Background: Animal and clinical studies suggest that impaired sensorimotor gating, as assessed with the prepulse inhibition (PPI) paradigm, may result from dysfunctional frontostriatal brain circuits and from neurochemical alterations which are also implied in the pathophysiology of obsessive-compulsive disorder (OCD). However, there is only preliminary evidence about impaired PPI in OCD so far.
Methods: Acoustic PPI was measured in 30 OCD patients and 30 matched healthy controls with a paradigm using different prepulse intensities. Psychopathology assessment included ratings for obsessions, compulsions, and depression.
Results: PPI was reduced in OCD patients, and this deficit was most pronounced for most intense (16 dB(A)) prepulses, where mean PPI was 39.6% in unmedicated patients (n = 4), 45.8% in medicated patients, and 58.9% in controls. No group differences were observed with regard to the habituation of acoustic startle magnitude. Startle measures were generally not associated with clinical measures, although such associations may have been obscured by medication effects.
Conclusions: The present study confirms deficient central inhibitory functioning in patients with OCD and supports the model of deficient frontostriatal circuits in OCD. The relationship of PPI deficits to pharmacological and behavioral treatment and to possible subtypes of OCD merits further study.