Prolonged cortical somatosensory evoked potential latencies in progressive myoclonus epilepsy.

In 9 mildly affected and 7 severely affected patients with progressive myoclonus epilepsy, we observed a distinct slowing in the short-latency median nerve SEP components N 19 (5.2% and 24.7%), P 22 (14.6% and 37.1%) and N 30 (4.8% and 17.1%, respectively). The P 22-N 30 amplitude increased in mild but decreased again in severe disease. These findings are indicative of mild affection of the peripheral and spinal sensory connections, and more severe involvement of the thalamocortical pathways. In controls, a clear correlation between the height and the latency of the N 19 and P 22 components was observed. We also often observed a small additional negative SEP component adjoining the P 22 component.