Presynaptic parkinsonism in multiple system atrophy mimicking Parkinson's disease: A clinicopathological case study
Identifieur interne : 002093 ( Istex/Curation ); précédent : 002092; suivant : 002094Presynaptic parkinsonism in multiple system atrophy mimicking Parkinson's disease: A clinicopathological case study
Auteurs : José Berciano [Espagne] ; Francesc Valldeoriola [Espagne] ; Isidre Ferrer [Espagne] ; Jordi Rumià [Espagne] ; Julio Pascual [Espagne] ; Concepci N Marín [Espagne] ; María J. Rey [Espagne] ; Eduardo Tolosa [Espagne]Source :
- Movement Disorders [ 0885-3185 ] ; 2002-07.
English descriptors
Abstract
We describe the clinicopathological findings in a patient aged 63 years at death who, at age 55 years, developed levodopa‐responsive parkinsonism with no atypical features. A diagnosis of idiopathic Parkinson's disease (PD) was made. During the clinical course, fluctuations and dyskinesias appeared. Eight years after onset, he was successfully treated with subthalamic nucleus stimulation but died 3 weeks postoperatively from pulmonary embolus. Brain autopsy showed marked neuronal loss and gliosis in the substantia nigra and locus coeruleus, and, to a much lesser extent, in the basis pontis, inferior olivary nuclei, and cerebellar cortex. Striatum was normal. There were numerous oligodendroglial and neuronal cytoplasmic inclusions and neuropil threads, the highest density being localized in the pons and cerebellar white matter. No Lewy bodies were observed. We conclude that nigral, presynaptic parkinsonism may occur in multiple system atrophy, which even in the long run can be indistinguishable from PD. Putaminal preservation accounts for good response to both levodopa therapy and subthalamic nucleus stimulation. © 2002 Movement Disorder Society
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DOI: 10.1002/mds.10190
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Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>New York</pubPlace><date type="published" when="2002-07">2002-07</date><biblScope unit="vol">17</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="812">812</biblScope><biblScope unit="page" to="816">816</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">57C84AA3F6FAEEE8D50716D4FD8A1BEC16C25B34</idno><idno type="DOI">10.1002/mds.10190</idno><idno type="ArticleID">MDS10190</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Parkinson's disease</term><term>multiple system atrophy</term><term>subthalamic nucleus stimulation</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We describe the clinicopathological findings in a patient aged 63 years at death who, at age 55 years, developed levodopa‐responsive parkinsonism with no atypical features. A diagnosis of idiopathic Parkinson's disease (PD) was made. During the clinical course, fluctuations and dyskinesias appeared. Eight years after onset, he was successfully treated with subthalamic nucleus stimulation but died 3 weeks postoperatively from pulmonary embolus. Brain autopsy showed marked neuronal loss and gliosis in the substantia nigra and locus coeruleus, and, to a much lesser extent, in the basis pontis, inferior olivary nuclei, and cerebellar cortex. Striatum was normal. There were numerous oligodendroglial and neuronal cytoplasmic inclusions and neuropil threads, the highest density being localized in the pons and cerebellar white matter. No Lewy bodies were observed. We conclude that nigral, presynaptic parkinsonism may occur in multiple system atrophy, which even in the long run can be indistinguishable from PD. Putaminal preservation accounts for good response to both levodopa therapy and subthalamic nucleus stimulation. © 2002 Movement Disorder Society</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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