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Bilateral medial medullary infarction manifested as sensory ataxia: a case report and review of the literature.

Medial medullary infarction is usually manifested as hypoglossal palsy, limb weakness, impairment of proprioception, and oculomotor disturbance. We report a case with the unusual presentation of sensory ataxia. A 71 year-old male presented with ataxia and disequilibrium. Bilateral dysmetria, truncal...

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Detalles Bibliográficos
Autores principales: Roh, J. K., Lee, Y. S.
Formato: Texto
Lenguaje:English
Publicado: Korean Academy of Medical Sciences 1996
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3053934/
https://www.ncbi.nlm.nih.gov/pubmed/8835770
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author Roh, J. K.
Lee, Y. S.
author_facet Roh, J. K.
Lee, Y. S.
author_sort Roh, J. K.
collection PubMed
description Medial medullary infarction is usually manifested as hypoglossal palsy, limb weakness, impairment of proprioception, and oculomotor disturbance. We report a case with the unusual presentation of sensory ataxia. A 71 year-old male presented with ataxia and disequilibrium. Bilateral dysmetria, truncal ataxia, Upbeat nystagmus, and impaired vibration and position sense were the clinical features. However, weakness of the limbs, tongue, or face was not definite. MRI revealed bilateral lesion in the medullary tegmentum, and cortical potentials of somatosensory evoked response were absent. Recovery was fair after treatment. According to the literature, motor weakness is a cardinal manifestation in medial medullary infarction, and there has been no reported case presented as sensory ataxia preserving motor power. Current development of diagnostic tools would contribute to define a variety of clinical manifestations, topography, vascular concomitants, and prognosis in medial medullary infarction.
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spelling pubmed-30539342011-03-15 Bilateral medial medullary infarction manifested as sensory ataxia: a case report and review of the literature. Roh, J. K. Lee, Y. S. J Korean Med Sci Research Article Medial medullary infarction is usually manifested as hypoglossal palsy, limb weakness, impairment of proprioception, and oculomotor disturbance. We report a case with the unusual presentation of sensory ataxia. A 71 year-old male presented with ataxia and disequilibrium. Bilateral dysmetria, truncal ataxia, Upbeat nystagmus, and impaired vibration and position sense were the clinical features. However, weakness of the limbs, tongue, or face was not definite. MRI revealed bilateral lesion in the medullary tegmentum, and cortical potentials of somatosensory evoked response were absent. Recovery was fair after treatment. According to the literature, motor weakness is a cardinal manifestation in medial medullary infarction, and there has been no reported case presented as sensory ataxia preserving motor power. Current development of diagnostic tools would contribute to define a variety of clinical manifestations, topography, vascular concomitants, and prognosis in medial medullary infarction. Korean Academy of Medical Sciences 1996-04 /pmc/articles/PMC3053934/ /pubmed/8835770 Text en
spellingShingle Research Article
Roh, J. K.
Lee, Y. S.
Bilateral medial medullary infarction manifested as sensory ataxia: a case report and review of the literature.
title Bilateral medial medullary infarction manifested as sensory ataxia: a case report and review of the literature.
title_full Bilateral medial medullary infarction manifested as sensory ataxia: a case report and review of the literature.
title_fullStr Bilateral medial medullary infarction manifested as sensory ataxia: a case report and review of the literature.
title_full_unstemmed Bilateral medial medullary infarction manifested as sensory ataxia: a case report and review of the literature.
title_short Bilateral medial medullary infarction manifested as sensory ataxia: a case report and review of the literature.
title_sort bilateral medial medullary infarction manifested as sensory ataxia: a case report and review of the literature.
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3053934/
https://www.ncbi.nlm.nih.gov/pubmed/8835770
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