Is amnesia caused by an activational deficit? A preliminary electrophysiological investigation of acquisition in amnesics.
Six alcoholic amnesics were compared with 6 matched controls in a task involving visual presentation of words under 'learn', 'repeat' and 'passive' instructions whilst their EEG was recorded from the vertex. Although the amnesics' N2-P3 component to word stimuli was similar to that of controls, their word-elicited N1-P2 component was of greater amplitude and their EEG showed an overall reduction in power in the period immediately following word offset. The group difference for N1-P2 was similar in all instructional conditions, but the EEG power difference was greater in the learn condition. It was argued that the N1-P2 enhancement may reflect an attempt by the amnesics to compensate for an unspecified activational impairment indicated by their reduced post-word EEG power.
D000437:Alcoholism / Q000150:complications; D000647:Amnesia / Q000209:etiology* / Q000503:physiopathology / Q000523:psychology; D001921:Brain / Q000503:physiopathology*; D004569:Electroencephalography; D006801:Humans; D008568:Memory; D008875:Middle Aged