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October 1994

Elevated Cerebrospinal Fluid Levels of Oxytocin in Obsessive-compulsive Disorder: Comparison With Tourette's Syndrome and Healthy Controls

Author Affiliations

From Child Study Center (Drs Leckman, Chappell, Pauls, Anderson, and Cohen) and General Clinical Research Centers (Dr Leckman), Depts of Psychiatry (Drs Leckman, Price, McDougle, Barr, and Cohen), Pediatrics (Drs Leckman and Cohen), and Genetics (Dr Pauls), and Abraham Ribicoff Research Facilities, Connecticut Mental Health Center (Drs Price and McDougle), Yale University School of Medicine, New Haven, Conn; Dept of Psychiatry, University of Florida College of Medicine, Gainesville (Dr Goodman); Dept of Physiology, Dartmouth Medical School, Hanover, NH (Dr North); Dept of Psychiatry and Behavioral Science, Johns Hopkins Medical Institutions, Baltimore, Md (Dr Riddle); and Dept of Psychiatry, Medical College of Georgia, Augusta (Ms McSwiggan-Hardin).

Arch Gen Psychiatry. 1994;51(10):782-792. doi:10.1001/archpsyc.1994.03950100030003

Background:  Limited neurobiological data have implicated central arginine vasopressin in the pathobiology of obsessive-compulsive disorder (OCD). Based on twin, family genetic, and pharmacological studies, some forms of OCD are etiologically related to Tourette's syndrome. The role of arginine vasopressin and related compounds such as oxytocin in Tourette's syndrome has not been previously explored.

Methods:  To compare cerebrospinal fluid (CSF) levels of arginine vasopressin and oxytocin, we collected CSF at midday in a standardized fashion from a total of 83 individuals (29 patients with OCD, 23 patients with Tourette's syndrome, and 31 normal controls). We also collected family study data on each subject to determine which subjects had a family history positive for Tourette's syndrome, OCD, or related syndromes.

Results:  In contrast to previous reports, we report similar concentrations of arginine vasopressin for all three groups but increased oxytocin levels in patients with OCD. Remarkably, this increase was observed only in a subset of patients with OCD (n=22) independently identified as being without a personal or family history of tic disorders (P=.0003). In this subgroup of patients, the CSF oxytocin level was correlated with current severity of OCD (n=19,r=.47, P<.05).

Conclusions:  A possible role for oxytocin in the neurobiology of a subtype of OCD is suggested by the elevated CSF levels of oxytocin and by the correlation between CSF oxytocin levels and OCD severity. These findings reinforce the value of family genetic data in identifying biologically homogeneous (and perhaps more etiologically homogeneous) groups of patients with OCD. Together with emerging pharmacological data showing differential responsiveness to treatment of tic-related OCD vs non—tic-related OCD, these data also argue strongly for the incorporation of tic-relatedness as a variable in biological and behavioral studies of patients with OCD.

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