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More MS news articles for August 2003

Working memory deficits in multiple sclerosis: a controlled study with auditory P600 correlates

J Neurol Neurosurg Psychiatry. 2003 Sep;74(9):1231-1235
Sfagos C, Papageorgiou CC, Kosma KK, Kodopadelis E, Uzunoglu NK, Vassilopoulos D, Rabavilas AD.
Department of Neurology, Eginition Hospital, University of Athens, Athens, Greece. Department of Psychiatry, Eginition Hospital, University of Athens. Department of Electrical and Computer Engineering, National Technical University of Athens. University Mental Health Research Institute, Athens.


Recently, the P600 component of event related potentials, a waveform that is conceived to be generated and/or modulated by basal ganglia and cingulate area has been considered an index of the completion of any synchronised operation after target detection, having much in common with working memory operation.

Moreover, dysfunction of these brain structures as well as working memory deficits have been implicated in the pathophysiology of multiple sclerosis.

The aim of this study was to investigate the patterns of P600 elicited during a working memory test in multiple sclerosis patients compared with healthy controls.


Twenty two definite, chronic progressive multiple sclerosis patients, with recent exacerbation of their illness, and 20 normal subjects matched for age, sex, and educational level, were studied with a computerised version of the digit span test of Wechsler batteries.

Auditory P600 were measured during the anticipatory period of this test.


The patient group, as compared with healthy controls, showed significantly reduced latencies of P600 at left frontal areas and reduced P600 amplitudes at left temporoparietal region.

Moreover, memory performance of patients was significantly more impaired when compared with healthy controls.


These findings may indicate that multiple sclerosis is associated with abnormal features of the completion of synchronised operation after target detection, as they are reflected by P600 amplitudes and latencies.

Dysfunction of this mechanism may contribute to the identification of basic cognitive processes that could account for the cognitive deficits in multiple sclerosis.