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Journal Article

Citation

Metzger LJ, Clark CR, McFarlane AC, Veltmeyer MD, Lasko NB, Paige SR, Pitman RK, Orr SP. Psychophysiology 2009; 46(1): 172-178.

Copyright

(Copyright © 2009, Society for Psychophysiological Research, Publisher John Wiley and Sons)

DOI

10.1111/j.1469-8986.2008.00720.x

PMID

unavailable

Abstract

Studies have demonstrated ERP abnormalities related to concentration difficulties in post‐traumatic stress disorder (PTSD). We used an identical‐twin, case‐control design to investigate whether these abnormalities reflect pre‐trauma vulnerability or the acquired consequence of PTSD. Vietnam combat veterans and their non‐combat‐exposed, identical twins completed a three‐tone oddball task. Veterans with PTSD had delayed target N2 latencies compared to veterans without PTSD. In a small nonmedicated, nonsmoking subsample, veterans with PTSD also had significantly diminished target P3b amplitudes. A mixed‐model, random‐effects analysis on the nonmedicated, nonsmoking subsample that included the combat‐unexposed co‐twins showed a significant Diagnosis × Combat Exposure interaction for target P3b amplitude. Results replicate increased N2 latency and diminished P3b amplitude in PTSD and suggest that diminished P3b amplitude is an acquired condition in PTSD.

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