Laser evoked potentials and prepulse inhibition of the blink reflex in patients with Wallenberg's syndrome.

Spinothalamic tract lesions in patients with Wallenberg's syndrome can be demonstrated by abnormalities in the laser evoked potentials (LEPs) to stimulation of the affected side. However, before reaching the structures generating LEPs, laser stimuli can induce effects at a subcortical level. We examined LEPs and laser-induced prepulse inhibition of the blink reflex in seven patients with Wallenberg's syndrome within a month after the infarct. All patients had abnormally elevated thresholds for temperature and pain sensation, and for pinprick pain induced by laser stimuli, in the affected vs the non-affected side. LEPs to stimulation of the affected side were abnormal because of absent, reduced or delayed responses. However, the same laser stimuli that were unable to induce LEPs generated normal inhibition of the blink reflex response when applied 250ms before a trigeminal nerve electrical stimulus. The percentage inhibition induced in the R2 response of the blink reflex by laser stimulation of the affected side was not different from that induced by stimulation of the non-affected side, or in control subjects. These results are compatible with either a different pathway for prepulse inhibition and evoked potentials or a reduced energy requirement of the sensory input generating prepulse inhibition in comparison to that generating evoked potentials.