Brain, Vol. 106, No. 2, 271-311, 1983
© 1983 Oxford University Press
research-article |
ASTEREOGNOSIS AND DISSOCIATED LOSS OF FRONTAL OR PARIETAL COMPONENTS OF SOMATOSENSORY EVOKED POTENTIALS IN HEMISPHERIC LESIONS
DETAILED CORRELATIONS WITH CLINICAL SIGNS AND COMPUTERIZED TOMOGRAPHIC SCANNING
From the EEG Department, Hôpital Nenrologique, Faculté de Médecine Lyon Nord 69394 Lyon Cedex 3, France, and the the Brain Research Unit, University of Brussels Brussels 1000, Belgium
Correspondence to:
Request for reprints to Professor J. E. Desmedt, Brain Research Unit, 115 Boulevard de Waterloo, 1000 Brussels, Belgium.
Detailed clinical sensory and motor signs were correlated case by case with somatosensory evoked potentials (SEP) in 22 selected patients with a single circumscribed hemisphere lesion. The lesions collectively mapped out a variety of cerebral sites from the anterior frontal to the posterior parietal regions. SEPs were averaged from 8 standard scalp sites with an earlobe reference electrode, so that parietal N20-P27-P45 were differentiated from prerolandic P22-N30 SEP components. SEP wave forms to stimulation on the unaffected side served as the patient's own control.
A complete parietal lesion produced contralateral hemianaesthesia without upper motor neuron signs and eliminated the parietal N20-P27-P45 while the prerolandic P22-N30 persisted at usual latencies. The neural generators for the N20 and the P22 components are thus distinct. It is also proposed that direct, short latency pathways convey somatosensory inputs to the motor cortex, independently of connections via parietal areas 2 and 5. Enhancement of P22-N30 after chronic parietal lesions suggests collateral reinnervation by residual inputs after partial deafferentiation of prerolandic cortex.
Small postcentral lesions produced astereognosis (with preserved tactile and deep sensation) and reduced or eliminated the N20 and P27 SEP components, but did not affect the P22-N30 components. Precentral lesions with severe hemiplegia (but not prefrontal lesions) eliminated the prerolandic P22-N30 SEP components and did not alter the parietal N20-P27-P45 components. The data are pertinent to the understanding of the pathophysiology of somatosensory deficits and for the diagnostic use of SEPs in cerebral lesions.
Received April 6, 1982.
Revised November 11, 1982.
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