Sensory gating and sensorimotor gating in medication-free obsessive-compulsive disorder patients.

Obsessive-compulsive disorder (OCD) is associated with deficits in inhibition mechanisms. This is reflected in reports showing impaired sensorimotor and sensory gating in OCD patients, as measured with prepulse inhibition (PPI) of the startle reflex and P50 suppression paradigms. However, most of the patients in these studies used medication and the results were not controlled for menstrual cycle phase in women. In this study PPI and P50 suppression were tested in 25 medication-free OCD patients and 25 healthy controls, using auditory stimuli and controlling for menstrual cycle effects. Subgroups were established, based on clinical variables (e.g. 'washers' and 'checkers'). No impairments in PPI or P50 suppression were found in the OCD group when compared with healthy controls. However, a subgroup of OCD patients ('checkers', n=12) showed increased P50 suppression. It was concluded that sensorimotor and sensory gating is not impaired in drug-free OCD patients, taking into account the menstrual cycle effects in women. These results do not support hypotheses linking deficits in these inhibition paradigms and the pathogenesis of OCD. The finding of an increased P50 suppression in the subgroup of 'checkers' deserves further investigation and underlines the value of studying subgroups of OCD.

Hypersensitivity of 5-HT2 receptors in OCD patients. An increased prolactin response after a challenge with meta-chlorophenylpiperazine and pre-treatment with ritanserin and placebo.

INTRODUCTION: Several studies in obsessive compulsive disorder (OCD) have provided circumstantial evidence that the 5-HT-system is involved in the pathophysiology of OCD. To further examine the role of 5-HT receptors we studied the behavioural and neuroendocrine effects of different doses of meta-chlorophenylpiperazine (mCPP) in OCD patients and healthy controls, after pre-treatment with ritanserin, a 5-HT2 receptor antagonist, and placebo. DESIGN: Twenty patients and 20 healthy controls received 0.1, 0.3 or 0.5 mg/kg mCPP or placebo orally. Each subject was tested two times, receiving both times the same dosage of mCPP or placebo with ritanserin or placebo pre-treatment. All was done under double-blind conditions. OC-symptoms and hormone levels were measured. RESULTS: The increase in prolactin level after mCPP administration was more robust in patients than in controls. The prolactin response following 0.5 mg/kg of mCPP was partially blocked by ritanserin in patients, but totally blocked in healthy controls. The cortisol responses in both groups did not differ statistically significant from each other and were entirely blocked by ritanserin. None of the subjects experienced an exacerbation of obsessive compulsive symptoms. CONCLUSION: The neuroendocrine results show an enhanced susceptibility of OCD patients for the mCPP-induced prolactin response, which effect seems to be due to an increased sensitivity of 5-HT2 receptors.