Pure Akinesia with Gait Freezing : A Third Clinical Phenotype of Progressive Supranuclear Palsy
Identifieur interne : 001869 ( PascalFrancis/Curation ); précédent : 001868; suivant : 001870Pure Akinesia with Gait Freezing : A Third Clinical Phenotype of Progressive Supranuclear Palsy
Auteurs : David R. Williams [Australie, Royaume-Uni] ; Janice L. Holton [Royaume-Uni] ; Kate Strand [Royaume-Uni] ; Tamas Revesz [Royaume-Uni] ; Andrew J. Lees [Royaume-Uni]Source :
- Movement disorders [ 0885-3185 ] ; 2007.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Congélation.
English descriptors
- KwdEn :
Abstract
The clinical syndrome of pure akinesia has most often been associated with progressive supranuclear palsy (PSP) and is characterized by difficulty initiating gait and "freezing" during walking, writing and speaking. Similar syndromes have been described under the rubrics of primary progressive freezing gait and primary gait ignition failure. We investigated the specificity of the clinical syndrome of pure akinesia with gait freezing (PAGF) for PSP-tau pathology. Among 749 patients archived at the QSBB, only 7 fulfilled proposed diagnostic criteria of: gradual onset of freezing of gait or speech; absent limb rigidity and tremor; no sustained response to levodopa; and no dementia or ophthalmoplegia in the first 5 years of disease. In these cases detailed pathological examination was performed. PSP was the pathological diagnosis in six patients, and Parkinson's disease (PD) in the seventh. As defined, this syndrome had a positive predictive value of 86% for PSP-tau pathology. In the cases with PSP there were no additional features of coexistent vascular or PD and the median PSP-tau score was 3, reflecting relative mild tau load. The clinical syndrome of PAGF appears to have a high specificity for PSP-tau pathology. This relatively uncommon presentation of PSP-tau pathology has less severe tau accumulation than in the more common, "classic" PSP clinical phenotype: Richardson's disease.
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Williams</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Faculty of Medicine (Neurosciences), Monash University (Alfred Hospital Campus)</s1><s2>Melbourne</s2><s3>AUS</s3><sZ>1 aut.</sZ></inist:fA14><country>Australie</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Reta Lila Weston Institute of Neurological Studies</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Royaume-Uni</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Queen Square Brain Bank for Neurological Disorders</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Royaume-Uni</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="04"><s1>Department of Molecular Neuroscience, Institute of Neurology, UCL</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Royaume-Uni</country></affiliation></author><author><name sortKey="Holton, Janice L" sort="Holton, Janice L" uniqKey="Holton J" first="Janice L." last="Holton">Janice L. Holton</name><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Reta Lila Weston Institute of Neurological Studies</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Royaume-Uni</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Queen Square Brain Bank for Neurological Disorders</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Royaume-Uni</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="04"><s1>Department of Molecular Neuroscience, Institute of Neurology, UCL</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Royaume-Uni</country></affiliation></author><author><name sortKey="Strand, Kate" sort="Strand, Kate" uniqKey="Strand K" first="Kate" last="Strand">Kate Strand</name><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Queen Square Brain Bank for Neurological Disorders</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Royaume-Uni</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="04"><s1>Department of Molecular Neuroscience, Institute of Neurology, UCL</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Royaume-Uni</country></affiliation></author><author><name sortKey="Revesz, Tamas" sort="Revesz, Tamas" uniqKey="Revesz T" first="Tamas" last="Revesz">Tamas Revesz</name><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Queen Square Brain Bank for Neurological Disorders</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Royaume-Uni</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="04"><s1>Department of Molecular Neuroscience, Institute of Neurology, UCL</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Royaume-Uni</country></affiliation></author><author><name sortKey="Lees, Andrew J" sort="Lees, Andrew J" uniqKey="Lees A" first="Andrew J." last="Lees">Andrew J. Lees</name><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Reta Lila Weston Institute of Neurological Studies</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Royaume-Uni</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Queen Square Brain Bank for Neurological Disorders</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Royaume-Uni</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="04"><s1>Department of Molecular Neuroscience, Institute of Neurology, UCL</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Royaume-Uni</country></affiliation></author></analytic><series><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno><imprint><date when="2007">2007</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Akinesia</term><term>Freezing</term><term>Nervous system diseases</term><term>Phenotype</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Pathologie du système nerveux</term><term>Akinésie</term><term>Congélation</term><term>Phénotype</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Congélation</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The clinical syndrome of pure akinesia has most often been associated with progressive supranuclear palsy (PSP) and is characterized by difficulty initiating gait and "freezing" during walking, writing and speaking. Similar syndromes have been described under the rubrics of primary progressive freezing gait and primary gait ignition failure. We investigated the specificity of the clinical syndrome of pure akinesia with gait freezing (PAGF) for PSP-tau pathology. Among 749 patients archived at the QSBB, only 7 fulfilled proposed diagnostic criteria of: gradual onset of freezing of gait or speech; absent limb rigidity and tremor; no sustained response to levodopa; and no dementia or ophthalmoplegia in the first 5 years of disease. In these cases detailed pathological examination was performed. PSP was the pathological diagnosis in six patients, and Parkinson's disease (PD) in the seventh. As defined, this syndrome had a positive predictive value of 86% for PSP-tau pathology. In the cases with PSP there were no additional features of coexistent vascular or PD and the median PSP-tau score was 3, reflecting relative mild tau load. The clinical syndrome of PAGF appears to have a high specificity for PSP-tau pathology. This relatively uncommon presentation of PSP-tau pathology has less severe tau accumulation than in the more common, "classic" PSP clinical phenotype: Richardson's disease.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0885-3185</s0></fA01><fA03 i2="1"><s0>Mov. disord.</s0></fA03><fA05><s2>22</s2></fA05><fA06><s2>15</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Pure Akinesia with Gait Freezing : A Third Clinical Phenotype of Progressive Supranuclear Palsy</s1></fA08><fA11 i1="01" i2="1"><s1>WILLIAMS (David R.)</s1></fA11><fA11 i1="02" i2="1"><s1>HOLTON (Janice L.)</s1></fA11><fA11 i1="03" i2="1"><s1>STRAND (Kate)</s1></fA11><fA11 i1="04" i2="1"><s1>REVESZ (Tamas)</s1></fA11><fA11 i1="05" i2="1"><s1>LEES (Andrew J.)</s1></fA11><fA14 i1="01"><s1>Faculty of Medicine (Neurosciences), Monash University (Alfred Hospital Campus)</s1><s2>Melbourne</s2><s3>AUS</s3><sZ>1 aut.</sZ></fA14><fA14 i1="02"><s1>Reta Lila Weston Institute of Neurological Studies</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>5 aut.</sZ></fA14><fA14 i1="03"><s1>Queen Square Brain Bank for Neurological Disorders</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></fA14><fA14 i1="04"><s1>Department of Molecular Neuroscience, Institute of Neurology, UCL</s1><s2>London</s2><s3>GBR</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ></fA14><fA20><s1>2235-2241</s1></fA20><fA21><s1>2007</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>20953</s2><s5>354000162671070150</s5></fA43><fA44><s0>0000</s0><s1>© 2008 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>54 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>08-0071411</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Movement disorders</s0></fA64><fA66 i1="01"><s0>USA</s0></fA66><fC01 i1="01" l="ENG"><s0>The clinical syndrome of pure akinesia has most often been associated with progressive supranuclear palsy (PSP) and is characterized by difficulty initiating gait and "freezing" during walking, writing and speaking. Similar syndromes have been described under the rubrics of primary progressive freezing gait and primary gait ignition failure. We investigated the specificity of the clinical syndrome of pure akinesia with gait freezing (PAGF) for PSP-tau pathology. Among 749 patients archived at the QSBB, only 7 fulfilled proposed diagnostic criteria of: gradual onset of freezing of gait or speech; absent limb rigidity and tremor; no sustained response to levodopa; and no dementia or ophthalmoplegia in the first 5 years of disease. In these cases detailed pathological examination was performed. PSP was the pathological diagnosis in six patients, and Parkinson's disease (PD) in the seventh. As defined, this syndrome had a positive predictive value of 86% for PSP-tau pathology. In the cases with PSP there were no additional features of coexistent vascular or PD and the median PSP-tau score was 3, reflecting relative mild tau load. The clinical syndrome of PAGF appears to have a high specificity for PSP-tau pathology. 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