hypothesis, either the PL or IL of adult female rats was bilaterally inactivated with GABAA agonist muscimol during acute inescapable swim stress. 24h later, all subjects were trained with classical eyeblink conditioning. Though stressed, females without neuronal activity in the PL learned well. In contrast, females with IL inactivation during the stressor did not learn well, behaving similar to stressed vehicle-treated females. These data suggest that exposure to a stressful event critically engages the PL, but not IL, to disrupt associative learning in females. Together with previous studies, these data indicate that the PL communicates with the BLA to suppress learning after a stressful experience in females. This circuit may be similarly engaged in women who become cognitively impaired after stressful life events.
    Frontiers in Neural Circuits 12/2013; 7:198. DOI:10.3389/fncir.2013.00198 · 3.60 Impact Factor
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