J Neuropsychiatry Clin Neurosci.2009; 21: 132-143
Rachel Yehuda, Ph.D., Philip D. Harvey, Ph.D., Julia A. Golier, M.D., Randall E. Newmark, B.A., Christopher R. Bowie, Ph.D., Janelle J. Wohltmann, B.A., Robert A. Grossman, M.D., James Schmeidler, Ph.D., Erin A. Hazlett, Ph.D. and Monte S. Buchsbaum, M.D.
The authors aimed to examine central glucocorticoids effects by measuring relative glucose metabolic rate (rGMR) in the hippocampus, amygdala, and anterior cingulate cortex (ACC) and the relationship between amygdala and ACC activity.
The participants were male combat veterans with and without PTSD, 52 to 81 years old.
The authors utilized randomized, double-blind, placebo-controlled examinations of the rGMR response to 17.5 mg hydrocortisone (HCORT) using 2-Deoxy-2-[18F]fluorodeoxyglucose (FDG) Positron Emission Tomography (PET) neuroimaging.
Group differences in hemispheric laterality of rGMR were observed following placebo administration, reflecting lower rGMR in the right hippocampus and ventral amygdala, and higher rGMR in the left ventral amygdala in the PTSD+ group compared to the PTSD– group.
HCORT reduced these group differences in laterality.
The net effect of HCORT was to restore a normal inverse association between the ACC and amygdala in the PTSD+ group, but disrupt this neural network in the PTSD– group.
The magnitude of improvement in working memory correlated with greater hemispheric laterality in the dorsal amygdala following HCORT in both groups.
The restorative effects of HCORT on metabolism and working memory provide a rationale for examining the therapeutic benefits of glucocorticoid manipulation in aging PTSD patients.