***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: BACKGROUND The study estimates the relative importance of specific types of traumas experienced in the community in terms of their prevalence and risk of leading to posttraumatic stress disorder ( PTSD ) . METHODS A representative sample of 2181 persons in the Detroit area aged 18 to 45 years were interviewed by telephone to assess the lifetime history of traumatic events and PTSD , according to DSM-IV . Posttraumatic stress disorder was assessed with respect to a r and omly selected trauma from the list of traumas reported by each respondent , using a modified version of the Diagnostic Interview Schedule , Version IV , and the World Health Organization Composite International Diagnostic Interview . RESULTS The conditional risk of PTSD following exposure to trauma was 9.2 % . The highest risk of PTSD was associated with assaultive violence ( 20.9 % ) . The trauma most often reported as the precipitating event among persons with PTSD ( 31 % of all PTSD cases ) was sudden unexpected death of a loved one , an event experienced by 60 % of the sample , and with a moderate risk of PTSD ( 14.3 % ) . Women were at higher risk of PTSD than men , controlling for type of trauma . CONCLUSIONS The risk of PTSD associated with a representative sample of traumas is less than previously estimated . Previous studies have overestimated the conditional risk of PTSD by focusing on the worst events the respondents had ever experienced . Although recent research has focused on combat , rape , and other assaultive violence as causes of PTSD , sudden unexpected death of a loved one is a far more important cause of PTSD in the community , accounting for nearly one third of PTSD cases An altered function of the hypothalamic-pituitary-adrenal axis is assumed to be characteristic for Posttraumatic Stress Disorder ( PTSD ) , although there is inconsistent empirical evidence . Only few studies examined the awakening cortisol response and a daytime profile in PTSD .  Salivary cortisol levels were measured at seven intervals from awakening until 8 PM in trauma-exposed subjects with ( N=29 ) and without PTSD ( N=19 ) and in 15 non-exposed controls . While the three groups did not differ with respect to their first cortisol level immediately after awakening , the expected cortisol increase to awakening 15 - 60 min later was significantly lower in PTSD patients compared to non-PTSD subjects and healthy controls . This effect remained stable when trauma-exposed subjects with comorbid major depression were excluded from the analysis . A significant negative correlation between the overall cortisol secretion ( AUC(G ) ) and overall PTSD symptomatology and hyper-arousal symptoms was found . The findings are discussed in light of the hypothesis of a counterregulation of hyper-arousal symptoms and chronic stress in PTSD BACKGROUND Exposure to intense physical and psychological stress during septic shock can result in posttraumatic stress disorder in survivors . Patients with chronic posttraumatic stress disorder often show sustained reductions in serum cortisol concentration . This investigation examines whether increasing serum cortisol levels with hydrocortisone treatment during septic shock reduces the incidence of posttraumatic stress disorder in survivors . METHODS Patients ( n = 20 ) were recruited from a prospect i ve , r and omized double-blind study on the hemodynamic effects of hydrocortisone during septic shock . Eleven patients had received placebo and nine  stress doses of hydrocortisone . Posttraumatic stress disorder was diagnosed 31 months ( median ) after intensive care unit discharge using SCID-IV ( DSM-IV- criteria ) . Furthermore , the number of categories of traumatic memory from ICU treatment was determined in both groups at that time . RESULTS Only one of nine patients from the hydrocortisone group developed posttraumatic stress disorder , compared with seven of 11 patients in the placebo group ( p = .02 ) . There was no significant difference with regard to the number of categories of traumatic memory between the hydrocortisone and placebo groups . CONCLUSIONS The administration of hydrocortisone during septic shock in a dosage similar to the endogenous maximal production rate was associated with a lower incidence of posttraumatic stress disorder in long-term survivors , which seems to be independent of the number of categories of traumatic memory BACKGROUND We examine whether traumatic events increase the risk for  major depression  independent of their effects on posttraumatic stress disorder ( PTSD ) . METHODS Data come from the Epidemiologic Study of Young Adults in southeast Michigan ( N = 1007 ) .  Retrospective and prospect i ve data were used to estimate the risk of major depression in persons with PTSD and persons exposed to trauma with no PTSD , compared with persons who did not experience a trauma . National Comorbidity Survey data were used to evaluate the influence of trauma type . RESULTS In the retrospective lifetime data , hazard ratios were , for first-onset major depression in exposed persons with PTSD , 2.8 and , in exposed persons with no PTSD , 1.3 ( not significant ) , as compared with persons who were not exposed . Corresponding estimates from the prospect i ve data were 11.7 and 1.4 ( not significant ) . The difference in the risk for depression associated with PTSD versus exposure without PTSD is unlikely to be due to differences in trauma type . CONCLUSIONS The findings of a markedly increased risk for major depression in persons with PTSD , but not in exposed persons without PTSD , do not support the hypothesis that PTSD and major depression in trauma victims are influenced by separate vulnerabilities BACKGROUND While enhanced cortisol suppression in response to dexamethasone is one of the most consistent biological findings in posttraumatic stress disorder ( PTSD ) , the relative contribution of trauma exposure to this finding remains unclear . METHODS Assessment of diurnal salivary cortisol levels and 1600 h salivary cortisol before and after oral administration of 0.5 mg dexamethasone in veterans with PTSD , veterans without PTSD ( trauma controls ) and healthy controls . Assessment of 1600 h plasma cortisol , ACTH and corticotrophin binding globulin ( CBG ) in response to dexamethasone in PTSD patients and trauma controls . RESULTS Both PTSD patients and trauma controls demonstrated significantly more salivary cortisol suppression compared to healthy controls . Salivary cortisol , plasma cortisol and ACTH suppression as well as CBG levels did not differ between PTSD patients and trauma controls . PTSD patients showed a reduced awakening cortisol response ( ACR ) compared to healthy controls that correlated significantly with PTSD symptoms . No significant differences were observed in ACR between PTSD patients and trauma controls . CONCLUSIONS These data suggest that enhanced cortisol suppression to  dexamethasone  is related to trauma exposure and not specifically to PTSD . The correlation between the ACR and PTSD severity suggests that a flattened ACR may be a result of clinical symptoms OBJECTIVE The purpose of this study was to prospect ively evaluate the onset , overlap , and course of posttraumatic stress disorder ( PTSD ) and major depression following traumatic events . METHOD The occurrence of PTSD and major depression and the intensity of related symptoms were assessed in 211 trauma survivors recruited from a general hospital 's emergency room .  Psychometrics and structured clinical interview ( the Structured Clinical Interview for DSM-III-R and the Clinician-Administered PTSD Scale ) were administered 1 week , 1 month , and 4 months after the traumatic event .  Heart rate  was assessed upon arrival at the emergency room for subjects with physical injury . Twenty-three subjects with PTSD and 35 matched comparison subjects were followed for 1 year . RESULTS Major depression and PTSD occurred early on after trauma ; patients with these diagnoses had similar recovery rates : 63 survivors ( 29.9 % ) met criteria for PTSD at 1 month , and 37 ( 17.5 % ) had PTSD at 4 months . Forty subjects ( 19.0 % ) met criteria for major depression at 1 month , and 30 ( 14.2 % ) had major depression at 4 months . Comorbid depression occurred in 44.5 % of PTSD patients at 1 month and in 43.2 % at 4 months . Comorbidity was associated with greater symptom severity and lower levels of functioning . Survivors with PTSD had higher heart rate levels at the emergency room and reported more intrusive symptoms , exaggerated startle , and peritraumatic dissociation than those with major depression . Prior depression was associated with a higher prevalence of major depression and with more reported symptoms . CONCLUSIONS Major depression and PTSD are independent sequelae of traumatic events , have similar prognoses , and interact to increase distress and dysfunction . Both should be targeted by early treatment interventions and by neurobiological research BACKGROUND The hypothalamic-pituitary-adrenal axis and the catecholaminergic system are involved in the pathophysiology of post-traumatic stress disorder ( PTSD ) . This was a prospect i ve and longitudinal study of neuroendocrine physiology in children with PTSD following a motor vehicle accident ( MVA ) .  METHODS Sixty children aged 7 - 18 were studied immediately after an MVA and 1 and 6 months later .  Fasting morning plasma catecholamine and serum cortisol concentrations  were measured . Salivary cortisol concentrations were measured serially five times daily to examine circadian variation in all three assessment s. Values were compared between those who did ( PTSD ) or did not develop PTSD ( non-PTSD ) after the trauma and a control group at months 1 and 6 . RESULTS Twenty-three of the children had PTSD at the 1-month and 9 children at the 6-month evaluations . 1 ) Plasma noradrenaline concentrations were higher in the PTSD group than in the other two groups at both months 1 and 6 ( p = .001 and p = .001 , respectively ) . Additionally , the PTSD patients presented with significantly higher salivary cortisol concentrations at 18.00 ( p = .03 ) and 21.00 ( p = .04 ) at month 1.2 ) Eight children suffering from PTSD at both months 1 and 6 had significantly elevated plasma noradrenaline concentrations at month 6 compared with those at month 1 and at baseline and to the other two groups ( within subjects : p < .001 ; between subjects : p = .005 ) . The initially elevated evening salivary cortisol concentrations in this group normalized at month 6 . CONCLUSIONS This progressive divergence of noradrenaline and cortisol concentrations over time might underlie the natural history and pathophysiology of PTSD BACKGROUND This study was design ed to examine the relationship between urinary hormone levels collected upon admission to the trauma unit following a motor vehicle accident and posttraumatic stress disorder symptomatology 1 month later . METHODS Fifteen-hour urine sample s were collected from 63 male and 36 female motor vehicle accident victims and were used to assess levels of catecholamines and cortisol reflecting peritraumatic and acute-phase posttraumatic levels . Presence of posttraumatic stress disorder symptomatology was assessed 1 month after the accident . RESULTS Motor vehicle accident victims subsequently diagnosed with acute posttraumatic stress disorder excreted significantly lower levels of cortisol in 15-hour urines collected upon admission to the hospital . In addition , urinary levels of cortisol predicted a significant percentage of the variance in intrusive and avoidant thoughts 1 month after the accident . CONCLUSIONS The results of our study suggest that initial cortisol levels in the immediate aftermath of a traumatic event contribute , in part , to subsequent symptoms of posttraumatic stress disorder BACKGROUND Because alterations in cortisol negative feedback inhibition associated with aging are generally opposite of those observed in posttraumatic stress disorder ( PTSD ) , we examined the cortisol and glucocorticoid receptor ( GR ) response to dexamethasone ( DEX ) in older trauma survivors . METHODS Twenty-three Holocaust survivors ( 9 men , 14 women ) , 27 combat veterans ( all male ) , and 10 comparison subjects ( 7 men , 3 women ) provided sample s for plasma or salivary cortisol and glucocorticoid receptor determination in mononuclear leukocytes at 8:00 AM on the day of , and following , 0.5 mg of DEX at 11:00 PM . RESULTS Greater percent suppression of cortisol and lymphocyte GR was observed in older trauma survivors with PTSD compared to survivors without PTSD and comparison subjects . There was a significant main effect of depression in the direction of reduced suppression following DEX , consistent with the effects of DEX in major depressive disorder patients . Responses to DEX were uncorrelated with PTSD symptom severity , but cortisol suppression was associated with years elapsed since the most recent , but not focal , traumatic event . CONCLUSIONS The response to DEX is generally similar in older and younger trauma survivors , but the findings suggest that age , symptom severity , and lifetime trauma exposure characteristics may influence this response OBJECTIVE To evaluate cortisol suppression following 0.5 mg of dexamethasone ( DEX ) in trauma survivors ( N=52 ) with posttraumatic stress disorder ( PTSD ) , major depressive disorder ( MDD ) , both , or neither disorder , and in subjects never exposed to trauma ( N=10 ) , in order to examine interactions between diagnosis and trauma history on cortisol negative feedback inhibition 
    Output:
    
These findings suggest that enhanced HPA feedback function may be a marker of trauma-exposure rather than a specific mechanism of vulnerability for PTSD , whereas lower daily cortisol output may be associated with PTSD in particular