par Maurage, P;Philippot, P;Verbanck, Paul ;Noël, Xavier ;Kornreich, Charles ;Hanak, Catherine ;Campanella, Salvatore
Référence Clinical neurophysiology, 118, 3, page (633-644)
Publication Publié, 2007-03
Référence Clinical neurophysiology, 118, 3, page (633-644)
Publication Publié, 2007-03
Article révisé par les pairs
Résumé : | OBJECTIVE: Studies exploring chronic alcoholism with event-related potentials (ERPs) have shown delayed latency and reduced amplitude of the P300, a long-lasting positive potential reflecting decisional processing. This P300 deficit in alcoholism is generally interpreted as a disturbance in central nervous system inhibition or in memory/attention. The present study aimed at identifying if this electrophysiological deficit is already present on earlier components, and advances a new hypothesis concerning the interpretation of the P300 alteration. METHODS: Patients suffering from alcoholism and matched healthy controls had to detect, in an oddball paradigm, emotional faces among a succession of neutral faces. Behavioral performance and ERP data (recorded from 32 electrodes) were analyzed. RESULTS: In line with previous studies, data showed that alcoholism led to a P300 deficit. Moreover, we observed for the first time that this deficit begins at earlier visual (P100) and face-processing (N170) stages, and we found high positive correlations between P100, N170 and P300 for amplitude and latency values, suggesting cumulative deficits on the cognitive continuum. CONCLUSIONS: We suggest that the P300 deficit observed in chronic alcoholism could be linked to earlier visuo-spatial deficits rather than being an impairment of the specific processes linked to the P300. SIGNIFICANCE: These results call for reconsidering the interpretation of P300 impairments at a fundamental and clinical level, and shows that earlier ERP components must be taken into account in future studies. |