4.7 Article Proceedings Paper

Resting regional cerebral perfusion in recent posttraumatic stress disorder

期刊

BIOLOGICAL PSYCHIATRY
卷 54, 期 10, 页码 1077-1086

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ELSEVIER SCIENCE INC
DOI: 10.1016/S0006-3223(03)00525-0

关键词

SPECT; rCBF; PTSD; cerebellum; cortisol

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Background: Brain imaging research in posttraumatic stress disorder has been largely performed on patients with chronic disease, often heavily medicated, with current or past alcohol and substance abuse. Additionally, virtually only activation brain imaging paradigms have been done in posttraumatic stress disorder, whereas in other mental disorders both resting and activation studies have been performed. Methods: Twenty-eight (11 posttraumatic stress disorder) trauma survivors underwent resting state hexamethylpro-pyleneamineoxime single photon emission computed tomography and magnetic resonance imaging 6 months after trauma. Eleven nontraumatized subjects served as healthy controls. Results: Regional cerebral blood flow in the cerebellum was higher in posttraumatic stress disorder than in both control groups. Regional cerebral blood flow in right precentral, superior temporal, and fusiform gyri in posttraumatic stress disorder was higher than in healthy controls. Cerebellar and extrastriate regional cerebral blood flow were positively correlated with continuous measures of depression and posttraumatic stress disorder. Cortisol level in posttraumatic stress disorder was negatively correlated with medial temporal lobe perfusion. Anterior cingulate perfusion and cortisol level were positively correlated in posttraumatic stress disorder and negatively correlated in trauma survivors without posttraumatic stress disorder. Conclusions: Recent posttraumatic stress disorder is accompanied by elevated regional cerebral bloodflow, particularly in the cerebellum. This warrants attention because the cerebellum is often used as a reference region in regional cerebral bloodflow studies. The inverse correlation between plasma cortisol and medial temporal lobe perfusion may herald hippocampal damage. Biol Psychiatry 2003;54: 1077-1086 (C) 2003 Society of Biological Psychiatry

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