Neuropsychological Functioning in a Subclinical Obsessive-compulsive Sample David Mataix-Cols, Carme Junque ´, Miquel Sa `nchez-Turet, Julio Vallejo, Katia Verger, and Maite Barrios Background: Previous neuropsychological research has suggested that the study of psychometrically defined sub- clinical samples might be a valid approach to understand the underlying pathophysiology of obsessive-compulsive disorder (OCD). This approach has the potential benefit of overcoming some of the methodological problems linked to the use of clinical samples. Methods: A group of subclinical obsessive-compulsive (OC) subjects (n = 35), selected on the basis of their scores on the Padua Inventory, and a control group were assessed on executive functioning tasks and other neuro- psychological tests which have been demonstrated to be impaired in clinical OCD patients and/or in those with several basal ganglia disorders. Results: Subclinical OC subjects needed significantly more moves than controls to reach the solution criteria on the Tower of Hanoi puzzle, and performance on this test was positively correlated with total score and the Check- ing factor of the Padua Inventory. There were no between- group differences on the other frontal lobe tests. Conclusions: The results suggest that deficits in manipulat- ing spatial information might be basic in OCD, and are congruent with the involvement of the frontostriatal circuits in the disorder. Biol Psychiatry 1999;45:898 –904 © 1999 Society of Biological Psychiatry Key Words: Obsessive-compulsive disorder, neuropsy- chology, executive functions, prefrontal, basal ganglia Introduction C urrent approaches to obsessive-compulsive disorder (OCD) suggest that specific frontosubcortical circuits are involved in the symptoms and cognitive deficits associated with the disorder. Evidence is provided by several findings. Both structural and functional neuroim- aging studies have identified selective neocortical (orbital prefrontal), cingulate, and striatum abnormalities in OCD (Rauch et al 1997). Lesioning the anterior cingulate or interrupting those frontosubcortical loops through neuro- surgery improves anxiety, depression, and obsessional thinking (Mindus and Jenike 1992). Comorbidity has been reported for OCD and Tourette’s syndrome, Parkinson’s disease, Huntington’s disease, Sydenham’s chorea, and other basal ganglia diseases (Rapoport 1990; Cummings 1996). Furthermore, psychological changes resemblant to obsessional illness have been reported in patients with head injury (McKeon et al 1984) and with discrete lesions in the basal ganglia (Laplane et al 1989). Neuropsychological findings are consistent with the frontostriatal etiologic hypothesis of OCD and include impairments in a variety of domains, such as visuospatial and visuoconstructional deficits (Insel et al 1983; Boone et al 1991; Zielinski et al 1991), nonverbal memory deficits (Christensen et al 1991; Savage et al 1996), spatial learning impairment as measured by the Tactual Perfor- mance Test (Flor-Henry et al 1979; Insel et al 1983), reduced verbal fluency (Harvey et al 1986), or cognitive set maintenance/shifting deficits (Harvey 1986; Head et al 1989). However, neuropsychological studies in OCD are still not definitive, since the use of tests sensitive to frontal lobe functioning has yielded discordant results. It is possible that such discordant results could depend on factors like clinical state, medication effects, intelligence, or the heterogeneity of OC symptoms. Indeed, clinical improvement could have an effect on neuropsychological performance. For instance, the study of Abbruzzese et al (1995) provided modest evidence that medicated patients may have a better performance on the Wisconsin Card Sorting Test (WCST) than nonmedicated patients, sug- gesting that card sorting deficits may not constitute trait markers of OCD, but may depend on the symptomatic state. Another study found that intelligence was more important than group membership to account for between- group differences on the WCST (Grau 1991a, b). Similar concerns on the specificity of the deficits have been noted, since patients with other anxiety disorders, such as social From the Department of Psychiatry and Clinical Psychobiology, University of Barcelona, Barcelona, Spain. Address reprint requests to David Mataix-Cols, Department of Psychiatry and Clinical Psychobiology, University of Barcelona, Passeig de la Vall d’Hebron, 171. E-08035 Barcelona, Catalonia, Spain. Received September 10, 1997; revised April 3, 1998; revised July 8, 1998; accepted July 24, 1998. © 1999 Society of Biological Psychiatry 0006-3223/99/$19.00 PII S0006-3223(98)00260-1