Corticobasal syndrome with novel argyrophilic glial inclusions
Identifieur interne : 003966 ( Main/Exploration ); précédent : 003965; suivant : 003967Corticobasal syndrome with novel argyrophilic glial inclusions
Auteurs : Gregory A. Rippon [États-Unis] ; S. M. Staugaitis [États-Unis] ; Steven S. M. Chin [États-Unis] ; James E. Goldman [États-Unis] ; K. Marder [États-Unis]Source :
- Movement Disorders [ 0885-3185 ] ; 2005-05.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Adult, Apraxia, Ideomotor (complications), Apraxia, Ideomotor (metabolism), Apraxia, Ideomotor (pathology), Atrophy (pathology), Basal Ganglia (metabolism), Basal Ganglia (pathology), Degeneration, Dysarthria (complications), Fatal Outcome, Female, Frontal Lobe (pathology), Glial Fibrillary Acidic Protein (metabolism), Humans, Inclusion, Muscle Rigidity (complications), Muscle Rigidity (metabolism), Muscle Rigidity (pathology), Nerve Degeneration (complications), Nerve Degeneration (metabolism), Nerve Degeneration (pathology), Nervous system diseases, Neuropathy, Syndrome, Ubiquitin (immunology), Ubiquitin (metabolism), alpha-Crystallins (immunology), alpha-Crystallins (metabolism), corticobasal degeneration, corticobasal syndrome, degenerative disorders, glial inclusions, neuropathology.
- MESH :
- chemical , immunology : Ubiquitin, alpha-Crystallins.
- chemical , metabolism : Glial Fibrillary Acidic Protein, Ubiquitin, alpha-Crystallins.
- complications : Apraxia, Ideomotor, Dysarthria, Muscle Rigidity, Nerve Degeneration.
- metabolism : Apraxia, Ideomotor, Basal Ganglia, Muscle Rigidity, Nerve Degeneration.
- pathology : Apraxia, Ideomotor, Atrophy, Basal Ganglia, Frontal Lobe, Muscle Rigidity, Nerve Degeneration.
- Adult, Fatal Outcome, Female, Humans, Syndrome.
Abstract
A 42‐year‐old, left‐handed woman first noted impaired dexterity of the dominant hand, soon followed by dysarthria and cognitive decline. Over a 4‐year period, she developed severe left‐sided apraxia with eventual neglect of the left arm and progressive extrapyramidal signs. Cognitive testing showed progressive executive, visuospatial, fluency, and naming impairment with relative preservation of memory. Single‐photon emission computed tomography demonstrated asymmetric right posterior frontal and superior parietal hypoperfusion. The clinical impression was corticobasal degeneration. At autopsy, severe atrophy was seen in the perirolandic and frontal regions. There was marked neuronal loss and gliosis in the posterior frontal and precentral regions and less severe pathology in prefrontal, temporal, and parietal areas. Mild to moderate gliosis and neuronal loss were also seen in the putamen, globus pallidus, subthalamic, and dentate nuclei. Gallyas silver stain revealed numerous inclusions adjacent to oligodendrocyte nuclei in white and gray matter of affected cortical and subcortical regions. The gracile inclusions were wavy, slender, and stained positively with antibodies to ubiquitin and αB‐crystallin but not to microtubule‐associated proteins (tau, MAP1B, MAP2), tubulin, neurofilaments, glial fibrillary acidic protein, or α‐synuclein. The argyrophilic inclusions identified in this case are distinct from those previously described in neurodegenerative diseases. © 2005 Movement Disorder Society
Url:
DOI: 10.1002/mds.20396
Affiliations:
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Le document en format XML
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<term>Apraxia, Ideomotor (metabolism)</term>
<term>Apraxia, Ideomotor (pathology)</term>
<term>Atrophy (pathology)</term>
<term>Basal Ganglia (metabolism)</term>
<term>Basal Ganglia (pathology)</term>
<term>Degeneration</term>
<term>Dysarthria (complications)</term>
<term>Fatal Outcome</term>
<term>Female</term>
<term>Frontal Lobe (pathology)</term>
<term>Glial Fibrillary Acidic Protein (metabolism)</term>
<term>Humans</term>
<term>Inclusion</term>
<term>Muscle Rigidity (complications)</term>
<term>Muscle Rigidity (metabolism)</term>
<term>Muscle Rigidity (pathology)</term>
<term>Nerve Degeneration (complications)</term>
<term>Nerve Degeneration (metabolism)</term>
<term>Nerve Degeneration (pathology)</term>
<term>Nervous system diseases</term>
<term>Neuropathy</term>
<term>Syndrome</term>
<term>Ubiquitin (immunology)</term>
<term>Ubiquitin (metabolism)</term>
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<term>alpha-Crystallins (metabolism)</term>
<term>corticobasal degeneration</term>
<term>corticobasal syndrome</term>
<term>degenerative disorders</term>
<term>glial inclusions</term>
<term>neuropathology</term>
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<term>alpha-Crystallins</term>
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<term>Dysarthria</term>
<term>Muscle Rigidity</term>
<term>Nerve Degeneration</term>
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<term>Basal Ganglia</term>
<term>Muscle Rigidity</term>
<term>Nerve Degeneration</term>
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<term>Basal Ganglia</term>
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<term>Muscle Rigidity</term>
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<term>Fatal Outcome</term>
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<front><div type="abstract" xml:lang="en">A 42‐year‐old, left‐handed woman first noted impaired dexterity of the dominant hand, soon followed by dysarthria and cognitive decline. Over a 4‐year period, she developed severe left‐sided apraxia with eventual neglect of the left arm and progressive extrapyramidal signs. Cognitive testing showed progressive executive, visuospatial, fluency, and naming impairment with relative preservation of memory. Single‐photon emission computed tomography demonstrated asymmetric right posterior frontal and superior parietal hypoperfusion. The clinical impression was corticobasal degeneration. At autopsy, severe atrophy was seen in the perirolandic and frontal regions. There was marked neuronal loss and gliosis in the posterior frontal and precentral regions and less severe pathology in prefrontal, temporal, and parietal areas. Mild to moderate gliosis and neuronal loss were also seen in the putamen, globus pallidus, subthalamic, and dentate nuclei. Gallyas silver stain revealed numerous inclusions adjacent to oligodendrocyte nuclei in white and gray matter of affected cortical and subcortical regions. The gracile inclusions were wavy, slender, and stained positively with antibodies to ubiquitin and αB‐crystallin but not to microtubule‐associated proteins (tau, MAP1B, MAP2), tubulin, neurofilaments, glial fibrillary acidic protein, or α‐synuclein. The argyrophilic inclusions identified in this case are distinct from those previously described in neurodegenerative diseases. © 2005 Movement Disorder Society</div>
</front>
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