ParkinsonCanadaV1, PascalFrancis, Curation, bibRecord, 001193

Clinical features differentiating patients with postmortem confirmed progressive supranuclear palsy and corticobasal degeneration

Identifieur interne : 001193 ( PascalFrancis/Curation ); précédent : 001192; suivant : 001194

Clinical features differentiating patients with postmortem confirmed progressive supranuclear palsy and corticobasal degeneration

Auteurs : I. Litvan [États-Unis] ; D. A. Grimes [Canada] ; A. E. Lang [Canada] ; J. Jankovic [États-Unis] ; A. Mckee [États-Unis] ; M. Verny [France] ; K. Jellinger [Autriche] ; K. R. Chaudhuri [Royaume-Uni] ; R. K. B. Pearce [Royaume-Uni]

Source :

Journal of neurology. Supplement [ 0939-1517 ] ; 1999.

RBID : Pascal:99-0515801

Descripteurs français

Pascal (Inist)
- Ophtalmoplégie supranucléaire, Progressif, Dégénérescence, Noyau gris central, Etude comparative, Diagnostic différentiel, Symptomatologie, Homme.
Wicri :
- topic : Homme.

English descriptors

KwdEn :
- Basal ganglion, Comparative study, Degeneration, Differential diagnostic, Human, Progressive, Supranuclear ophthalmoplegia, Symptomatology.

Abstract

Progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD) are often clinically confused with each other because they share a rapid disease progression, parkinsonism that responds poorly or transiently to levodopa therapy, and associated signs (e.g., ocular abnormalities, pyramidal signs and cognitive involvement). To improve the accuracy in diagnosing these disorders, this study examined the clinical features of 51 patients pathologically diagnosed with PSP and CBD. Logistic regression analysis identified two sets of predictors (models) for CBD patients, one consisting of asymmetric parkinsonism, cognitive disturbances at onset and instability and falls at first clinic visit, and the other one of asymmetric parkinsonism, cognitive disturbances at symptom onset and speech disturbances. While PSP patients often had severe postural instability at onset, symmetric parkinsonism, vertical supranuclear gaze palsy, speech and frontal lobe-type features, CBD patients presented with lateralized motor (e.g., parkinsonism, dystonia or myoclonus) and cognitive signs (e.g., ideomotor apraxia, aphasia or alien limb). On the other hand, CBD patients presenting with an alternate phenotype characterized by early severe frontal dementia and bilateral parkinsonism were generally misdiagnosed. PSP patients without vertical supranuclear gaze palsy were misdiagnosed. Recognizing the features which differentiate these disorders and the less obvious disease presentations as well as developing an increased index of suspicion will improve the diagnostic accuracy of these disorders.

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C01	`01`		`ENG`	@0 Progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD) are often clinically confused with each other because they share a rapid disease progression, parkinsonism that responds poorly or transiently to levodopa therapy, and associated signs (e.g., ocular abnormalities, pyramidal signs and cognitive involvement). To improve the accuracy in diagnosing these disorders, this study examined the clinical features of 51 patients pathologically diagnosed with PSP and CBD. Logistic regression analysis identified two sets of predictors (models) for CBD patients, one consisting of asymmetric parkinsonism, cognitive disturbances at onset and instability and falls at first clinic visit, and the other one of asymmetric parkinsonism, cognitive disturbances at symptom onset and speech disturbances. While PSP patients often had severe postural instability at onset, symmetric parkinsonism, vertical supranuclear gaze palsy, speech and frontal lobe-type features, CBD patients presented with lateralized motor (e.g., parkinsonism, dystonia or myoclonus) and cognitive signs (e.g., ideomotor apraxia, aphasia or alien limb). On the other hand, CBD patients presenting with an alternate phenotype characterized by early severe frontal dementia and bilateral parkinsonism were generally misdiagnosed. PSP patients without vertical supranuclear gaze palsy were misdiagnosed. Recognizing the features which differentiate these disorders and the less obvious disease presentations as well as developing an increased index of suspicion will improve the diagnostic accuracy of these disorders.
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Le document en format XML

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<front><div type="abstract" xml:lang="en">Progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD) are often clinically confused with each other because they share a rapid disease progression, parkinsonism that responds poorly or transiently to levodopa therapy, and associated signs (e.g., ocular abnormalities, pyramidal signs and cognitive involvement). To improve the accuracy in diagnosing these disorders, this study examined the clinical features of 51 patients pathologically diagnosed with PSP and CBD. Logistic regression analysis identified two sets of predictors (models) for CBD patients, one consisting of asymmetric parkinsonism, cognitive disturbances at onset and instability and falls at first clinic visit, and the other one of asymmetric parkinsonism, cognitive disturbances at symptom onset and speech disturbances. While PSP patients often had severe postural instability at onset, symmetric parkinsonism, vertical supranuclear gaze palsy, speech and frontal lobe-type features, CBD patients presented with lateralized motor (e.g., parkinsonism, dystonia or myoclonus) and cognitive signs (e.g., ideomotor apraxia, aphasia or alien limb). On the other hand, CBD patients presenting with an alternate phenotype characterized by early severe frontal dementia and bilateral parkinsonism were generally misdiagnosed. PSP patients without vertical supranuclear gaze palsy were misdiagnosed. Recognizing the features which differentiate these disorders and the less obvious disease presentations as well as developing an increased index of suspicion will improve the diagnostic accuracy of these disorders.</div>
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<fA09 i1="01" i2="1" l="ENG"><s1>7th Symposium on the Treatment of Parkinson's Disease</s1>
</fA09>
<fA11 i1="01" i2="1"><s1>LITVAN (I.)</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>GRIMES (D. A.)</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>LANG (A. E.)</s1>
</fA11>
<fA11 i1="04" i2="1"><s1>JANKOVIC (J.)</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>MCKEE (A.)</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>VERNY (M.)</s1>
</fA11>
<fA11 i1="07" i2="1"><s1>JELLINGER (K.)</s1>
</fA11>
<fA11 i1="08" i2="1"><s1>CHAUDHURI (K. R.)</s1>
</fA11>
<fA11 i1="09" i2="1"><s1>PEARCE (R. K. B.)</s1>
</fA11>
<fA12 i1="01" i2="1"><s1>HIROSE (Genjiro)</s1>
<s9>ed.</s9>
</fA12>
<fA12 i1="02" i2="1"><s1>KANAZAWA (Ichiro)</s1>
<s9>ed.</s9>
</fA12>
<fA12 i1="03" i2="1"><s1>KUNO (Sadako)</s1>
<s9>ed.</s9>
</fA12>
<fA12 i1="04" i2="1"><s1>MIZUNO (Yoshikuni)</s1>
<s9>ed.</s9>
</fA12>
<fA12 i1="05" i2="1"><s1>NOMOTO (Masahiro)</s1>
<s9>ed.</s9>
</fA12>
<fA12 i1="06" i2="1"><s1>OGAWA (Norio)</s1>
<s9>ed.</s9>
</fA12>
<fA12 i1="07" i2="1"><s1>YAMAMOTO (Mitsutoshi)</s1>
<s9>ed.</s9>
</fA12>
<fA12 i1="08" i2="1"><s1>YANAGISAWA (Nobuo)</s1>
<s9>ed.</s9>
</fA12>
<fA14 i1="01"><s1>Neuropharmacology Unit, Defense & Veteran Head Injury Program, Henry M. Jackson Foundation, Federal Building, Room 714</s1>
<s2>Bethesda, Maryland 20892-9130</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>The Toronto Hospital Movement Disorders Centre</s1>
<s2>Toronto</s2>
<s3>CAN</s3>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Department of Neurology, Baylor College of Medicine</s1>
<s2>Houston, TX</s2>
<s3>USA</s3>
<sZ>4 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Department of Neuropathology Massachusetts General Hospital and GRECC Bedford VA Medical Center</s1>
<s2>Boston, MA</s2>
<s3>USA</s3>
<sZ>5 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>Raymond Escourolle Neuropathology, Laboratory, INSERM U 360, Hôpital de la Salpêtrière</s1>
<s2>Paris</s2>
<s3>FRA</s3>
<sZ>6 aut.</sZ>
</fA14>
<fA14 i1="06"><s1>The Ludwig Boltzmann Institute of Clinical Neurobiology</s1>
<s2>Vienna</s2>
<s3>AUT</s3>
<sZ>7 aut.</sZ>
</fA14>
<fA14 i1="07"><s1>The Department of Neurology, Institute of Psychiatry</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>8 aut.</sZ>
</fA14>
<fA14 i1="08"><s1>The Parkinson's Disease Society Brain Tissue Bank, Institute of Neurology</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>9 aut.</sZ>
</fA14>
<fA15 i1="01"><s1>Kanazawa Medical School</s1>
<s3>JPN</s3>
<sZ>1 aut.</sZ>
</fA15>
<fA15 i1="02"><s1>Tokyo University</s1>
<s3>JPN</s3>
<sZ>2 aut.</sZ>
</fA15>
<fA15 i1="03"><s1>Utano Hospital</s1>
<s3>JPN</s3>
<sZ>3 aut.</sZ>
</fA15>
<fA15 i1="04"><s1>Juntendo University</s1>
<s3>JPN</s3>
<sZ>4 aut.</sZ>
</fA15>
<fA15 i1="05"><s1>Kagoshima University</s1>
<s3>JPN</s3>
<sZ>5 aut.</sZ>
</fA15>
<fA15 i1="06"><s1>Okayama University</s1>
<s3>JPN</s3>
<sZ>6 aut.</sZ>
</fA15>
<fA15 i1="07"><s1>Kagawa Prefectural Hospital</s1>
<s3>JPN</s3>
<sZ>7 aut.</sZ>
</fA15>
<fA15 i1="08"><s1>Chubu National Hospital</s1>
<s3>JPN</s3>
<sZ>8 aut.</sZ>
</fA15>
<fA20><s2>II1-II5</s2>
</fA20>
<fA21><s1>1999</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>4826S</s2>
<s5>354000089729040010</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 1999 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>22 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>99-0515801</s0>
</fA47>
<fA60><s1>P</s1>
<s2>C</s2>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>Journal of neurology. Supplement</s0>
</fA64>
<fA66 i1="01"><s0>DEU</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>Progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD) are often clinically confused with each other because they share a rapid disease progression, parkinsonism that responds poorly or transiently to levodopa therapy, and associated signs (e.g., ocular abnormalities, pyramidal signs and cognitive involvement). To improve the accuracy in diagnosing these disorders, this study examined the clinical features of 51 patients pathologically diagnosed with PSP and CBD. Logistic regression analysis identified two sets of predictors (models) for CBD patients, one consisting of asymmetric parkinsonism, cognitive disturbances at onset and instability and falls at first clinic visit, and the other one of asymmetric parkinsonism, cognitive disturbances at symptom onset and speech disturbances. While PSP patients often had severe postural instability at onset, symmetric parkinsonism, vertical supranuclear gaze palsy, speech and frontal lobe-type features, CBD patients presented with lateralized motor (e.g., parkinsonism, dystonia or myoclonus) and cognitive signs (e.g., ideomotor apraxia, aphasia or alien limb). On the other hand, CBD patients presenting with an alternate phenotype characterized by early severe frontal dementia and bilateral parkinsonism were generally misdiagnosed. PSP patients without vertical supranuclear gaze palsy were misdiagnosed. Recognizing the features which differentiate these disorders and the less obvious disease presentations as well as developing an increased index of suspicion will improve the diagnostic accuracy of these disorders.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B17G</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Ophtalmoplégie supranucléaire</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Supranuclear ophthalmoplegia</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Oftalmoplejía supranuclear</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Progressif</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Progressive</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Progresivo</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Dégénérescence</s0>
<s5>04</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Degeneration</s0>
<s5>04</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Degeneración</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Noyau gris central</s0>
<s5>05</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Basal ganglion</s0>
<s5>05</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Núcleo basal</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Etude comparative</s0>
<s5>16</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Comparative study</s0>
<s5>16</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Estudio comparativo</s0>
<s5>16</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Diagnostic différentiel</s0>
<s5>17</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Differential diagnostic</s0>
<s5>17</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Diagnóstico diferencial</s0>
<s5>17</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Symptomatologie</s0>
<s5>18</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Symptomatology</s0>
<s5>18</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Sintomatología</s0>
<s5>18</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Homme</s0>
<s5>20</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Human</s0>
<s5>20</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Hombre</s0>
<s5>20</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Oeil pathologie</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Eye disease</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Ojo patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Oculomotricité syndrome</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Oculomotor syndrome</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Oculomotricidad síndrome</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Système nerveux pathologie</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>40</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Tronc cérébral syndrome</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Brain stem syndrome</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Tallo encefalico sindrome</s0>
<s5>41</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Encéphale pathologie</s0>
<s5>42</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>42</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>42</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>43</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>43</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>43</s5>
</fC07>
<fN21><s1>333</s1>
</fN21>
</pA>
<pR><fA30 i1="01" i2="1" l="ENG"><s1>Symposium on the Treatment of Parkinson's Disease</s1>
<s2>7</s2>
<s3>Osaka JPN</s3>
<s4>1998-10-03</s4>
</fA30>
</pR>
</standard>
</inist>
</record>

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	La maladie de Parkinson au Canada (serveur d'exploration)
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La maladie de Parkinson au Canada (serveur d'exploration)

Clinical features differentiating patients with postmortem confirmed progressive supranuclear palsy and corticobasal degeneration

Clinical features differentiating patients with postmortem confirmed progressive supranuclear palsy and corticobasal degeneration

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