Auditory middle-latency responses were recorded in 45 neurological patients. In 4 patients with localized lesions in the thalamus, or subcortical white matter, the component Na was attenuated or delayed at T3, Cz and T4, exclusively on stimulation of the ear contralateral to the lesion. In 5 patients with temporal lobe lesions with receptive aphasia, the amplitude of component Pa was decreased on the lesion side (T3), regardless of the side of stimulation. These findings suggest that Na is generated from a subcortical structure and Pa is generated from the temporal cortex. In 25 patients with diffuse CNS lesions, V-Na interpeak latency was prolonged in 2 cases.