Presynaptic parkinsonism in multiple system atrophy mimicking Parkinson's disease: a clinicopathological case study.
Identifieur interne : 003A04 ( PubMed/Curation ); précédent : 003A03; suivant : 003A05Presynaptic parkinsonism in multiple system atrophy mimicking Parkinson's disease: a clinicopathological case study.
Auteurs : José Berciano [Espagne] ; Francesc Valldeoriola ; Isidre Ferrer ; Jordi Rumià ; Julio Pascual ; Concepci N Marín ; María J. Rey ; Eduardo TolosaSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2002.
English descriptors
- KwdEn :
- Brain (pathology), Brain (physiopathology), Combined Modality Therapy, Diagnosis, Differential, Electric Stimulation Therapy, Electrodes, Implanted, Humans, Levodopa (therapeutic use), Male, Middle Aged, Multiple System Atrophy (diagnosis), Multiple System Atrophy (pathology), Multiple System Atrophy (therapy), Neurologic Examination, Parkinson Disease (diagnosis), Parkinson Disease (pathology), Parkinson Disease (therapy), Parkinsonian Disorders (diagnosis), Parkinsonian Disorders (pathology), Parkinsonian Disorders (therapy), Receptors, Presynaptic (physiology), Subthalamic Nucleus (pathology), Subthalamic Nucleus (physiopathology).
- MESH :
- chemical , physiology : Receptors, Presynaptic.
- chemical , therapeutic use : Levodopa.
- diagnosis : Multiple System Atrophy, Parkinson Disease, Parkinsonian Disorders.
- pathology : Brain, Multiple System Atrophy, Parkinson Disease, Parkinsonian Disorders, Subthalamic Nucleus.
- physiopathology : Brain, Subthalamic Nucleus.
- therapy : Multiple System Atrophy, Parkinson Disease, Parkinsonian Disorders.
- Combined Modality Therapy, Diagnosis, Differential, Electric Stimulation Therapy, Electrodes, Implanted, Humans, Male, Middle Aged, Neurologic Examination.
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.
DOI: 10.1002/mds.10190
PubMed: 12210882
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Rey</name></author><author><name sortKey="Tolosa, Eduardo" sort="Tolosa, Eduardo" uniqKey="Tolosa E" first="Eduardo" last="Tolosa">Eduardo Tolosa</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2002">2002</date><idno type="RBID">pubmed:12210882</idno><idno type="pmid">12210882</idno><idno type="doi">10.1002/mds.10190</idno><idno type="wicri:Area/PubMed/Corpus">003A04</idno><idno type="wicri:Area/PubMed/Curation">003A04</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Presynaptic parkinsonism in multiple system atrophy mimicking Parkinson's disease: a clinicopathological case study.</title><author><name sortKey="Berciano, Jose" sort="Berciano, Jose" uniqKey="Berciano J" first="José" last="Berciano">José Berciano</name><affiliation wicri:level="1"><nlm:affiliation>Service of Neurology, University Hospital Marqués de Valdecilla, University of Cantabria, Santander, Spain. neuro@humv.es</nlm:affiliation><country xml:lang="fr">Espagne</country><wicri:regionArea>Service of Neurology, University Hospital Marqués de Valdecilla, University of Cantabria, Santander</wicri:regionArea></affiliation></author><author><name sortKey="Valldeoriola, Francesc" sort="Valldeoriola, Francesc" uniqKey="Valldeoriola F" first="Francesc" last="Valldeoriola">Francesc Valldeoriola</name></author><author><name sortKey="Ferrer, Isidre" sort="Ferrer, Isidre" uniqKey="Ferrer I" first="Isidre" last="Ferrer">Isidre Ferrer</name></author><author><name sortKey="Rumia, Jordi" sort="Rumia, Jordi" uniqKey="Rumia J" first="Jordi" last="Rumià">Jordi Rumià</name></author><author><name sortKey="Pascual, Julio" sort="Pascual, Julio" uniqKey="Pascual J" first="Julio" last="Pascual">Julio Pascual</name></author><author><name sortKey="Marin, Concepci N" sort="Marin, Concepci N" uniqKey="Marin C" first="Concepci N" last="Marín">Concepci N Marín</name></author><author><name sortKey="Rey, Maria J" sort="Rey, Maria J" uniqKey="Rey M" first="María J" last="Rey">María J. Rey</name></author><author><name sortKey="Tolosa, Eduardo" sort="Tolosa, Eduardo" uniqKey="Tolosa E" first="Eduardo" last="Tolosa">Eduardo Tolosa</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="2002" type="published">2002</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Brain (pathology)</term><term>Brain (physiopathology)</term><term>Combined Modality Therapy</term><term>Diagnosis, Differential</term><term>Electric Stimulation Therapy</term><term>Electrodes, Implanted</term><term>Humans</term><term>Levodopa (therapeutic use)</term><term>Male</term><term>Middle Aged</term><term>Multiple System Atrophy (diagnosis)</term><term>Multiple System Atrophy (pathology)</term><term>Multiple System Atrophy (therapy)</term><term>Neurologic Examination</term><term>Parkinson Disease (diagnosis)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (therapy)</term><term>Parkinsonian Disorders (diagnosis)</term><term>Parkinsonian Disorders (pathology)</term><term>Parkinsonian Disorders (therapy)</term><term>Receptors, Presynaptic (physiology)</term><term>Subthalamic Nucleus (pathology)</term><term>Subthalamic Nucleus (physiopathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Receptors, Presynaptic</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Multiple System Atrophy</term><term>Parkinson Disease</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain</term><term>Multiple System Atrophy</term><term>Parkinson Disease</term><term>Parkinsonian Disorders</term><term>Subthalamic Nucleus</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Brain</term><term>Subthalamic Nucleus</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Multiple System Atrophy</term><term>Parkinson Disease</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Combined Modality Therapy</term><term>Diagnosis, Differential</term><term>Electric Stimulation Therapy</term><term>Electrodes, Implanted</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Neurologic Examination</term></keywords></textClass></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.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">12210882</PMID><DateCreated><Year>2002</Year><Month>09</Month><Day>04</Day></DateCreated><DateCompleted><Year>2002</Year><Month>11</Month><Day>20</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>17</Volume><Issue>4</Issue><PubDate><Year>2002</Year><Month>Jul</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. 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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. 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ValidYN="Y"><LastName>Marín</LastName><ForeName>Concepción</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Rey</LastName><ForeName>María J</ForeName><Initials>MJ</Initials></Author><Author ValidYN="Y"><LastName>Tolosa</LastName><ForeName>Eduardo</ForeName><Initials>E</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017661">Receptors, Presynaptic</NameOfSubstance></Chemical><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance 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