Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Email this article to a Colleague Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to My Articles & Searches Download to citation manager Citing Articles via HighWire Citing Articles via Google Scholar Articles by Lewine, J. D. Articles by Canive, J. M. Search for Related Content PubMed Citation Articles by Lewine, J. D. Articles by Canive, J. M. Neurophysiology Posttraumatic Stress Disorder Other Research Techniques

Abnormal Stimulus-Response Intensity Functions in Posttraumatic Stress Disorder: An Electrophysiological Investigation

OBJECTIVE: The purpose of this study was to explore the relationship between combat-related posttraumatic stress disorder (PTSD) and specific augmentation versus reduction patterns for the N100 and P200 components of auditory event-related potentials evoked by tones of increasing intensity. METHOD: Event-related potentials of subjects with PTSD (N=36), subjects with no psychopathology (N=20), subjects with major depression but no PTSD (N=10), and subjects with a history of chronic alcohol abuse but no PTSD (N=8) were recorded. Brain responses were evoked by a 2000-Hz tone presented in intensity blocks of 65, 72.5, 80, 87.5, and 95 dB (SPL). RESULTS: Evoked data from five PTSD subjects were of poor quality and excluded from further analyses. For all but one subject with no psychopathology and for all subjects with a history of alcohol abuse or major depression (but no PTSD), the Cz amplitude of the P200 response component showed augmentation as a nearly linear function of tone intensity. As a group, subjects with PTSD showed no such increase in P200 response magnitude. Examination of the data from individual subjects with PTSD showed that 42% exhibited augmentation patterns similar to those seen for subjects in the comparison groups. However, 58% showed evidence of P200 reduction, with the response to the loudest tone being smaller than responses to tones of intermediate intensity. CONCLUSIONS: The data suggest that there is a significant subgroup of patients with combat-related PTSD who enter into a state of protective inhibition at relatively low stimulus intensities. It is hypothesized that this is an appropriate adaptive mechanism for these subjects rather than an indication of a core neurobiological abnormality.

This article has been cited by other articles:

				K. Al-Abduljawad, F. Baqui, R. Langley, C. Bradshaw, and E. Szabadi Effects of threat of electric shock and diazepam on the N1/P2 auditory-evoked potential elicited by low-intensity auditory stimuli J Psychopharmacol, November 1, 2008; 22(8): 828 - 835. [Abstract] [PDF]

				J. C. Scaife, R. H. Hou, E. R. Samuels, F. Baqui, R. W. Langley, C. M. Bradshaw, and E. Szabadi Diazepam-induced disruption of classically-conditioned fear-potentiation of late-latency auditory evoked potentials is prevented by flumazenil given before, but not after, CS/US pairing J Psychopharmacol, January 1, 2007; 21(1): 93 - 101. [Abstract] [PDF]

				J. C. Scaife, R. W. Langley, C. M. Bradshaw, and E. Szabadi Diazepam suppresses the acquisition but not the expression of 'fearpotentiation' of the acoustic startle response in man J Psychopharmacol, July 1, 2005; 19(4): 347 - 356. [Abstract] [PDF]

Get information about faster international access.

Privacy Policy

Copyright © 2002 American Psychiatric Association. All rights reserved.

Home | Search | Current Issue | Past Issues | Subscribe | All APPI Journals | Help | Contact Us