Freezing of gait in postmortem‐confirmed atypical parkinsonism
Identifieur interne : 001889 ( Main/Exploration ); précédent : 001888; suivant : 001890Freezing 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.
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- topic : Congélation.
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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
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DOI: 10.1002/mds.10234
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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="2002-09">2002-09</date><biblScope unit="volume">17</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="1041">1041</biblScope><biblScope unit="page" to="1045">1045</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">E1CB40BE27539036803823AC72C4BB232A34BCC6</idno><idno type="DOI">10.1002/mds.10234</idno><idno type="ArticleID">MDS10234</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Freezing</term><term>corticobasal degeneration</term><term>dementia with Lewy bodies</term><term>gait</term><term>multiple system atrophy</term><term>progressive supranuclear palsy</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Congélation</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></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. © 2002 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>Autriche</li><li>États-Unis</li></country><region><li>Maryland</li><li>Tyrol (Land)</li></region><settlement><li>Innsbruck</li></settlement><orgName><li>Université de médecine d'Innsbruck</li></orgName></list><tree><country name="Autriche"><noRegion><name sortKey="Muller, Jorg" sort="Muller, Jorg" uniqKey="Muller J" first="Jörg" last="Müller">Jörg Müller</name></noRegion><name sortKey="Poewe, Werner" sort="Poewe, Werner" uniqKey="Poewe W" first="Werner" last="Poewe">Werner Poewe</name><name sortKey="Seppi, Klaus" sort="Seppi, Klaus" uniqKey="Seppi K" first="Klaus" last="Seppi">Klaus Seppi</name><name sortKey="Stefanova, Nadia" sort="Stefanova, Nadia" uniqKey="Stefanova N" first="Nadia" last="Stefanova">Nadia Stefanova</name><name sortKey="Wenning, Gregor K" sort="Wenning, Gregor K" uniqKey="Wenning G" first="Gregor K." last="Wenning">Gregor K. Wenning</name></country><country name="États-Unis"><region name="Maryland"><name sortKey="Litvan, Irene" sort="Litvan, Irene" uniqKey="Litvan I" first="Irene" last="Litvan">Irene Litvan</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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