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pseudobulbar palsy/inflamació
L'enllaç es desa al porta-retalls
6 resultats
Bilateral thalamic infarcts presenting as acute pseudobulbar palsy.
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A 28-year-old, previously healthy, normotensive woman suddenly developed an acute pseudobulbar palsy with dysarthria, dysphagia, hypernasal voice and mild right arm paresis. Extensive laboratory investigations excluded all other possible causes of acute pseudobulbar palsy (neoplastic, inflammatory,
Alexander's disease: a report and reappraisal.
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A boy with juvenile onset of symptoms of Alexander's disease had a clinical picture of pseudobulbar palsy, ataxia, and spastic paraparesis. Pathologic examination of the central nervous system revealed the diffuse presence of Rosenthal fibers and patchy demyelination. This may be the first report of
Central pontine myelinolysis.
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Central pontine myelinolysis (CPM), a neurologic disorder caused most frequently by rapid correction of hyponatremia, is characterized by demyelination that affects the central portion of the base of the pons. There are no inflammatory changes, and blood vessels are normal. Clinical features usually
[Paucisymptomatic and reversible myelinolysis after an anaphylactic shock].
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Myelinolysis is characterized by a non inflammatory demyelination, affecting the central portion of the pons. Clinical features usually reflect damage to the descending motor tracts and include spastic tetraparesis, pseudobulbar paralysis, and the locked-in syndrome. We describe the case of a
A clinical comparative study of multiple sclerosis and neuro-Behçet's syndrome.
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Clinical comparisons were made between Japanese patients with multiple sclerosis (66 cases) and neuro-Behçet's syndrome (23 cases). Those with neuro-Behçet showed marked male predominance, while those with multiple sclerosis showed slight female preponderance. Both showed encephalomyelopathy
[The role of immunologic reactions in the pathogenesis in Binswanger's disease; a clue to therapeutic approach].
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We examined the alterations of glial cells in the brains with Binswanger's disease. In comparison to the brains with lacunar cerebral infarction and those from non-neurological controls, oligodendroglia was decreased in number, and microglia was increased and activated in the white matter lesions in
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