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Results of a Twin Study

Tamara V. Gurvits, MD, PhD; Linda J. Metzger, PhD; Natasha B. Lasko, PhD; Paul A. Cannistraro, MD; Alexandra S. Tarhan, MD, PhD; Mark W. Gilbertson, PhD; Scott P. Orr, PhD; Anna M. Charbonneau, BA; Michelle M. Wedig, BS; Roger K. Pitman, MD

Arch Gen Psychiatry. 2006;63:571-576.

Context  Previous studies have demonstrated subtle neurologic dysfunction in chronic posttraumatic stress disorder (PTSD) manifest as increased neurologic soft signs (NSSs). The origin of this dysfunction is undetermined.

Objective  To resolve competing origins of increased NSSs in PTSD, namely, preexisting vulnerability factor vs acquired PTSD sign.

Design  Case-control study of identical twins.

Setting  A Veterans Affairs and academic medical center (ambulatory).

Participants  A convenience sample of male Vietnam veteran twins with (n = 25) and without (n = 24) PTSD and their combat-unexposed identical (monozygotic) co-twins.

Interventions  Neurologic examination for 45 NSSs.

Main Outcome Measure  Average scores for 45 NSSs, each scored on an ordinal scale from 0 to 3, masked to diagnosis and combat exposure status.

Results  There was a significant between-pair main effect of PTSD diagnosis (as determined in the combat-exposed twin) on average NSS score in the absence of a significant combat exposure main effect or diagnosis x exposure interaction. Combat veterans with PTSD had significantly higher NSS scores than combat veterans without PTSD. The "high-risk," unexposed co-twins of the former also had significantly higher NSS scores than the "low-risk," unexposed co-twins of the latter. This result could not be explained by age, number of potentially traumatic lifetime noncombat events, alcoholism, or the presence of a comorbid affective or anxiety disorder. The average NSS score in unexposed co-twins was not significantly associated with combat severity in combat-exposed twins.

Conclusions  These results replicate previous findings of increased NSSs in Vietnam combat veterans with PTSD. Furthermore, results from their combat-unexposed identical co-twins support the conclusion that subtle neurologic dysfunction in PTSD is not acquired along with the trauma or PTSD but rather represents an antecedent familial vulnerability factor for developing chronic PTSD on exposure to a traumatic event.

Author Affiliations: Research Service, Veterans Affairs Medical Center, Manchester, NH (Drs Gurvits, Metzger, Lasko, Gilbertson, and Orr and Ms Charbonneau); Department of Psychiatry, Massachusetts General Hospital, Boston (Drs Metzger, Lasko, Cannistraro, Orr, and Pitman and Ms Wedig); Bekhterev Psychoneurological Research Institute, St Petersburg, Russia (Dr Tarhan); and Department of Psychiatry, Harvard Medical School, Boston (Drs Gurvits, Metzger, Lasko, Cannistraro, Gilbertson, Orr, and Pitman).

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