Parkinsonian syndromes associated with hydrocephalus: Case reports, a review of the literature, and pathophysiological hypotheses
Identifieur interne : 000440 ( Istex/Corpus ); précédent : 000439; suivant : 000441Parkinsonian syndromes associated with hydrocephalus: Case reports, a review of the literature, and pathophysiological hypotheses
Auteurs : Terry Curran ; LangSource :
- Movement Disorders [ 0885-3185 ] ; 1994.
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- KwdEn :
Abstract
We present nine cases of obstructive hydrocephalus (OH) associated with marked parkinsonism. Four patients had noncommunicating OH (NCOH) [three nontumoral aqueductal stenosis (AS), one tumoral AS]. The presentation was that of acute or subacute parkinsonism, usually at the time of acute recurrent ventricular obstruction. Three had a marked response to levodopa and required short‐term treatment after shunting. However, one has remained levodopa dependent after 21/2 years. Three of the five patients with communicating OH (COH) presented with shunt‐responsive normal pressure hydrocephalus (NPH), only later to develop progressive parkinsonism. One of these was found to have progressive supranuclear palsy (PSP) at autopsy and PSP was clinically susepected in one other patient. A third had an atypical course suggestive of PSP; however, autopsy demonstrated the combination of Lewy body parkinsonism and the sequelae of hydrocephalus. The remaining two COH patients presented with levodopa‐responsive parkinsonism. Subsequent clinical features and imaging studies suggested the presence of NPH. The pathophysiology of hydrocephalic parkinsonism probably involves variable sites of dysfunction in the nigrostriatal pathway and/or the cortico‐striato‐pallido‐thalamo‐cortical circuit. At certain locations these pathways lie in close proximity to the ventricular system and may be subjected to mass effects and ischemic changes secondary to ventriculomegaly. The additional importance of possible associations between subcortical cerebral ischemia, NPH, and “degenerative” disorders such as PSP and Parkinson's disease is discussed.
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DOI: 10.1002/mds.870090503
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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>Hoboken</pubPlace><date type="published" when="1994">1994</date><biblScope unit="vol">9</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="508">508</biblScope><biblScope unit="page" to="520">520</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">0BFD4262D4B803658D5CCD421D9D06677FC2DE77</idno><idno type="DOI">10.1002/mds.870090503</idno><idno type="ArticleID">MDS870090503</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Hydrocephalus</term><term>Normal pressure hydrocephalus</term><term>Parkinsonian syndromes</term><term>Progressive supranuclear palsy</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We present nine cases of obstructive hydrocephalus (OH) associated with marked parkinsonism. Four patients had noncommunicating OH (NCOH) [three nontumoral aqueductal stenosis (AS), one tumoral AS]. The presentation was that of acute or subacute parkinsonism, usually at the time of acute recurrent ventricular obstruction. Three had a marked response to levodopa and required short‐term treatment after shunting. However, one has remained levodopa dependent after 21/2 years. Three of the five patients with communicating OH (COH) presented with shunt‐responsive normal pressure hydrocephalus (NPH), only later to develop progressive parkinsonism. One of these was found to have progressive supranuclear palsy (PSP) at autopsy and PSP was clinically susepected in one other patient. A third had an atypical course suggestive of PSP; however, autopsy demonstrated the combination of Lewy body parkinsonism and the sequelae of hydrocephalus. The remaining two COH patients presented with levodopa‐responsive parkinsonism. Subsequent clinical features and imaging studies suggested the presence of NPH. The pathophysiology of hydrocephalic parkinsonism probably involves variable sites of dysfunction in the nigrostriatal pathway and/or the cortico‐striato‐pallido‐thalamo‐cortical circuit. At certain locations these pathways lie in close proximity to the ventricular system and may be subjected to mass effects and ischemic changes secondary to ventriculomegaly. The additional importance of possible associations between subcortical cerebral ischemia, NPH, and “degenerative” disorders such as PSP and Parkinson's disease is discussed.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Terry Curran</name><affiliations><json:string>Morton and Gloria Shulman Movement Disorders Centre, The Toronto Hospital, Western Division, Toronto, Ontario, Canada</json:string></affiliations></json:item><json:item><name>Dr. Lang</name><affiliations><json:string>Morton and Gloria Shulman Movement Disorders Centre, The Toronto Hospital, Western Division, Toronto, Ontario, Canada</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Parkinsonian syndromes</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Hydrocephalus</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Normal pressure hydrocephalus</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Progressive supranuclear palsy</value></json:item></subject><language><json:string>eng</json:string></language><abstract>We present nine cases of obstructive hydrocephalus (OH) associated with marked parkinsonism. Four patients had noncommunicating OH (NCOH) [three nontumoral aqueductal stenosis (AS), one tumoral AS]. The presentation was that of acute or subacute parkinsonism, usually at the time of acute recurrent ventricular obstruction. Three had a marked response to levodopa and required short‐term treatment after shunting. However, one has remained levodopa dependent after 21/2 years. Three of the five patients with communicating OH (COH) presented with shunt‐responsive normal pressure hydrocephalus (NPH), only later to develop progressive parkinsonism. One of these was found to have progressive supranuclear palsy (PSP) at autopsy and PSP was clinically susepected in one other patient. A third had an atypical course suggestive of PSP; however, autopsy demonstrated the combination of Lewy body parkinsonism and the sequelae of hydrocephalus. The remaining two COH patients presented with levodopa‐responsive parkinsonism. Subsequent clinical features and imaging studies suggested the presence of NPH. The pathophysiology of hydrocephalic parkinsonism probably involves variable sites of dysfunction in the nigrostriatal pathway and/or the cortico‐striato‐pallido‐thalamo‐cortical circuit. At certain locations these pathways lie in close proximity to the ventricular system and may be subjected to mass effects and ischemic changes secondary to ventriculomegaly. 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Disord.</title><idno type="pISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><idno type="DOI">10.1002/(ISSN)1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1994"></date><biblScope unit="vol">9</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="508">508</biblScope><biblScope unit="page" to="520">520</biblScope></imprint></monogr><idno type="istex">0BFD4262D4B803658D5CCD421D9D06677FC2DE77</idno><idno type="DOI">10.1002/mds.870090503</idno><idno type="ArticleID">MDS870090503</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1994</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>We present nine cases of obstructive hydrocephalus (OH) associated with marked parkinsonism. Four patients had noncommunicating OH (NCOH) [three nontumoral aqueductal stenosis (AS), one tumoral AS]. The presentation was that of acute or subacute parkinsonism, usually at the time of acute recurrent ventricular obstruction. Three had a marked response to levodopa and required short‐term treatment after shunting. However, one has remained levodopa dependent after 21/2 years. Three of the five patients with communicating OH (COH) presented with shunt‐responsive normal pressure hydrocephalus (NPH), only later to develop progressive parkinsonism. One of these was found to have progressive supranuclear palsy (PSP) at autopsy and PSP was clinically susepected in one other patient. A third had an atypical course suggestive of PSP; however, autopsy demonstrated the combination of Lewy body parkinsonism and the sequelae of hydrocephalus. The remaining two COH patients presented with levodopa‐responsive parkinsonism. Subsequent clinical features and imaging studies suggested the presence of NPH. The pathophysiology of hydrocephalic parkinsonism probably involves variable sites of dysfunction in the nigrostriatal pathway and/or the cortico‐striato‐pallido‐thalamo‐cortical circuit. At certain locations these pathways lie in close proximity to the ventricular system and may be subjected to mass effects and ischemic changes secondary to ventriculomegaly. 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Four patients had <i>noncommunicating OH</i> (NCOH) [three nontumoral aqueductal stenosis (AS), one tumoral AS]. The presentation was that of acute or subacute parkinsonism, usually at the time of acute recurrent ventricular obstruction. Three had a marked response to levodopa and required short‐term treatment after shunting. However, one has remained levodopa dependent after 21/2 years. Three of the five patients with <i>communicating OH</i> (COH) presented with shunt‐responsive normal pressure hydrocephalus (NPH), only later to develop progressive parkinsonism. One of these was found to have progressive supranuclear palsy (PSP) at autopsy and PSP was clinically susepected in one other patient. A third had an atypical course suggestive of PSP; however, autopsy demonstrated the combination of Lewy body parkinsonism and the sequelae of hydrocephalus. The remaining two COH patients presented with levodopa‐responsive parkinsonism. Subsequent clinical features and imaging studies suggested the presence of NPH. The pathophysiology of hydrocephalic parkinsonism probably involves variable sites of dysfunction in the nigrostriatal pathway and/or the cortico‐striato‐pallido‐thalamo‐cortical circuit. At certain locations these pathways lie in close proximity to the ventricular system and may be subjected to mass effects and ischemic changes secondary to ventriculomegaly. The additional importance of possible associations between subcortical cerebral ischemia, NPH, and “degenerative” disorders such as PSP and Parkinson's disease is discussed.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 4-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Parkinsonian syndromes associated with hydrocephalus: Case reports, a review of the literature, and pathophysiological hypotheses</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>PARKINSONIAN SYNDROMES AND HYDROCEPHALUS</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Parkinsonian syndromes associated with hydrocephalus: Case reports, a review of the literature, and pathophysiological hypotheses</title></titleInfo><name type="personal"><namePart type="given">Terry</namePart><namePart type="family">Curran</namePart><affiliation>Morton and Gloria Shulman Movement Disorders Centre, The Toronto Hospital, Western Division, Toronto, Ontario, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="termsOfAddress">Dr.</namePart><namePart type="family">Lang</namePart><affiliation>Morton and Gloria Shulman Movement Disorders Centre, The Toronto Hospital, Western Division, Toronto, Ontario, Canada</affiliation><description>Correspondence: Morton and Gloria Shulman Movement Disorders Centre, The Toronto Hospital, Western Division, 399 Bathurst Street, MP11‐304, Toronto, Ontario, Canada M5T 2S8</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">1994</dateIssued><copyrightDate encoding="w3cdtf">1994</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">5</extent><extent unit="tables">2</extent><extent unit="references">62</extent></physicalDescription><abstract lang="en">We present nine cases of obstructive hydrocephalus (OH) associated with marked parkinsonism. Four patients had noncommunicating OH (NCOH) [three nontumoral aqueductal stenosis (AS), one tumoral AS]. The presentation was that of acute or subacute parkinsonism, usually at the time of acute recurrent ventricular obstruction. Three had a marked response to levodopa and required short‐term treatment after shunting. However, one has remained levodopa dependent after 21/2 years. Three of the five patients with communicating OH (COH) presented with shunt‐responsive normal pressure hydrocephalus (NPH), only later to develop progressive parkinsonism. One of these was found to have progressive supranuclear palsy (PSP) at autopsy and PSP was clinically susepected in one other patient. A third had an atypical course suggestive of PSP; however, autopsy demonstrated the combination of Lewy body parkinsonism and the sequelae of hydrocephalus. The remaining two COH patients presented with levodopa‐responsive parkinsonism. Subsequent clinical features and imaging studies suggested the presence of NPH. The pathophysiology of hydrocephalic parkinsonism probably involves variable sites of dysfunction in the nigrostriatal pathway and/or the cortico‐striato‐pallido‐thalamo‐cortical circuit. At certain locations these pathways lie in close proximity to the ventricular system and may be subjected to mass effects and ischemic changes secondary to ventriculomegaly. The additional importance of possible associations between subcortical cerebral ischemia, NPH, and “degenerative” disorders such as PSP and Parkinson's disease is discussed.</abstract><subject lang="en"><genre>Keywords</genre><topic>Parkinsonian syndromes</topic><topic>Hydrocephalus</topic><topic>Normal pressure hydrocephalus</topic><topic>Progressive supranuclear palsy</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. 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