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)

The study of two groups of right handed aphasics, group A and group B, is presented. Each group was formed by four subjects, both groups showed an aphasic syndrome craracterized by alteration in the efferent sphere of oral and written language, principally in the latter. There was almost no alteration in the sensory interchange sphere, except for a right hypoesthesia and astereognosis in two subjects of each group. The aspect in which both groups differed profoundly was the efferent sphere of written language. Group B patients could not write with the dominant hand because of a right hemiplegia. Nevertheless, they could do it with the left, nondominant hand. Group A patients were unable to write with either hand in spite of the absence of motor deficit or incoordination which could explain this inability. The different possible topographical localizations responsible for the deficit are analyzed. It is concluded that there are three main possibilities that could explain the writing difficulty found in group B patients: a) a lesion located in the white frontal matter of the left hemisphere just underneath the kinesthetic area; b) a lesion in the kinesthetic dominant area itself; c) a lesion in the dominant cerebral hemisphere white matter underlying the primary receptor somesthetic and the primary effector areas, but without directly involving them, and extending also in depth toward the anterior third of the corpus callosum. Any one of these lesions could impair the transmission of information from the dominant kinesthetic hand area to the primary effector motor area of both cerebral hemispheres.
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PMID:Aphasia due to lesions of the kinesthetic speech areas. 61 25

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