“…Dementia is also seen in neurological disorders that involve predominantly subcortical structures as the brainstem and basal ganglia, exemplified in Parkinson's disease (PD) [1,2] and Huntington's chorea (HD) [3], Although qualitative differences in cognitive functioning have been described between 'cortical' and 'subcortical' dementias [3], the nature of these differences, if any, is controversial [4], Among the electrophysiological correlates of demen tia, the event-related potentials, generated in response to infrequent, attended, task-relevant stimuli, are consid ered to reflect some, still undetermined, aspects of the cognitive processing [5][6][7], The latency of the P3 (or P300) component of event-related potentials was shown in a number of studies to correlate well with the cogni tive capabilities and to increase with age and in patients with dementing illness [8,9], However, particularly in triguing were the findings of Goodin and Aminoff [10,11] that, although the N2 and P3 components of audi tory event-related potentials (aERPs) were prolonged in latency among patients with dementia caused by DAT, PD and HD, the latencies of the N1 and P2 components differed between the groups. While they were normal in DAT patients, the N 1 latencies were prolonged in those with HD and PD, whereas P2 was prolonged only in the group with HD.…”