Cerebellar involvement in progressive supranuclear palsy: A clinicopathological study
Identifieur interne : 002C73 ( Main/Merge ); précédent : 002C72; suivant : 002C74Cerebellar involvement in progressive supranuclear palsy: A clinicopathological study
Auteurs : Masato Kanazawa [Japon] ; Takayoshi Shimohata [Japon] ; Yasuko Toyoshima [Japon] ; Mari Tada [Japon] ; Akiyoshi Kakita [Japon] ; Takashi Morita [Japon] ; Tetsutaro Ozawa [Japon] ; Hitoshi Takahashi [Japon] ; Masatoyo Nishizawa [Japon]Source :
- Movement Disorders [ 0885-3185 ] ; 2009-07-15.
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Cell Death (physiology), Cerebellum (metabolism), Cerebellum (pathology), Cerebellum (physiopathology), Female, Humans, Longitudinal Studies, Male, Nerve Tissue Proteins (metabolism), Neurons (metabolism), Neurons (pathology), Neurons (ultrastructure), Parkinson's disease, Retrospective Studies, Silver Staining (methods), Supranuclear Palsy, Progressive (classification), Supranuclear Palsy, Progressive (pathology), Supranuclear Palsy, Progressive (physiopathology), parkinsonian disorders, progressive supranuclear palsy, spinocerebellar ataxias, tau Proteins (metabolism).
- MESH :
- chemical , metabolism : Nerve Tissue Proteins, tau Proteins.
- classification : Supranuclear Palsy, Progressive.
- metabolism : Cerebellum, Neurons.
- methods : Silver Staining.
- pathology : Cerebellum, Neurons, Supranuclear Palsy, Progressive.
- physiology : Cell Death.
- physiopathology : Cerebellum, Supranuclear Palsy, Progressive.
- ultrastructure : Neurons.
- Aged, Aged, 80 and over, Female, Humans, Longitudinal Studies, Male, Retrospective Studies.
Abstract
The clinical heterogeneity of progressive supranuclear palsy (PSP), which is classified as classic Richardson's syndrome (RS) and PSP‐Parkinsonism (PSP‐P), has been previously discussed. We retrospectively analyzed 22 consecutive Japanese patients with pathologically proven PSP to investigate the clinicopathological heterogeneity. We investigated the clinical features both early in and at any time during the disease course. The pathological severities of neuronal loss with gliosis and tau pathology were also evaluated. On the basis of the clinical features, 10 patients were categorized as having RS, and 8 were categorized as having PSP‐P. Four patients presenting with cerebellar ataxia or cerebral cortical signs were categorized as having unclassifiable PSP. Among them, 3 developed cerebellar ataxia as the initial and principal symptom. Notably, tau‐positive inclusion bodies in Purkinje cells were significantly more frequently observed in the patients with cerebellar ataxia than in those without cerebellar ataxia. All the patients with cerebellar ataxia exhibited more neuronal loss with gliosis and higher densities of coiled bodies in the cerebellar dentate nucleus than those without cerebellar ataxia. This study confirms the wide spectrum of clinicopathological manifestations associated with PSP regardless of different ethnic origin, and demonstrates that PSP patients manifest cerebellar ataxia. © 2009 Movement Disorder Society
Url:
DOI: 10.1002/mds.22583
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Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. 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="2009-07-15">2009-07-15</date><biblScope unit="vol">24</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="1312">1312</biblScope><biblScope unit="page" to="1318">1318</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">794DDA51BBCBE22D672130D09EA1D289879D5C07</idno><idno type="DOI">10.1002/mds.22583</idno><idno type="ArticleID">MDS22583</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Cell Death (physiology)</term><term>Cerebellum (metabolism)</term><term>Cerebellum (pathology)</term><term>Cerebellum (physiopathology)</term><term>Female</term><term>Humans</term><term>Longitudinal Studies</term><term>Male</term><term>Nerve Tissue Proteins (metabolism)</term><term>Neurons (metabolism)</term><term>Neurons (pathology)</term><term>Neurons (ultrastructure)</term><term>Parkinson's disease</term><term>Retrospective Studies</term><term>Silver Staining (methods)</term><term>Supranuclear Palsy, Progressive (classification)</term><term>Supranuclear Palsy, Progressive (pathology)</term><term>Supranuclear Palsy, Progressive (physiopathology)</term><term>parkinsonian disorders</term><term>progressive supranuclear palsy</term><term>spinocerebellar ataxias</term><term>tau Proteins (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Nerve Tissue Proteins</term><term>tau Proteins</term></keywords><keywords scheme="MESH" qualifier="classification" xml:lang="en"><term>Supranuclear Palsy, Progressive</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Cerebellum</term><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Silver Staining</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Cerebellum</term><term>Neurons</term><term>Supranuclear Palsy, Progressive</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Cell Death</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Cerebellum</term><term>Supranuclear Palsy, Progressive</term></keywords><keywords scheme="MESH" qualifier="ultrastructure" xml:lang="en"><term>Neurons</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Female</term><term>Humans</term><term>Longitudinal Studies</term><term>Male</term><term>Retrospective Studies</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The clinical heterogeneity of progressive supranuclear palsy (PSP), which is classified as classic Richardson's syndrome (RS) and PSP‐Parkinsonism (PSP‐P), has been previously discussed. We retrospectively analyzed 22 consecutive Japanese patients with pathologically proven PSP to investigate the clinicopathological heterogeneity. We investigated the clinical features both early in and at any time during the disease course. The pathological severities of neuronal loss with gliosis and tau pathology were also evaluated. On the basis of the clinical features, 10 patients were categorized as having RS, and 8 were categorized as having PSP‐P. Four patients presenting with cerebellar ataxia or cerebral cortical signs were categorized as having unclassifiable PSP. Among them, 3 developed cerebellar ataxia as the initial and principal symptom. Notably, tau‐positive inclusion bodies in Purkinje cells were significantly more frequently observed in the patients with cerebellar ataxia than in those without cerebellar ataxia. All the patients with cerebellar ataxia exhibited more neuronal loss with gliosis and higher densities of coiled bodies in the cerebellar dentate nucleus than those without cerebellar ataxia. This study confirms the wide spectrum of clinicopathological manifestations associated with PSP regardless of different ethnic origin, and demonstrates that PSP patients manifest cerebellar ataxia. © 2009 Movement Disorder Society</div></front></TEI><double doi="10.1002/mds.22583"><ISTEX><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Cerebellar involvement in progressive supranuclear palsy: A clinicopathological study</title><author><name sortKey="Kanazawa, Masato" sort="Kanazawa, Masato" uniqKey="Kanazawa M" first="Masato" last="Kanazawa">Masato Kanazawa</name></author><author><name sortKey="Shimohata, Takayoshi" sort="Shimohata, Takayoshi" uniqKey="Shimohata T" first="Takayoshi" last="Shimohata">Takayoshi Shimohata</name></author><author><name sortKey="Toyoshima, Yasuko" sort="Toyoshima, Yasuko" uniqKey="Toyoshima Y" first="Yasuko" last="Toyoshima">Yasuko Toyoshima</name></author><author><name sortKey="Tada, Mari" sort="Tada, Mari" uniqKey="Tada M" first="Mari" last="Tada">Mari Tada</name></author><author><name sortKey="Kakita, Akiyoshi" sort="Kakita, Akiyoshi" uniqKey="Kakita A" first="Akiyoshi" last="Kakita">Akiyoshi Kakita</name></author><author><name sortKey="Morita, Takashi" sort="Morita, Takashi" uniqKey="Morita T" first="Takashi" last="Morita">Takashi Morita</name></author><author><name sortKey="Ozawa, Tetsutaro" sort="Ozawa, Tetsutaro" uniqKey="Ozawa T" first="Tetsutaro" last="Ozawa">Tetsutaro Ozawa</name></author><author><name sortKey="Takahashi, Hitoshi" sort="Takahashi, Hitoshi" uniqKey="Takahashi H" first="Hitoshi" last="Takahashi">Hitoshi Takahashi</name></author><author><name sortKey="Nishizawa, Masatoyo" sort="Nishizawa, Masatoyo" uniqKey="Nishizawa M" first="Masatoyo" last="Nishizawa">Masatoyo Nishizawa</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:794DDA51BBCBE22D672130D09EA1D289879D5C07</idno><date when="2009" year="2009">2009</date><idno type="doi">10.1002/mds.22583</idno><idno type="url">https://api.istex.fr/document/794DDA51BBCBE22D672130D09EA1D289879D5C07/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">001604</idno><idno type="wicri:Area/Istex/Curation">001604</idno><idno type="wicri:Area/Istex/Checkpoint">001014</idno><idno type="wicri:doubleKey">0885-3185:2009:Kanazawa M:cerebellar:involvement:in</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Cerebellar involvement in progressive supranuclear palsy: A clinicopathological study</title><author><name sortKey="Kanazawa, Masato" sort="Kanazawa, Masato" uniqKey="Kanazawa M" first="Masato" last="Kanazawa">Masato Kanazawa</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Neurology, Brain Research Institute, Niigata University, Niigata</wicri:regionArea><wicri:noRegion>Niigata</wicri:noRegion></affiliation></author><author><name sortKey="Shimohata, Takayoshi" sort="Shimohata, Takayoshi" uniqKey="Shimohata T" first="Takayoshi" last="Shimohata">Takayoshi Shimohata</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Neurology, Brain Research Institute, Niigata University, Niigata</wicri:regionArea><wicri:noRegion>Niigata</wicri:noRegion></affiliation></author><author><name sortKey="Toyoshima, Yasuko" sort="Toyoshima, Yasuko" uniqKey="Toyoshima Y" first="Yasuko" last="Toyoshima">Yasuko Toyoshima</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Pathology, Brain Research Institute, Niigata University, Niigata</wicri:regionArea><wicri:noRegion>Niigata</wicri:noRegion></affiliation></author><author><name sortKey="Tada, Mari" sort="Tada, Mari" uniqKey="Tada M" first="Mari" last="Tada">Mari Tada</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Neurology, Brain Research Institute, Niigata University, Niigata</wicri:regionArea><wicri:noRegion>Niigata</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Pathology, Brain Research Institute, Niigata University, Niigata</wicri:regionArea><wicri:noRegion>Niigata</wicri:noRegion></affiliation></author><author><name sortKey="Kakita, Akiyoshi" sort="Kakita, Akiyoshi" uniqKey="Kakita A" first="Akiyoshi" last="Kakita">Akiyoshi Kakita</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Pathology, Brain Research Institute, Niigata University, Niigata</wicri:regionArea><wicri:noRegion>Niigata</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Pathological Neuroscience, Resource Branch for Brain Disease Research CBBR, Brain Research Institute, Niigata University, Niigata</wicri:regionArea><wicri:noRegion>Niigata</wicri:noRegion></affiliation></author><author><name sortKey="Morita, Takashi" sort="Morita, Takashi" uniqKey="Morita T" first="Takashi" last="Morita">Takashi Morita</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Pathology, Shinrakuen Hospital, Niigata</wicri:regionArea><wicri:noRegion>Niigata</wicri:noRegion></affiliation></author><author><name sortKey="Ozawa, Tetsutaro" sort="Ozawa, Tetsutaro" uniqKey="Ozawa T" first="Tetsutaro" last="Ozawa">Tetsutaro Ozawa</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Neurology, Brain Research Institute, Niigata University, Niigata</wicri:regionArea><wicri:noRegion>Niigata</wicri:noRegion></affiliation></author><author><name sortKey="Takahashi, Hitoshi" sort="Takahashi, Hitoshi" uniqKey="Takahashi H" first="Hitoshi" last="Takahashi">Hitoshi Takahashi</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Pathology, Brain Research Institute, Niigata University, Niigata</wicri:regionArea><wicri:noRegion>Niigata</wicri:noRegion></affiliation></author><author><name sortKey="Nishizawa, Masatoyo" sort="Nishizawa, Masatoyo" uniqKey="Nishizawa M" first="Masatoyo" last="Nishizawa">Masatoyo Nishizawa</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Neurology, Brain Research Institute, Niigata University, Niigata</wicri:regionArea><wicri:noRegion>Niigata</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. 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="2009-07-15">2009-07-15</date><biblScope unit="vol">24</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="1312">1312</biblScope><biblScope unit="page" to="1318">1318</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">794DDA51BBCBE22D672130D09EA1D289879D5C07</idno><idno type="DOI">10.1002/mds.22583</idno><idno type="ArticleID">MDS22583</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>parkinsonian disorders</term><term>progressive supranuclear palsy</term><term>spinocerebellar ataxias</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The clinical heterogeneity of progressive supranuclear palsy (PSP), which is classified as classic Richardson's syndrome (RS) and PSP‐Parkinsonism (PSP‐P), has been previously discussed. We retrospectively analyzed 22 consecutive Japanese patients with pathologically proven PSP to investigate the clinicopathological heterogeneity. We investigated the clinical features both early in and at any time during the disease course. The pathological severities of neuronal loss with gliosis and tau pathology were also evaluated. On the basis of the clinical features, 10 patients were categorized as having RS, and 8 were categorized as having PSP‐P. Four patients presenting with cerebellar ataxia or cerebral cortical signs were categorized as having unclassifiable PSP. Among them, 3 developed cerebellar ataxia as the initial and principal symptom. Notably, tau‐positive inclusion bodies in Purkinje cells were significantly more frequently observed in the patients with cerebellar ataxia than in those without cerebellar ataxia. All the patients with cerebellar ataxia exhibited more neuronal loss with gliosis and higher densities of coiled bodies in the cerebellar dentate nucleus than those without cerebellar ataxia. This study confirms the wide spectrum of clinicopathological manifestations associated with PSP regardless of different ethnic origin, and demonstrates that PSP patients manifest cerebellar ataxia. © 2009 Movement Disorder Society</div></front></TEI></ISTEX><PubMed><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Cerebellar involvement in progressive supranuclear palsy: A clinicopathological study.</title><author><name sortKey="Kanazawa, Masato" sort="Kanazawa, Masato" uniqKey="Kanazawa M" first="Masato" last="Kanazawa">Masato Kanazawa</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neurology, Brain Research Institute, Niigata University, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Neurology, Brain Research Institute, Niigata University</wicri:regionArea><wicri:noRegion>Niigata University</wicri:noRegion></affiliation></author><author><name sortKey="Shimohata, Takayoshi" sort="Shimohata, Takayoshi" uniqKey="Shimohata T" first="Takayoshi" last="Shimohata">Takayoshi Shimohata</name></author><author><name sortKey="Toyoshima, Yasuko" sort="Toyoshima, Yasuko" uniqKey="Toyoshima Y" first="Yasuko" last="Toyoshima">Yasuko Toyoshima</name></author><author><name sortKey="Tada, Mari" sort="Tada, Mari" uniqKey="Tada M" first="Mari" last="Tada">Mari Tada</name></author><author><name sortKey="Kakita, Akiyoshi" sort="Kakita, Akiyoshi" uniqKey="Kakita A" first="Akiyoshi" last="Kakita">Akiyoshi Kakita</name></author><author><name sortKey="Morita, Takashi" sort="Morita, Takashi" uniqKey="Morita T" first="Takashi" last="Morita">Takashi Morita</name></author><author><name sortKey="Ozawa, Tetsutaro" sort="Ozawa, Tetsutaro" uniqKey="Ozawa T" first="Tetsutaro" last="Ozawa">Tetsutaro Ozawa</name></author><author><name sortKey="Takahashi, Hitoshi" sort="Takahashi, Hitoshi" uniqKey="Takahashi H" first="Hitoshi" last="Takahashi">Hitoshi Takahashi</name></author><author><name sortKey="Nishizawa, Masatoyo" sort="Nishizawa, Masatoyo" uniqKey="Nishizawa M" first="Masatoyo" last="Nishizawa">Masatoyo Nishizawa</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2009">2009</date><idno type="doi">10.1002/mds.22583</idno><idno type="RBID">pubmed:19412943</idno><idno type="pmid">19412943</idno><idno type="wicri:Area/PubMed/Corpus">001D36</idno><idno type="wicri:Area/PubMed/Curation">001D36</idno><idno type="wicri:Area/PubMed/Checkpoint">001F15</idno><idno type="wicri:Area/Ncbi/Merge">002641</idno><idno type="wicri:Area/Ncbi/Curation">002641</idno><idno type="wicri:Area/Ncbi/Checkpoint">002641</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Cerebellar involvement in progressive supranuclear palsy: A clinicopathological study.</title><author><name sortKey="Kanazawa, Masato" sort="Kanazawa, Masato" uniqKey="Kanazawa M" first="Masato" last="Kanazawa">Masato Kanazawa</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neurology, Brain Research Institute, Niigata University, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Neurology, Brain Research Institute, Niigata University</wicri:regionArea><wicri:noRegion>Niigata University</wicri:noRegion></affiliation></author><author><name sortKey="Shimohata, Takayoshi" sort="Shimohata, Takayoshi" uniqKey="Shimohata T" first="Takayoshi" last="Shimohata">Takayoshi Shimohata</name></author><author><name sortKey="Toyoshima, Yasuko" sort="Toyoshima, Yasuko" uniqKey="Toyoshima Y" first="Yasuko" last="Toyoshima">Yasuko Toyoshima</name></author><author><name sortKey="Tada, Mari" sort="Tada, Mari" uniqKey="Tada M" first="Mari" last="Tada">Mari Tada</name></author><author><name sortKey="Kakita, Akiyoshi" sort="Kakita, Akiyoshi" uniqKey="Kakita A" first="Akiyoshi" last="Kakita">Akiyoshi Kakita</name></author><author><name sortKey="Morita, Takashi" sort="Morita, Takashi" uniqKey="Morita T" first="Takashi" last="Morita">Takashi Morita</name></author><author><name sortKey="Ozawa, Tetsutaro" sort="Ozawa, Tetsutaro" uniqKey="Ozawa T" first="Tetsutaro" last="Ozawa">Tetsutaro Ozawa</name></author><author><name sortKey="Takahashi, Hitoshi" sort="Takahashi, Hitoshi" uniqKey="Takahashi H" first="Hitoshi" last="Takahashi">Hitoshi Takahashi</name></author><author><name sortKey="Nishizawa, Masatoyo" sort="Nishizawa, Masatoyo" uniqKey="Nishizawa M" first="Masatoyo" last="Nishizawa">Masatoyo Nishizawa</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2009" type="published">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Cell Death (physiology)</term><term>Cerebellum (metabolism)</term><term>Cerebellum (pathology)</term><term>Cerebellum (physiopathology)</term><term>Female</term><term>Humans</term><term>Longitudinal Studies</term><term>Male</term><term>Nerve Tissue Proteins (metabolism)</term><term>Neurons (metabolism)</term><term>Neurons (pathology)</term><term>Neurons (ultrastructure)</term><term>Retrospective Studies</term><term>Silver Staining (methods)</term><term>Supranuclear Palsy, Progressive (classification)</term><term>Supranuclear Palsy, Progressive (pathology)</term><term>Supranuclear Palsy, Progressive (physiopathology)</term><term>tau Proteins (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Nerve Tissue Proteins</term><term>tau Proteins</term></keywords><keywords scheme="MESH" qualifier="classification" xml:lang="en"><term>Supranuclear Palsy, Progressive</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Cerebellum</term><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Silver Staining</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Cerebellum</term><term>Neurons</term><term>Supranuclear Palsy, Progressive</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Cell Death</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Cerebellum</term><term>Supranuclear Palsy, Progressive</term></keywords><keywords scheme="MESH" qualifier="ultrastructure" xml:lang="en"><term>Neurons</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Female</term><term>Humans</term><term>Longitudinal Studies</term><term>Male</term><term>Retrospective Studies</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The clinical heterogeneity of progressive supranuclear palsy (PSP), which is classified as classic Richardson's syndrome (RS) and PSP-Parkinsonism (PSP-P), has been previously discussed. We retrospectively analyzed 22 consecutive Japanese patients with pathologically proven PSP to investigate the clinicopathological heterogeneity. We investigated the clinical features both early in and at any time during the disease course. The pathological severities of neuronal loss with gliosis and tau pathology were also evaluated. On the basis of the clinical features, 10 patients were categorized as having RS, and 8 were categorized as having PSP-P. Four patients presenting with cerebellar ataxia or cerebral cortical signs were categorized as having unclassifiable PSP. Among them, 3 developed cerebellar ataxia as the initial and principal symptom. Notably, tau-positive inclusion bodies in Purkinje cells were significantly more frequently observed in the patients with cerebellar ataxia than in those without cerebellar ataxia. All the patients with cerebellar ataxia exhibited more neuronal loss with gliosis and higher densities of coiled bodies in the cerebellar dentate nucleus than those without cerebellar ataxia. This study confirms the wide spectrum of clinicopathological manifestations associated with PSP regardless of different ethnic origin, and demonstrates that PSP patients manifest cerebellar ataxia.</div></front></TEI></PubMed></double></record>Pour manipuler ce document sous Unix (Dilib)
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