Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018991 (hemiplegia)
 3,997 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Scalp distributions and topographies of early cortical somatosensory evoked potentials (SEPs) to median nerve stimulation were studied in 22 patients with 5 different types of cerebral lesion due to cerebrovascular disease or tumor (thalamic, postcentral subcortical, precentral subcortical, diffuse subcortical and parieto-occipital lesions) in order to investigate the origins of frontal (P20, N24) and central-parietal SEPs (N20, P22, P23). In 2 patients with thalamic syndrome, N16 was delayed in latency and N20/P20 were not recorded. No early SEP except for N16 was recorded in 2 patients with pure hemisensory loss due to postcentral subcortical lesion. In all 11 patients with pure hemiparesis or hemiplegia due to precentral subcortical lesion N20/P20 and P22, P23/N24 components were of normal peak latencies. The amplitude of N24 was significantly decreased in all 3 patients with complete hemiplegia. These findings support the hypothesis that N20/P20 are generated as a horizontal dipole in the central sulcus (3b), whereas P23/N24 are a reflection of multiple generators in pre- and post-rolandic fissures. P22 was very localized in the central area contralateral to the stimulation.
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PMID:Topography of somatosensory evoked potentials to median nerve stimulation in patients with cerebral lesions. 245 93

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.
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PMID: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. 685 Feb 71