Movement Disorders (revue)

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Presynaptic parkinsonism in multiple system atrophy mimicking Parkinson's disease: A clinicopathological case study

Identifieur interne : 000642 ( PascalFrancis/Curation ); précédent : 000641; suivant : 000643

Presynaptic parkinsonism in multiple system atrophy mimicking Parkinson's disease: A clinicopathological case study

Auteurs : José Berciano [Espagne] ; Francesc Valldeoriola [Espagne] ; Isidre Ferrer [Espagne] ; Jordi Rumia [Espagne] ; Julio Pascual [Espagne] ; Concepcion Marin [Espagne] ; Maria J. Rey [Espagne] ; Eduardo Tolosa [Espagne]

Source :

RBID : Pascal:02-0456878

Descripteurs français

English descriptors

Abstract

We describe the clinicopathological findings in a patient aged 63 years at death who, at age 55 years, developed levodopa-responsive parkinsonism with no atypical features. A diagnosis of idiopathic Parkinson's disease (PD) was made. During the clinical course, fluctuations and dyskinesias appeared. Eight years after onset, he was successfully treated with subthalamic nucleus stimulation but died 3 weeks postoperatively from pulmonary embolus. Brain autopsy showed marked neuronal loss and gliosis in the substantia nigra and locus coeruleus, and, to a much lesser extent, in the basis pontis, inferior olivary nuclei, and cerebellar cortex. Striatum was normal. There were numerous oligodendroglial and neuronal cytoplasmic inclusions and neuropil threads, the highest density being localized in the pons and cerebellar white matter. No Lewy bodies were observed. We conclude that nigral, presynaptic parkinsonism may occur in multiple system atrophy, which even in the long run can be indistinguishable from PD. Putaminal preservation accounts for good response to both levodopa therapy and subthalamic nucleus stimulation.
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A08 01  1  ENG  @1 Presynaptic parkinsonism in multiple system atrophy mimicking Parkinson's disease: A clinicopathological case study
A11 01  1    @1 BERCIANO (José)
A11 02  1    @1 VALLDEORIOLA (Francesc)
A11 03  1    @1 FERRER (Isidre)
A11 04  1    @1 RUMIA (Jordi)
A11 05  1    @1 PASCUAL (Julio)
A11 06  1    @1 MARIN (Concepcion)
A11 07  1    @1 REY (Maria J.)
A11 08  1    @1 TOLOSA (Eduardo)
A14 01      @1 Service of Neurology, University Hospital Marqués de Valdecilla, University of Cantabria @2 Santander @3 ESP @Z 1 aut. @Z 5 aut.
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C01 01    ENG  @0 We describe the clinicopathological findings in a patient aged 63 years at death who, at age 55 years, developed levodopa-responsive parkinsonism with no atypical features. A diagnosis of idiopathic Parkinson's disease (PD) was made. During the clinical course, fluctuations and dyskinesias appeared. Eight years after onset, he was successfully treated with subthalamic nucleus stimulation but died 3 weeks postoperatively from pulmonary embolus. Brain autopsy showed marked neuronal loss and gliosis in the substantia nigra and locus coeruleus, and, to a much lesser extent, in the basis pontis, inferior olivary nuclei, and cerebellar cortex. Striatum was normal. There were numerous oligodendroglial and neuronal cytoplasmic inclusions and neuropil threads, the highest density being localized in the pons and cerebellar white matter. No Lewy bodies were observed. We conclude that nigral, presynaptic parkinsonism may occur in multiple system atrophy, which even in the long run can be indistinguishable from PD. Putaminal preservation accounts for good response to both levodopa therapy and subthalamic nucleus stimulation.
C02 01  X    @0 002B17G
C03 01  X  FRE  @0 Atrophie multisystématisée @2 NM @5 01
C03 01  X  ENG  @0 Multiple system atrophy @2 NM @5 01
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C03 03  X  SPA  @0 Parkinson síndrome @2 NM @5 07
C03 04  X  FRE  @0 Présynaptique @5 08
C03 04  X  ENG  @0 Presynaptic @5 08
C03 04  X  SPA  @0 Presináptico @5 08
C03 05  X  FRE  @0 Etude cas @5 17
C03 05  X  ENG  @0 Case study @5 17
C03 05  X  SPA  @0 Estudio caso @5 17
C03 06  X  FRE  @0 Diagnostic différentiel @5 18
C03 06  X  ENG  @0 Differential diagnostic @5 18
C03 06  X  SPA  @0 Diagnóstico diferencial @5 18
C03 07  X  FRE  @0 Anatomopathologie @5 19
C03 07  X  ENG  @0 Pathology @5 19
C03 07  X  SPA  @0 Anatomía patológica @5 19
C03 08  X  FRE  @0 Personne âgée @5 20
C03 08  X  ENG  @0 Elderly @5 20
C03 08  X  SPA  @0 Anciano @5 20
C03 09  X  FRE  @0 Mâle @5 21
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C03 09  X  SPA  @0 Macho @5 21
C07 01  X  FRE  @0 Homme
C07 01  X  ENG  @0 Human
C07 01  X  SPA  @0 Hombre
C07 02  X  FRE  @0 Système nerveux pathologie @5 45
C07 02  X  ENG  @0 Nervous system diseases @5 45
C07 02  X  SPA  @0 Sistema nervioso patología @5 45
C07 03  X  FRE  @0 Système nerveux central pathologie @5 46
C07 03  X  ENG  @0 Central nervous system disease @5 46
C07 03  X  SPA  @0 Sistema nervosio central patología @5 46
C07 04  X  FRE  @0 Encéphale pathologie @5 47
C07 04  X  ENG  @0 Cerebral disorder @5 47
C07 04  X  SPA  @0 Encéfalo patología @5 47
C07 05  X  FRE  @0 Extrapyramidal syndrome @5 48
C07 05  X  ENG  @0 Extrapyramidal syndrome @5 48
C07 05  X  SPA  @0 Extrapiramidal síndrome @5 48
C07 06  X  FRE  @0 Maladie dégénérative @5 49
C07 06  X  ENG  @0 Degenerative disease @5 49
C07 06  X  SPA  @0 Enfermedad degenerativa @5 49
C07 07  X  FRE  @0 Trouble neurologique @5 53
C07 07  X  ENG  @0 Neurological disorder @5 53
C07 07  X  SPA  @0 Trastorno neurológico @5 53
N21       @1 266
N82       @1 PSI

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Pascal:02-0456878

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<div type="abstract" xml:lang="en">We describe the clinicopathological findings in a patient aged 63 years at death who, at age 55 years, developed levodopa-responsive parkinsonism with no atypical features. A diagnosis of idiopathic Parkinson's disease (PD) was made. During the clinical course, fluctuations and dyskinesias appeared. Eight years after onset, he was successfully treated with subthalamic nucleus stimulation but died 3 weeks postoperatively from pulmonary embolus. Brain autopsy showed marked neuronal loss and gliosis in the substantia nigra and locus coeruleus, and, to a much lesser extent, in the basis pontis, inferior olivary nuclei, and cerebellar cortex. Striatum was normal. There were numerous oligodendroglial and neuronal cytoplasmic inclusions and neuropil threads, the highest density being localized in the pons and cerebellar white matter. No Lewy bodies were observed. We conclude that nigral, presynaptic parkinsonism may occur in multiple system atrophy, which even in the long run can be indistinguishable from PD. Putaminal preservation accounts for good response to both levodopa therapy and subthalamic nucleus stimulation.</div>
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<s3>CC</s3>
</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>We describe the clinicopathological findings in a patient aged 63 years at death who, at age 55 years, developed levodopa-responsive parkinsonism with no atypical features. A diagnosis of idiopathic Parkinson's disease (PD) was made. During the clinical course, fluctuations and dyskinesias appeared. Eight years after onset, he was successfully treated with subthalamic nucleus stimulation but died 3 weeks postoperatively from pulmonary embolus. Brain autopsy showed marked neuronal loss and gliosis in the substantia nigra and locus coeruleus, and, to a much lesser extent, in the basis pontis, inferior olivary nuclei, and cerebellar cortex. Striatum was normal. There were numerous oligodendroglial and neuronal cytoplasmic inclusions and neuropil threads, the highest density being localized in the pons and cerebellar white matter. No Lewy bodies were observed. We conclude that nigral, presynaptic parkinsonism may occur in multiple system atrophy, which even in the long run can be indistinguishable from PD. Putaminal preservation accounts for good response to both levodopa therapy and subthalamic nucleus stimulation.</s0>
</fC01>
<fC02 i1="01" i2="X">
<s0>002B17G</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE">
<s0>Atrophie multisystématisée</s0>
<s2>NM</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG">
<s0>Multiple system atrophy</s0>
<s2>NM</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA">
<s0>Atrofia multisistematizada</s0>
<s2>NM</s2>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE">
<s0>Parkinson maladie</s0>
<s5>04</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG">
<s0>Parkinson disease</s0>
<s5>04</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA">
<s0>Parkinson enfermedad</s0>
<s5>04</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE">
<s0>Parkinsonisme</s0>
<s2>NM</s2>
<s5>07</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG">
<s0>Parkinsonism</s0>
<s2>NM</s2>
<s5>07</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA">
<s0>Parkinson síndrome</s0>
<s2>NM</s2>
<s5>07</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE">
<s0>Présynaptique</s0>
<s5>08</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG">
<s0>Presynaptic</s0>
<s5>08</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA">
<s0>Presináptico</s0>
<s5>08</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE">
<s0>Etude cas</s0>
<s5>17</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG">
<s0>Case study</s0>
<s5>17</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA">
<s0>Estudio caso</s0>
<s5>17</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE">
<s0>Diagnostic différentiel</s0>
<s5>18</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG">
<s0>Differential diagnostic</s0>
<s5>18</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA">
<s0>Diagnóstico diferencial</s0>
<s5>18</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE">
<s0>Anatomopathologie</s0>
<s5>19</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG">
<s0>Pathology</s0>
<s5>19</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA">
<s0>Anatomía patológica</s0>
<s5>19</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE">
<s0>Personne âgée</s0>
<s5>20</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG">
<s0>Elderly</s0>
<s5>20</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA">
<s0>Anciano</s0>
<s5>20</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE">
<s0>Mâle</s0>
<s5>21</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG">
<s0>Male</s0>
<s5>21</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA">
<s0>Macho</s0>
<s5>21</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE">
<s0>Homme</s0>
</fC07>
<fC07 i1="01" i2="X" l="ENG">
<s0>Human</s0>
</fC07>
<fC07 i1="01" i2="X" l="SPA">
<s0>Hombre</s0>
</fC07>
<fC07 i1="02" i2="X" l="FRE">
<s0>Système nerveux pathologie</s0>
<s5>45</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG">
<s0>Nervous system diseases</s0>
<s5>45</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA">
<s0>Sistema nervioso patología</s0>
<s5>45</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE">
<s0>Système nerveux central pathologie</s0>
<s5>46</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG">
<s0>Central nervous system disease</s0>
<s5>46</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA">
<s0>Sistema nervosio central patología</s0>
<s5>46</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Encéphale pathologie</s0>
<s5>47</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Cerebral disorder</s0>
<s5>47</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Encéfalo patología</s0>
<s5>47</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE">
<s0>Extrapyramidal syndrome</s0>
<s5>48</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG">
<s0>Extrapyramidal syndrome</s0>
<s5>48</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA">
<s0>Extrapiramidal síndrome</s0>
<s5>48</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE">
<s0>Maladie dégénérative</s0>
<s5>49</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG">
<s0>Degenerative disease</s0>
<s5>49</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA">
<s0>Enfermedad degenerativa</s0>
<s5>49</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE">
<s0>Trouble neurologique</s0>
<s5>53</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG">
<s0>Neurological disorder</s0>
<s5>53</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA">
<s0>Trastorno neurológico</s0>
<s5>53</s5>
</fC07>
<fN21>
<s1>266</s1>
</fN21>
<fN82>
<s1>PSI</s1>
</fN82>
</pA>
</standard>
</inist>
</record>

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