INTRODUCTION I was one of the people who were skeptical about the initial ï¬ndings 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 ï¬ndings of smaller hippocampal volumes of PTSD and many of the theories that have developed to explain them. My skepticism of the original ï¬ndings of reduced hippocampal volume in PTSD was not, as Dr. Bremner suggests in his position paper, due to an inability to âbelieve that events in the environment can lead to structural damage in the brain.â 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. Sapolskyâs 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 ï¬ndings in PTSD, because it was discrepant with the empirical data demonstrating lower, and not higher, cortisol levels in trauma survivors who develop this condition.
Hippocampus – Wiley
Published: Jan 1, 2001
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