In order to identify the neural structures which may be involved in th
e generation of the P300, 73 patients with focal brain damage were tes
ted using an auditory ''oddball''-paradigm. Included were fourteen pat
ients with frontal, ten with parietal and sixteen with subcortical les
ion sites. The latency of the P3b in the grand averages was delayed by
approximately 20 ms in all patient groups compared to the control gro
up (n = 12) a nd the amplitude of the P3b was significantly reduced. I
n addition we found differential effects according to lesion sites. Fr
ontal damage resulted in a prolonged latency and reduced amplitude of
the NZ in frontal areas, whereas the P3b was quite normal in the parie
tal region. The opposite was found for patients with parietal lesions:
a frontal increased amplitude of the NZ was combined with a decreased
parietal P3b amplitude. Subcortical lesions exhibited an irradiation
of the N2 with increased amplitude from the frontal to the parietal ar
eas. Our results indicate that subcortical structures play a central r
ole in the generation or modulation of the P3-complex.