-
[show abstract]
[hide abstract]
ABSTRACT: Abstract There is a large literature demonstrating that individuals who have experienced traumatic events have alterations in the hypothalamic-pituitary-adrenal (HPA) axis. However, the existing literature does not address the extent to which these alterations represent pre-existing risk factors for developing psychopathology upon exposure to a significant stressor. In the current study, we examined the relationship between waking salivary cortisol level and physiological, personality, and psychological measures in 60 firefighters and police trainees during training, and then again after exposure to a highly stressful, potentially traumatic event (PTE). Waking cortisol was negatively associated with neuroticism, but positively associated with physiological reactivity to loud tones and fear conditioning when assessed during training. Longitudinally, there were significant negative correlations between pre-PTE waking cortisol and post-PTE negative mood and anxiety symptoms, but a positive correlation (trend) between pre-PTE waking cortisol and post-PTE physiological reactivity during recollection of the PTE. Thus, waking cortisol level may serve to predict divergent types of emotional sequelae following PTEs.
Anxiety, stress, and coping 03/2012; · 1.55 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: This study sought to characterize the variability of the acute cortisol response following trauma and its relationship to posttraumatic stress disorder (PTSD). Forty eight participants were recruited within 24h of a traumatic accident requiring hospital admission. A saliva sample was collected at 08.00 h and 16.00 h 2 days, 1 month and 6 months after hospital admission, together with 24-h urine collection. Participants completed a dexamethasone suppression test (0.5mg DEX at 21.00 h) at each follow up, together with self-report questionnaires. The Clinician Administered PTSD Scale (CAPS) was administered at 1 and 6 months to identify PTSD. Prevalence of PTSD was 27% at 1 month and 21% at 6 months. PTSD symptoms at 6 months were negatively correlated with salivary cortisol at 08.00 h on day 2 (r=-0.36, p=0.04), but positively correlated with 16.00 h cortisols (r=0.41, p=0.03). A lower rise in cortisol at 08.00 h on day 2 was associated with an increase in risk of PTSD at both 1 month (OR=1.411 (1.017, 1.957)) and 6 months (OR=1.411 (1.066, 1.866)). At 1 month, 70% of participants with PTSD suppressed cortisol to more than 90% of pre-dex levels compared with 25% without PTSD (χ(2)=6.77, p=0.034). Urinary cortisol excretion was not different between groups at any time point. The findings support a hypothesis that sensitization of the HPA axis and enhanced suppression of cortisol following the dexamethasone suppression test are established early in the disease process.
Psychoneuroendocrinology 11/2010; 36(5):720-7. · 5.81 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: The diagnosis of posttraumatic stress disorder (PTSD) is unique in that its criteria are embedded with a presumed causal agent, viz, a traumatic event. This assumption has come under scrutiny as a number of recent studies have suggested that many symptoms of PTSD may not necessarily be the result of trauma and may merely represent general psychiatric symptoms that would have existed even in the absence of a trauma event but are subsequently misattributed to it. The current study tests this hypothesis.
A case-control twin study conducted between 1996-2001 examined psychopathologic symptoms in a national convenience sample of 104 identical twin pairs discordant for combat exposure in Vietnam, with (n = 50) or without (n = 54) combat-related PTSD (DSM-IV-diagnosed) in the exposed twin. Psychometric measures used were the Symptom Checklist-90-Revised, the Clinician-Administered PTSD Scale, and the Mississippi Scale for Combat-Related PTSD. If a psychopathologic feature represents a factor that would have existed even without traumatic exposure, then there is a high chance that it would also be found at elevated rates in the non-trauma-exposed, identical cotwins of trauma-exposed twins with PTSD. In contrast, if a psychopathologic feature is acquired as a result of an environmental factor unique to the exposed twin, eg, the traumatic event, their cotwins should not have an increased incidence of the feature.
Combat veterans with PTSD demonstrated significantly higher scores (P < .0001) on the Symptom Checklist-90-Revised and other psychometric measures of psychopathology than their own combat-unexposed cotwins (and than combat veterans without PTSD and their cotwins).
These results support the conclusion that the majority of psychiatric symptoms reported by combat veterans with PTSD would not have been present were it not for their exposure to traumatic events.
The Journal of Clinical Psychiatry 10/2010; 71(10):1324-30. · 5.80 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: It has been suggested that discrepant findings regarding low basal cortisol levels and enhanced suppression of cortisol in response to dexamethasone (DEX) administration in post-traumatic stress disorder (PTSD) may reflect individual differences in gender, trauma type, stage of development at trauma occurrence (e.g., childhood vs. adulthood), early pre-traumatic risk factors, or other individual differences. This study examined salivary cortisol levels at 08.00h and 16.00h as well as cortisol response to 0.50 mg DEX in 40 female Vietnam nurse veterans who had current, chronic PTSD (Current) vs. 43 who never had PTSD (Never). Repeated measures analyses of covariance did not reveal significant group differences in cortisol levels or cortisol suppression. Given that nurses who served in Vietnam had similar exposures, ages at exposure, and duration since exposure to previously studied male Vietnam combat veterans, the present lack of evidence for low cortisol and cortisol hyper-suppression in nurses with PTSD suggests that previous findings of low cortisol and cortisol hyper-suppression in male Vietnam veterans, females sexually abused as children, and other populations may reflect risk factors beyond simply having PTSD.
Psychiatry Research 11/2008; 161(3):330-5. · 2.52 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: The aim of the study was to prospectively evaluate the association between the occurrence of post-traumatic stress disorder (PTSD) and the adrenergic response to the traumatic event, and additionally, to explore the link between PTSD and the initial norepinephrine:cortisol ratio. Plasma levels and urinary excretion of norepinephrine (NE) were measured in 155 survivors of traumatic events during their admission to a general hospital emergency room (ER) and at 10 d, 1 month and 5 months later. Symptoms of peri-traumatic dissociation, PTSD and depression were assessed in each follow-up session. The Clinician-Administered PTSD Scale (CAPS) conferred a diagnosis of PTSD at 5 months. Trauma survivors with (n=31) and without (n=124) PTSD had similar levels of plasma NE, urinary NE excretion, and NE:cortisol ratio in the ER. Plasma NE levels were lower in subjects with PTSD at 10 d, 1 month, and 5 months. There was a weak but significant positive correlation between plasma levels of NE in the ER and concurrent heart rate, and a negative correlation between NE in the ER and dissociation symptoms. Peripheral levels of NE, shortly after traumatic events, are poor risk indicators of subsequent PTSD among civilian trauma victims. Simplified biological models may not properly capture the complex aetiology of PTSD.
The International Journal of Neuropsychopharmacology 06/2008; 11(3):373-80. · 4.58 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: The aim of the study was to evaluate the association between post-traumatic disorder (PTSD) and hypothalamic-pituitary-adrenal (HPA) axis responses to the triggering trauma. A companion paper evaluates the adrenergic response and interactions between the two. We measured plasma and saliva cortisol, hourly urinary excretion of cortisol, plasma levels of adrenocorticotropin (ACTH), and the leukocyte glucocorticoid receptor (GR) density of 155 non-injured survivors of traumatic events (91 males and 64 females; 125 road traffic accidents, 19 terrorist attacks, 11 others). Measurements were taken during survivors' admissions to an emergency room (ER) of a general hospital, and in the mornings, 10 d, 1 month, and 5 months later. Symptoms of peri-traumatic dissociation, PTSD, and depression were assessed on each follow-up session. The clinician-administered PTSD scale (CAPS) conferred a diagnosis of PTSD at 5 months. Survivors with (n=31) and without (n=124) PTSD at 5 months had similar levels of hormones at all times. Plasma cortisol levels decreased with time in both groups. Female subjects had lower ACTH levels than males. PTSD in females was associated with higher levels of ACTH. In unselected cohorts of trauma survivors, PTSD is not preceded by a detectable abnormality of peripheral HPA axis hormones.
The International Journal of Neuropsychopharmacology 06/2008; 11(3):365-72. · 4.58 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: A biological abnormality found to be associated with posttraumatic stress disorder (PTSD) may be, among other things, a pretrauma vulnerability factor, that is, it may have been present prior to the event's occurrence and increased the individual's likelihood of developing PTSD upon traumatic exposure. Alternately, it may be an acquired PTSD sign, that is, it may have developed after the traumatic exposure, along with the PTSD. We have studied pairs of Vietnam combat veterans and their noncombat-exposed, identical twins in an effort to resolve these competing origins. Combat veterans were diagnosed as current PTSD or non-PTSD (i.e., never had). Average heart rate responses (HRRs) to a series of sudden, loud-tone presentations were larger in Vietnam combat veteran twins with PTSD, but these larger responses were not shared by their noncombat-exposed cotwins, whose responses were similar to those of the non-PTSD combat veterans and their noncombat-exposed cotwins. These results suggest that larger HRRs to sudden, loud tones represent an acquired sign of PTSD. In contrast, increased neurological soft signs (NSSs), diminished hippocampal volume, and presence of abnormal cavum septum pellucidum (CSP) were found in Vietnam combat veteran twins with PTSD and their "high-risk," unexposed cotwins compared to Vietnam combat veteran twins without PTSD and their "low-risk," unexposed cotwins. These results support the conclusion that the latter abnormalities represent antecedent, familial vulnerability factors for developing chronic PTSD upon exposure to a traumatic event.
Annals of the New York Academy of Sciences 08/2006; 1071:242-54. · 3.15 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Following exposure to trauma, a large number of survivors will develop acute symptoms of posttraumatic stress disorder (PTSD), which mostly dissipate within a short time. In a minority, however, these symptoms will evolve into chronic and persistent PTSD. A number of factors increase the likelihood of this occurring, including characteristic autonomic and hypothalamic-pituitary-adrenal axis responses. PTSD often presents with comorbid depression, or in the form of somatization, both of which significantly reduce the possibilities of a correct diagnosis and appropriate treatment. Mainstay treatments include exposure-based psychosocial therapy and selective serotonin reuptake inhibitors, such as paroxetine and sertraline, both of which have been found to be effective in PTSD. This paper looks at the course of PTSD, its disabling effect, its recognition and treatment, and considers possible new research directions.
Journal of Neuropsychiatry 02/2004; 16(2):135-47. · 2.51 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: To provide an update to the "Consensus Statement on Posttraumatic Stress Disorder From the International Consensus Group on Depression and Anxiety" that was published in a supplement to The Journal of Clinical Psychiatry (2000) by presenting important developments in the field, the latest recommendations for patient care, and suggestions for future research.
The 4 members of the International Consensus Group on Depression and Anxiety were James C. Ballenger (chair), Jonathan R. T. Davidson, Yves Lecrubier, and David J. Nutt. Other faculty who were invited by the chair were Randall D. Marshall, Charles B. Nemeroff, Arieh Y. Shalev, and Rachel Yehuda.
The consensus statement is based on the 7 review articles in this supplement and the related scientific literature.
Group meetings were held over a 2-day period. On day 1, the group discussed topics to be represented by the 7 review articles in this supplement, and the chair identified key issues for further debate. On day 2, the group discussed these issues to arrive at a consensus view. After the group meetings, the consensus statement was drafted by the chair and approved by all faculty.
There have been advancements in the science and treatment of posttraumatic stress disorder. Attention to this disorder has increased with recent world events; however, continued efforts are needed to improve diagnosis, treatment, and prevention of posttraumatic stress disorder.
The Journal of Clinical Psychiatry 02/2004; 65 Suppl 1:55-62. · 5.80 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Hypothalamic pituitary adrenal axis abnormalities have been described in posttraumatic stress disorder (PTSD), and among the recently traumatized. Plasma cortisol and continuous measures of PTSD symptoms were obtained from 21 survivors, at 1 week and 6 months after traumatic events. Eight survivors met Clinician Administered PTSD Scale criteria for PTSD at 6 months. Cortisol levels at 1 week did not predict subsequent PTSD. Survivors with and without PTSD had similar mean levels of cortisol at both time points. Cortisol levels at 6 months negatively correlated with self-reported PTSD symptoms within PTSD subjects.
Psychiatry Research 08/2003; 119(1-2):171-5. · 2.52 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Neural networks and their behavior provide an information-processing model for initiation and maintenance of the biologic aspects of post-traumatic stress disorder (PTSD). The repeated replaying of the intrusive and distressing recollections that follow a trauma modifies the structure of the neural networks involved in the processing of traumatic memories. The hypothesis is proposed that this repetition instigates the mechanisms of iterative learning, top-down activation and pruning. The development of the symptoms of PTSD can be explained by current knowledge about modeling disturbances of parallel distributing processing. The noradrenergic neurons play a central role in coordinating the interaction of multiple cortical regions, which is an essential aspect of parallel distributed processing. Disturbances of this system in PTSD are likely to be manifest as a dysfunctional modulation of working memory and involuntary traumatic recollection. Modifications of neural networks have a secondary effect of kindling in the hippocampus that further moderates the individual's sensitivity to a range of stressors. Therefore, a neural network model of PTSD provides a method for conceptualizing the onset of PTSD symptoms and their subsequent modification with the passage of time.
Psychiatric Clinics of North America 07/2002; 25(2):253-70, v. · 2.13 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Objective: This paper highlights some of the recent findings in the field of posttraumatic stress disorder (PTSD) and examines their impact on conceptions of trauma-focused clinical treatment.Method: A series of research findings in the area of epidemiology, phenomenology, neurobiology and treatment are summarised.Results: The findings from these studies present critical challenges for clinicians who wish to treat trauma survivors using specialised trauma treatments. The major challenge is one of avoiding a simplistic view of PTSD as a singular response to trauma, as this perception may result in an underestimation of the complexity and disabling quality of the disorder, and lead to the formulation of treatment plans that are simplistic or incomplete.Conclusions: A more precise characterisation of the nature and range of the stress responses of trauma victims will significantly improve treatments of trauma survivors.
Australian and New Zealand Journal of Psychiatry 12/2000; 34(6):940 - 953. · 2.93 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: This chapter discusses some of the factors that might influence why exposure to extreme events sometimes results in posttraumatic stress disorder (PTSD), sometimes results in other psychiatric disorders, and sometimes is not followed by psychiatric disorders at all. In and of itself this approach challenges the traditional approach to studying the effects of traumatic events, which largely consisted of retrospectively evaluating their intensity and their contribution to predefined disorders. However, the authors believe that such an approach has perpetuated a post hoc definition of trauma, starting from its presumed consequences and inferring backward, about causation, mediation, and progression.
Topics include: the relationship between traumatic events and their psychological sequelae; the phenomenology of posttraumatic disorders; design and methods in studies of traumatic stress disorders; and inferred mechanisms. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
10/1998;
