Hypofunctioning of sensory gating mechanisms in patients with obsessive-compulsive disorder

In obsessive-compulsive disorder (OCD) patients, functional abnormalities in basal ganglia/precentral circuitries cause cortical hyperexcitability and lack of inhibitory control. These loops can be partly explored by median-nerve somatosensory evoked potentials (SEPs), which functionally reflect the brain responsiveness to somatosensory stimuli. In healthy humans, SEPs' amplitude during voluntary finger movements is lower than during muscular relaxation (i.e., sensory gating). Cortical hyperexcitability in OCD could be eventually responsible for a reduction of sensory gating. This might have pathophysiologic implications for motor compulsions.

Median-nerve SEPs were recorded in 11 OCD patients and 9 healthy volunteers during muscle relaxation ("Relax") or finger movements of the stimulated hand ("Move"). Latencies and amplitudes of pre- and postcentral SEP components were compared between groups during "Relax" and "Move" conditions.

In OCD patients, the responsiveness to sensory stimuli was enhanced for precentral SEPs. Sensory gating ("Relax" vs. "Move") in control subjects involved both pre- and postcentral SEPs, the former being reduced in amplitude by approximately 60%. In OCD patients, sensory gating was spatially restricted to precentral SEP components and was significantly reduced compared with control subjects (approximately 30%).

Enhanced precentral SEPs and hypofunctioning of centrifugal sensory gating in OCD might reflect the inability to modulate sensory information due to a "tonic" high level of cortical excitability of motor and related areas, likely resulting from basal ganglia dysfunction. This might offer new insights into the pathophysiology of OCD.