Citation

Stein MB, Hanna C, Koverola C, Torchia M, McClarty B. Ann. N. Y. Acad. Sci. 1997; 821: 76-82.

Affiliation

Department of Psychiatry, San Diego Veterans Affairs Medical Center, California 92161, USA.

Copyright

(Copyright © 1997, John Wiley and Sons)

DOI

unavailable

PMID

9238195

Abstract

Although the impetus for studying hippocampal morphology and functioning in PTSD was the finding that stress could result in hippocampal damage in rodent and primate models, it is far from proven that the findings to date in PTSD represent defects that have been caused by trauma. It is equally possible that the findings represent a preexisting anomaly which might serve as a risk factor for the development of PTSD following trauma exposure. To resolve this dilemma, it is necessary to study persons at high risk for trauma (e.g., soldiers) prior to trauma exposure and ag in after exposure. Such methods will permit the determination not only of whether trauma alters hippocampal morphology, but also, if so, of whether this effect is limited to persons with PTSD. At the present time, the field would be well advised to proceed vigorously but with appropriate caution along these lines of research. As just outlined, sample sizes have been small, and potentially confounding variables have abounded in most studies. The next few years of research may well continue to replicate the finding of abnormal hippocampal morphology in PTSD. However, it would not be surprising to find that other brain regions are also involved and that these represent part of a broader risk spectrum for the development of psychopathology under stress. Until these issues are clarified, the neuroanatomical findings to date in PTSD should be viewed as tentative, tantalizing, and in need of additional study.

Language: en