Movement Disorders (revue)

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Acute movement disorders with bilateral basal ganglia lesions in uremia

Identifieur interne : 002067 ( Istex/Curation ); précédent : 002066; suivant : 002068

Acute movement disorders with bilateral basal ganglia lesions in uremia

Auteurs : Wang [Taïwan] ; Peter Brown [Royaume-Uni] ; Andrew J. Lees [Royaume-Uni]

Source :

RBID : ISTEX:65A53E80CAD6B3F87E21FC29685852F8114EF920

English descriptors

Abstract

Acute and subacute extrapyramidal movement disorders are rarely reported in uremic patients. We report three such cases with basal ganglia lesions. All three had advanced renal failure with high serum creatinine levels. One of the patients had a history of ischemic heart disease and acute pulmonary edema with hypoxemia. Another patient had experienced arterial hypotension during previous hemodialysis. The third had prominent metabolic acidosis. One of the patients developed generalized dyskinesias, whereas the other two developed gait disturbances. Neuroimaging studies in all three cases showed bilateral changes in the basal ganglia. The natural history was self‐limiting with gradual improvement. Diminution of the basal ganglia lesions was demonstrated on follow‐up imaging in two of the three cases. We conclude that acute or subacute movement disorders with bilateral basal ganglia lesions may occur in uremia. Hypoperfusion with global brain ischemia and selective vulnerability of the basal ganglia to uremic toxins may account for these lesions.

Url:
DOI: 10.1002/mds.870130615

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ISTEX:65A53E80CAD6B3F87E21FC29685852F8114EF920

Le document en format XML

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<div type="abstract" xml:lang="en">Acute and subacute extrapyramidal movement disorders are rarely reported in uremic patients. We report three such cases with basal ganglia lesions. All three had advanced renal failure with high serum creatinine levels. One of the patients had a history of ischemic heart disease and acute pulmonary edema with hypoxemia. Another patient had experienced arterial hypotension during previous hemodialysis. The third had prominent metabolic acidosis. One of the patients developed generalized dyskinesias, whereas the other two developed gait disturbances. Neuroimaging studies in all three cases showed bilateral changes in the basal ganglia. The natural history was self‐limiting with gradual improvement. Diminution of the basal ganglia lesions was demonstrated on follow‐up imaging in two of the three cases. We conclude that acute or subacute movement disorders with bilateral basal ganglia lesions may occur in uremia. Hypoperfusion with global brain ischemia and selective vulnerability of the basal ganglia to uremic toxins may account for these lesions.</div>
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