Freezing of gait in postmortem‐confirmed atypical parkinsonism
Identifieur interne : 006459 ( Main/Merge ); précédent : 006458; suivant : 006460Freezing of gait in postmortem‐confirmed atypical parkinsonism
Auteurs : Jörg Müller [Autriche] ; Klaus Seppi [Autriche] ; Nadia Stefanova [Autriche] ; Werner Poewe [Autriche] ; Irene Litvan [États-Unis] ; Gregor K. Wenning [Autriche]Source :
- Movement Disorders [ 0885-3185 ] ; 2002-09.
Descripteurs français
- Wicri :
- topic : Congélation.
English descriptors
- KwdEn :
- Aged, Basal Ganglia Diseases (pathology), Brain (pathology), Culture Techniques, Female, Freezing, Gait Disorders, Neurologic (epidemiology), Gait Disorders, Neurologic (etiology), Humans, Lewy Body Disease (pathology), Male, Middle Aged, Multiple System Atrophy (pathology), Parkinsonian Disorders (complications), Parkinsonian Disorders (pathology), corticobasal degeneration, dementia with Lewy bodies, gait, multiple system atrophy, progressive supranuclear palsy.
- MESH :
- complications : Parkinsonian Disorders.
- epidemiology : Gait Disorders, Neurologic.
- etiology : Gait Disorders, Neurologic.
- pathology : Basal Ganglia Diseases, Brain, Lewy Body Disease, Multiple System Atrophy, Parkinsonian Disorders.
- Aged, Culture Techniques, Female, Humans, Male, Middle Aged.
Abstract
The frequency and pathophysiology of freezing of gait (FoG) in atypical parkinsonism is unknown. We analysed the frequency of FoG in postmortem‐confirmed atypical parkinsonian disorders (APD) comprising corticobasal degeneration (CBD), dementia with Lewy bodies (DLB), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP). Sixty‐six patients with pathologically confirmed APD (CBD, n = 13; DLB, n = 14; MSA, n = 15; PSP, n = 24) formed the basis for a multicenter clinicopathological study. Clinical features at first and last clinical visit were abstracted from patient records on standardized forms following strict instructions. At the first visit (median 36 months after symptom onset), 24% of APD had FoG (CBD, 8%; DLB, 21%; PSP, 25%; MSA, 40%). Logistic regression analysis showed a significant association of FoG and urinary incontinence (P = 0.04) at first visit. At last visit, 47% of APD had FoG (CBD, 25%; PSP, 53%; DLB, 54%; MSA, 54%). Clinicopathological correlation based on routine postmortem examination failed to identify a consistent neuropathological substrate of FoG. This study demonstrates that (1) FoG is common in APD, and (2) urinary incontinence is significantly associated with FoG in these disorders. Whether FoG and urinary incontinence share similar neuropathological substrates remains to be determined by future studies. © 2002 Movement Disorder Society
Url:
DOI: 10.1002/mds.10234
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<front><div type="abstract" xml:lang="en">The frequency and pathophysiology of freezing of gait (FoG) in atypical parkinsonism is unknown. We analysed the frequency of FoG in postmortem‐confirmed atypical parkinsonian disorders (APD) comprising corticobasal degeneration (CBD), dementia with Lewy bodies (DLB), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP). Sixty‐six patients with pathologically confirmed APD (CBD, n = 13; DLB, n = 14; MSA, n = 15; PSP, n = 24) formed the basis for a multicenter clinicopathological study. Clinical features at first and last clinical visit were abstracted from patient records on standardized forms following strict instructions. At the first visit (median 36 months after symptom onset), 24% of APD had FoG (CBD, 8%; DLB, 21%; PSP, 25%; MSA, 40%). Logistic regression analysis showed a significant association of FoG and urinary incontinence (P = 0.04) at first visit. At last visit, 47% of APD had FoG (CBD, 25%; PSP, 53%; DLB, 54%; MSA, 54%). Clinicopathological correlation based on routine postmortem examination failed to identify a consistent neuropathological substrate of FoG. This study demonstrates that (1) FoG is common in APD, and (2) urinary incontinence is significantly associated with FoG in these disorders. Whether FoG and urinary incontinence share similar neuropathological substrates remains to be determined by future studies. © 2002 Movement Disorder Society</div>
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<front><div type="abstract" xml:lang="en">The frequency and pathophysiology of freezing of gait (FoG) in atypical parkinsonism is unknown. We analysed the frequency of FoG in postmortem‐confirmed atypical parkinsonian disorders (APD) comprising corticobasal degeneration (CBD), dementia with Lewy bodies (DLB), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP). Sixty‐six patients with pathologically confirmed APD (CBD, n = 13; DLB, n = 14; MSA, n = 15; PSP, n = 24) formed the basis for a multicenter clinicopathological study. Clinical features at first and last clinical visit were abstracted from patient records on standardized forms following strict instructions. At the first visit (median 36 months after symptom onset), 24% of APD had FoG (CBD, 8%; DLB, 21%; PSP, 25%; MSA, 40%). Logistic regression analysis showed a significant association of FoG and urinary incontinence (P = 0.04) at first visit. At last visit, 47% of APD had FoG (CBD, 25%; PSP, 53%; DLB, 54%; MSA, 54%). Clinicopathological correlation based on routine postmortem examination failed to identify a consistent neuropathological substrate of FoG. This study demonstrates that (1) FoG is common in APD, and (2) urinary incontinence is significantly associated with FoG in these disorders. Whether FoG and urinary incontinence share similar neuropathological substrates remains to be determined by future studies. © 2002 Movement Disorder Society</div>
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<author><name sortKey="Seppi, Klaus" sort="Seppi, Klaus" uniqKey="Seppi K" first="Klaus" last="Seppi">Klaus Seppi</name>
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<author><name sortKey="Stefanova, Nadia" sort="Stefanova, Nadia" uniqKey="Stefanova N" first="Nadia" last="Stefanova">Nadia Stefanova</name>
</author>
<author><name sortKey="Poewe, Werner" sort="Poewe, Werner" uniqKey="Poewe W" first="Werner" last="Poewe">Werner Poewe</name>
<affiliation><country>Autriche</country>
<placeName><settlement type="city">Innsbruck</settlement>
<region nuts="2" type="region">Tyrol (Land)</region>
</placeName>
<orgName type="university">Université de médecine d'Innsbruck</orgName>
</affiliation>
</author>
<author><name sortKey="Litvan, Irene" sort="Litvan, Irene" uniqKey="Litvan I" first="Irene" last="Litvan">Irene Litvan</name>
</author>
<author><name sortKey="Wenning, Gregor K" sort="Wenning, Gregor K" uniqKey="Wenning G" first="Gregor K" last="Wenning">Gregor K. Wenning</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>Aged</term>
<term>Basal Ganglia Diseases (pathology)</term>
<term>Brain (pathology)</term>
<term>Culture Techniques</term>
<term>Female</term>
<term>Gait Disorders, Neurologic (epidemiology)</term>
<term>Gait Disorders, Neurologic (etiology)</term>
<term>Humans</term>
<term>Lewy Body Disease (pathology)</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Multiple System Atrophy (pathology)</term>
<term>Parkinsonian Disorders (complications)</term>
<term>Parkinsonian Disorders (pathology)</term>
</keywords>
<keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinsonian Disorders</term>
</keywords>
<keywords scheme="MESH" qualifier="epidemiology" xml:lang="en"><term>Gait Disorders, Neurologic</term>
</keywords>
<keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Gait Disorders, Neurologic</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Basal Ganglia Diseases</term>
<term>Brain</term>
<term>Lewy Body Disease</term>
<term>Multiple System Atrophy</term>
<term>Parkinsonian Disorders</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Aged</term>
<term>Culture Techniques</term>
<term>Female</term>
<term>Humans</term>
<term>Male</term>
<term>Middle Aged</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">The frequency and pathophysiology of freezing of gait (FoG) in atypical parkinsonism is unknown. We analysed the frequency of FoG in postmortem-confirmed atypical parkinsonian disorders (APD) comprising corticobasal degeneration (CBD), dementia with Lewy bodies (DLB), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP). Sixty-six patients with pathologically confirmed APD (CBD, n = 13; DLB, n = 14; MSA, n = 15; PSP, n = 24) formed the basis for a multicenter clinicopathological study. Clinical features at first and last clinical visit were abstracted from patient records on standardized forms following strict instructions. At the first visit (median 36 months after symptom onset), 24% of APD had FoG (CBD, 8%; DLB, 21%; PSP, 25%; MSA, 40%). Logistic regression analysis showed a significant association of FoG and urinary incontinence (P = 0.04) at first visit. At last visit, 47% of APD had FoG (CBD, 25%; PSP, 53%; DLB, 54%; MSA, 54%). Clinicopathological correlation based on routine postmortem examination failed to identify a consistent neuropathological substrate of FoG. This study demonstrates that (1) FoG is common in APD, and (2) urinary incontinence is significantly associated with FoG in these disorders. Whether FoG and urinary incontinence share similar neuropathological substrates remains to be determined by future studies.</div>
</front>
</TEI>
</PubMed>
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