Neurologic Soft Signs in Borderline Personality Disorder

José Manuel De la Fuente, M.D., Ph.D.; Julio Bobes, M.D., Ph.D.; Coro Vizuete, M.D.; Maria-Teresa Bascaran, M.D.; Ignacio Morlán, Ph.D.; and Julien Mendlewicz, M.D., Ph.D.

Objective: Borderline personality disorder is a disabling and dramatic psychiatric condition. To date, its pathophysiology remains unclear. Scientific evidence seems to have found underlying, nonfocal, central nervous system dysfunction in borderline personality disorder. Neurologic soft signs are anomalies only evidenced by specific motor, sensory, or integrative testing when no other sign of a neurologic lesion is present. Neurologic soft signs have been proposed to be nonfocal in origin and to reflect central nervous system failure. The assessment of neurologic soft signs now appears reliable and stable. Assuming that neurologic soft signs reflect nonfocal central nervous system dysfunction, we hypothesized that patients with borderline personality disorder should have an increased frequency of neurologic soft signs, therefore enhancing the possibility of the existence in borderline personality disorder of a nonlocalized brain dysfunction.

Method: To test this hypothesis, we compared 29 neurologic soft signs in 20 drug-free patients with DSM-III-R borderline personality disorder and 20 controls, using an examination adapted from the literature on neurologic soft signs. The study was conducted from February 1991 to March 1993.

Results: Thirteen neurologic soft signs were significantly more frequent in the borderline group. Patients with borderline personality disorder showed more left side, right side, and total neurologic soft signs than controls (p = .0001). All patients in the borderline group exhibited at least 1 neurologic soft sign, while only 7 controls did (p = .0001).

Conclusion: Our hypothesis was confirmed. These results add evidence to the possibility of the existence of a nonfocal central nervous system failure in borderline personality disorder.

(J Clin Psychiatry 2006;67:541-546)

Received Aug. 30, 2005; accepted Oct. 6, 2005. From the Department of Psychiatry, Erasme Hospital, Free University of Brussels, Brussels, Belgium (Drs. De la Fuente and Mendlewicz); the Faculty of Medicine, Oviedo University, Oviedo, Spain (Drs. De la Fuente, Bobes, and Bascaran); the Psychiatric Hospital of Lannemezan, Lannemezan, France (Drs. De la Fuente and Vizuete); and the Faculty of Computer Science, Basque Country University, Guipúzcoa Campus, San Sebastián, Spain (Dr. Morlán).

The authors report no financial or other relationships relevant to the subject of this article.

Corresponding author and reprints: José Manuel De la Fuente, Hôpital Psychiatrique de Lannemezan, Route de Toulouse, F-65300 Lannemezan, France (e-mail: jdlf@ch-lannemezan.fr).