Are glucocortoids responsible for putative hippocampal damage in PTSD? How and when to decide

Are glucocortoids responsible for putative hippocampal damage in PTSD? How and when to decide INTRODUCTION I was one of the people who were skeptical about the initial findings of smaller hippocampal volumes in posttraumatic stress disorder (PTSD), and have been invited to participate in this debate to articulate why I could not (and still cannot) uncritically accept both the findings of smaller hippocampal volumes of PTSD and many of the theories that have developed to explain them. My skepticism of the original findings of reduced hippocampal volume in PTSD was not, as Dr. Bremner suggests in his position paper, due to an inability to “believe that events in the environment can lead to structural damage in the brain.” Indeed, my own previous experience examining the impact of adrenalectomy and glucocorticoid treatment on cell proliferation (1) and cell death (2) in the rat brain is consistent with Dr. Sapolsky’s conclusion that both experience and glucocorticoids directly alter the microarchitecture, cell number, and volume of the brain (see his position paper). Rather, the proposed theory of stress-induced glucocorticoid toxicity did not seem like a reasonable explanation for the hippocampal findings in PTSD, because it was discrepant with the empirical data demonstrating lower, and not higher, cortisol levels in trauma survivors who develop this condition. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Hippocampus Wiley

Are glucocortoids responsible for putative hippocampal damage in PTSD? How and when to decide

Hippocampus, Volume 11 (2) – Jan 1, 2001

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Publisher
Wiley
Copyright
Copyright © 2001 Wiley‐Liss, Inc.
ISSN
1050-9631
eISSN
1098-1063
DOI
10.1002/hipo.1025
pmid
11345128
Publisher site
See Article on Publisher Site

Abstract

INTRODUCTION I was one of the people who were skeptical about the initial findings of smaller hippocampal volumes in posttraumatic stress disorder (PTSD), and have been invited to participate in this debate to articulate why I could not (and still cannot) uncritically accept both the findings of smaller hippocampal volumes of PTSD and many of the theories that have developed to explain them. My skepticism of the original findings of reduced hippocampal volume in PTSD was not, as Dr. Bremner suggests in his position paper, due to an inability to “believe that events in the environment can lead to structural damage in the brain.” Indeed, my own previous experience examining the impact of adrenalectomy and glucocorticoid treatment on cell proliferation (1) and cell death (2) in the rat brain is consistent with Dr. Sapolsky’s conclusion that both experience and glucocorticoids directly alter the microarchitecture, cell number, and volume of the brain (see his position paper). Rather, the proposed theory of stress-induced glucocorticoid toxicity did not seem like a reasonable explanation for the hippocampal findings in PTSD, because it was discrepant with the empirical data demonstrating lower, and not higher, cortisol levels in trauma survivors who develop this condition.

Journal

HippocampusWiley

Published: Jan 1, 2001

References

  • Enhanced brain cell proliferation following early adrenalectomy in rats
    Yehuda, Yehuda; Fairman, Fairman; Meyer, Meyer
  • Stress and cognitive function
    McEwen, McEwen; Sapolsky, Sapolsky

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