References: Post Traumatic Stress Disorder 1997; Volume 3 Issue 10

1. AUTHOR	Bronisch-T.
INSTITUTION	Max-Planc-Institut fur Psychiatire, Munchen.
TITLE	(Post-traumatic stress disorder. New research findings). TT Posttraumatic Stress Disorder-Posttraumatische Belastungsstorung. Neure Forschungsergebnisse.
SOURCE	Fortschr-Neurol-Psychiatr 1997 May, VOL: 65 (5), P: 195-207, ISSN: 0720-4299 108 Refs.
ABSTRACT	This article reviews recent research results on posttraumatic stress disorder (PTSD). Epidemiological studies show that PTSD is a common disorder within the normal population with a high degree of chronic courses. Degree of severity as well as dissociative symptoms during the traumatic event seem to have an impact on course and outcome of PTSD. A genetic disposition, familial psychopathology and premorbid personality traits as background variables seem to have an influence on the development of PTSD whereas coping strategies, as well as social support, modify the course of the disease. The investigation of biological parameters refers to the hypothalamic-pituitary- adrenal-axis system, provocation studies, psychophysiological studies, and studies of the endogenous opiate system. In regard to therapy studies only those with a randomised allocation to two different therapies as well as with a control group without therapy or a waiting list group are considered, using the DSM-III or DSM-III- R diagnostic criteria for PtSD. Five pharmacological studies could show a positive effect by antidepressants. Six behaviour therapy studies (two systematic desensitisation and four flioding) produced an improvement of PTSD symptomatology. The pathogenetic models discussed here are memory imprinting, kindling, dysregulation of the opioid neuromodulation, classical conditioning and disturbed cognitive schemas, which reflect as single models only a facet of the pathogenesis. Author.

2. AUTHOR	Briggs-L, Joyce-P-R.
INSTITUTION	University Department of Psychological Medicine, Christchurch School of Medicine, New Zealand.
TITLE	What determines post-traumatic stress disorder symptomatology for survivors of childhood sexual abuse?
SOURCE	Child-Abuse-Negl 1997 Jun, VOL: 21 (6), P: 575-82, ISSN: 0145-2134.
ABSTRACT	OBJECTIVE: The aim of this paper was to ascertain which childhood abuse experiences are associated with post-traumatic stress disorder (PTSD) symptomatology for women survivors of childhood sexual abuse (CSA). METHOD: Seventy-three women attending a Family Health Counselling Service's Sexual Abuse Program were invited to participate in a study looking at the effectiveness of sexual abuse counselling. Initially, the women completed a series of self-report questionnaires including a measure of PTSD symptoms, and were interviewed about childhood abuse experiences. RESULTS: PTSD symptoms were associated with higher levels of all psychopathology. However, more interestingly, the severity of PTSD symptoms was also associated with the extent of CSA which involved actual sexual intercourse. This association of repeated abuse involving sexual intercourse with PTSD symptoms was still significant (partial coefficient = .30, p, .000) even when controlling for general level of psychopathology. CONCLUSIONS: One of the long-term effects of child sexual abuse (CSA) is post-traumatic stress disorder (PTSD), and the women who reported multiple abusive episodes which involved sexual intercourse had increased symptoms of PTSD. Author.

3. AUTHOR	Heim-C, Owens-M-J, Plotsky-P-M, Nemeroff-C-B.
INSTITUTION	Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GA 30322, USA.
TITLE	Persistent changes in corticotropin-releasing factor systems due to early life stress: relationship to the pathophysiology of major depression and post-traumatic stress disorder.
SOURCE	Psychopharmacol-Bull 1997, VOL: 33 (2), P: 185-92, ISSN: 0048-5764 63 Refs.
ABSTRACT	In addition to a genetic contribution to the vulnerability for mood and anxiety disorders, such as major depressive disorder (MDD) and post-traumatic stress disorder (PTSD), a preeminent role of early adverse life events in the pathogenesis of these disorders has been postulated. Corticotropin releasing factor (CRF), which has been conclusively documented to be the major regulator of the mammalian stress response, may be the seminal neurobiological substrate mediating the effects of early life stress on subsequent psychopathology. Central administration of CRF produces many of the physiological and behavioral effects of stress and of anxiety and depression. Clinical studies have provided evidence for increased activation of CRF neuronal systems in both MDD and PTSD. Similar hyperactivity of CRF neurons and sensitization of the pituitary- adrenal stress response has been observed in adult animals exposed to stress early in life. We propose that early adverse life events might render the human individual vulnerable to the effects of stress later in life, resulting in an increased risk for developing psychopathology via long-lived alterations in CRF-containing neural circuits. Based on these findings, new therapies including early intervention can now be developed to treat individuals exposed to severe stress early in life. Author.

4. AUTHOR	Baker-D-G, West-S-A, Orth-D-N, Hill-K-K, Nicholson-W-E, Ekhator-N-N, Bruce-A-B, Wortman-M-D, Keck-P-E-Jr, Geracioti-T-D-Jr.
INSTITUTION	Psychiatry Service, Cincinnati Veterans Affairs Medical Center, OH 15220, USA. BAKERDG@ucbeh.san.uc.edu.
TITLE	Cerebrospinal fluid and plasma beta-endorphin in combat veterans with post-traumatic stress disorder.
SOURCE	Psychoneuroendocrinology 1997 Oct, VOL: 22 (7), P: 517-29, ISSN: 0306-4530.
ABSTRACT	Opioid-mediated analgesia develops in experimental animals following traumatic stress and increased opioid-mediated analgesia has been observed in combat veterans with post-traumatic stress disorder (PTSD). These observations have led to the hypothesis that increased central nervous system (CNS) opioidergic activity exists in patients with PTSD. However, direct CNS data on opioid peptide concentrations and dynamics in patients with PTSD are lacking. We withdrew cerebrospinal fluid (CSF) via a flexible, indwelling subarachnoid catheter over a 6-h period and determined hourly CSF concentrations of immunoreactive beta-endorphin (ir beta END) in 10 well- characterized combat veterans with PTSD and nine matched normal volunteers. Blood was simultaneously withdrawn to obtain plasma for ir beta END. PTSD symptom clusters, as measured by the CAPS, were correlated with neuroendocrine data. Mean CSF ir beta END was significantly greater in patients with PTSD compared with normals and there was a negative correlation between the ir beta END and PTSD intrusive and avoidant symptoms of PTSD. No intergroup difference between plasma ir beta END was found, nor was there a significant correlation between CSF and plasma ir beta END. Immunoreactive beta- lipotropin (ir beta LPH) and pro-opiomelanocortin (irPOMC), both precursors of beta END, were much more plentiful in human CSF than was beta-endorphin itself, as has been previously reported. It remains to be determined whether the increased CNS opioid concentrations predate traumatic stress, thereby conferring a vulnerability to dissociative states and PTSD itself, or result from the trauma. The negative correlation between CSF ir beta END and avoidant and intrusive symptoms suggests that CNS hypersecretion of opioids might constitute an adaptive response to traumatic experience. Poor correlation between CSF and plasma ir beta END limits use of plasma measures to assess CNS opioid activity. Author.

5. AUTHOR	Lucey-J-V, Costa-D-C, Adshead-G, Deahl-M, Busatto-G, Gacinovic-S, Travis-M, Pilowsky-L, Ell-P-J, Marks-I-M, Kerwin-R-W.
INSTITUTION	St Bartholomew's, London. j.v.lucey@mds.qmw.ac.uk.
TITLE	Brain blood flow in anxiety disorders. OCD, panic disorder with agoraphobia, and post-traumatic stress disorder on 99mTcHMPAO single photon emission tomography (SPET).
SOURCE	Br-J-Psychiatry 1997 Oct, VOL: 171, P: 346-50, ISSN: 0007-1250.
ABSTRACT	BACKGROUND: We compared regional cerebral blood flow (rCBF) in three groups of patients with DSM-III-R anxiety disorders. METHOD: Fifteen patients with obsessive -compulsive disorder (OCD), 15 with panic disorder with agoraphobia (PA), and 16 with post-traumatic stress disorder (PTSD) and a similar group of healthy controls were assessed on brain-dedicated high-resolution SPET. RESULTS: MANOVA revealed significant rCBF differences between diagnostic groups (F = 4.4; d.f. = 3, 57; P = 0.007) and between cerebral regions (F = 6.4; d.f. = 1, 57; P = 0.01) in OCD and PTSD compared with PA and healthy controls, limited to bilateral superior frontal cortices and right caudate nuclei. Whole brain blood flow correlated positively with anxiety (r = 0.24, n = 46, P = 0.05). Beck depression scores correlated significantly negatively with left caudate rCBF (r = -0.24, n = 46, P = 0.05) and right caudate rCBF (r = -0.31, n = 46, P = 0.02). PTSD syndrome severity correlated significantly negatively with the left caudate (r = -0.49, n = 16, P = 0.03) and with right caudate rCBF (r = -0.7, n = 16, P = 0.001). CONCLUSIONS: Functional rCBF differences in anxiety disorders could relate to repetitive, intrusive, distressing mental activity, prominent in both OCD and PTSD. Author.

6. AUTHOR	Davis-L-L, Suris-A, Lambert-M-T, Heimberg-C, Petty-F.
INSTITUTION	Veterans Affairs Medical Center, Tuscaloosa, AL 35404, USA. Davis.lori@tuscaloosa.va.gov.
TITLE	Post-traumatic stress disorder and serotonin: new directions for research and treatment.
SOURCE	J-Psychiatry-Neurosci 1997 Nov, VOL: 22 (5), P: 318-26, ISSN: 1180-4882 57 Refs.
ABSTRACT	The overlap in clinical phenomenology and morbidity between post- traumatic stress disorder (PTSD) and such conditions as major depression, anxiety disorders and aggression, in which a serotonin dysfunction is implicated, suggests a role for serotonin in the pathophysiology of PTSD. In this paper, we review current knowledge concerning the role of serotonergic mechanisms and interventions in PTSD. Since there is no clearly effective pharmacologic intervention for this disorder, the underlying neurochemical dysfunction needs to be carefully defined so that more effective treatment can be developed. Preclinical and clinical studies of the serotonergic mechanisms in the pathophysiology of PTSD and treatment trials involving serotonergic agents are limited, but indicate considerable promise. Further investigation of a serotonergic dysfunction in PTSD and of its treatment with serotonergic agents is warranted. Author.

7. AUTHOR	Neal-L-A, Shapland-W, Fox-C.
INSTITUTION	Defence Medical Services, Duchess of Kent Hospital, Catterick, North Yorkshire, UK.
TITLE	An open trial of moclobemide in the treatment of post-traumatic stress disorder.
SOURCE	Int-Clin-Psychopharmacol 1997 Jul, VOL: 12 (4), P: 231-7, ISSN: 0268-1315.
ABSTRACT	Traditional monoamine oxidase inhibitors have shown efficacy in the treatment of post-traumatic stress disorder, but their use is limited by some serious drug and food interactions. Moclobemide, which is a reversible inhibitor of monoamine oxidase-A, is relatively free of these limitations and is therefore potentially useful in the treatment of post-traumatic stress disorder. Twenty patients who met Diagnostic and Statistical Manual of Mental Disorders, Third Edition Revised (DSM-III-R) criteria for post-traumatic stress disorder were entered into a 12-week open study with moclobemide. Assessments were completed every 4 weeks. Eleven participants no longer met DSM-III-R criteria for post-traumatic stress disorder by week 12. The severity of post-traumatic stress disorder reduced by 2.09 SD (95% confidence interval 1.49-2.69; p < 0.001) and functional impairment improved by 1.08 SD (95% confidence interval 0.46-1.69; p < 0.01). Adverse events were minimal. Controlled, double-blind studies should be considered to confirm these findings. Author.