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

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Neuropathy as a Potential Complication of Levodopa Use in Parkinson's Disease

Identifieur interne : 000701 ( PascalFrancis/Curation ); précédent : 000700; suivant : 000702

Neuropathy as a Potential Complication of Levodopa Use in Parkinson's Disease

Auteurs : Cory Toth [Canada] ; Martin Sutton Brown [Canada] ; Sarah Furtado [Canada] ; Oksana Suchowersky [Canada] ; Douglas Zochodne [Canada]

Source :

RBID : Pascal:08-0522196

Descripteurs français

English descriptors

Abstract

The presence and potential etiologies of peripheral neuropathy (PN) in patients with Parkinson's Disease (PD) is unknown. We examined for presence of PN in patients with PD. From a PD patient population of 500 patients screened for features of symptomatic PN, patients were further selected for clinical, electrophysiological, and laboratory studies related to PN. This PD patient population with idiopathic PN (PD-IPN) was compared to a group of PD patients without PN (PD-only), and a large group of patients without PD with idiopathic PN (IPN) for abnormalities in Cbl, fasting homocysteine (Hcy), and fasting methylmalonic acid (MMA) levels. PD-IPN and IPN patients identified with abnormalities in Cbl, Hcy, or MMA levels were treated with intramuscular Cbl for 1 to 2 years. Of 49 PD patients with symptomatic PN, 34 patients (69%) had PD-IPN, and 32/34 (94%) had abnormal Hcy or MMA levels as compared to 26/258 (10%) of IPN patients. Cumulative lifetime L-dopa dosage and fasting MMA levels were associated with PN severity. Cbl therapy led to improvements in Hcy and MMA levels in all groups, and PN in PD-IPN patients stabilized during therapy. PN in PD patients may be associated with iatrogenic Cbl metabolic abnormalities. Alternatively PN may be a peripheral nervous system manifestation of PD.
pA  
A01 01  1    @0 0885-3185
A03   1    @0 Mov. disord.
A05       @2 23
A06       @2 13
A08 01  1  ENG  @1 Neuropathy as a Potential Complication of Levodopa Use in Parkinson's Disease
A11 01  1    @1 TOTH (Cory)
A11 02  1    @1 BROWN (Martin Sutton)
A11 03  1    @1 FURTADO (Sarah)
A11 04  1    @1 SUCHOWERSKY (Oksana)
A11 05  1    @1 ZOCHODNE (Douglas)
A14 01      @1 Department of Clinical Neurosciences, The Hotchkiss Brain Institute, and the University of Calgary @2 Calgary, Alberta @3 CAN @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 4 aut. @Z 5 aut.
A20       @1 1850-1859
A21       @1 2008
A23 01      @0 ENG
A43 01      @1 INIST @2 20953 @5 354000184468160090
A44       @0 0000 @1 © 2008 INIST-CNRS. All rights reserved.
A45       @0 40 ref.
A47 01  1    @0 08-0522196
A60       @1 P
A61       @0 A
A64 01  1    @0 Movement disorders
A66 01      @0 USA
C01 01    ENG  @0 The presence and potential etiologies of peripheral neuropathy (PN) in patients with Parkinson's Disease (PD) is unknown. We examined for presence of PN in patients with PD. From a PD patient population of 500 patients screened for features of symptomatic PN, patients were further selected for clinical, electrophysiological, and laboratory studies related to PN. This PD patient population with idiopathic PN (PD-IPN) was compared to a group of PD patients without PN (PD-only), and a large group of patients without PD with idiopathic PN (IPN) for abnormalities in Cbl, fasting homocysteine (Hcy), and fasting methylmalonic acid (MMA) levels. PD-IPN and IPN patients identified with abnormalities in Cbl, Hcy, or MMA levels were treated with intramuscular Cbl for 1 to 2 years. Of 49 PD patients with symptomatic PN, 34 patients (69%) had PD-IPN, and 32/34 (94%) had abnormal Hcy or MMA levels as compared to 26/258 (10%) of IPN patients. Cumulative lifetime L-dopa dosage and fasting MMA levels were associated with PN severity. Cbl therapy led to improvements in Hcy and MMA levels in all groups, and PN in PD-IPN patients stabilized during therapy. PN in PD patients may be associated with iatrogenic Cbl metabolic abnormalities. Alternatively PN may be a peripheral nervous system manifestation of PD.
C02 01  X    @0 002B17
C02 02  X    @0 002B17G
C03 01  X  FRE  @0 Maladie de Parkinson @2 NM @5 01
C03 01  X  ENG  @0 Parkinson disease @2 NM @5 01
C03 01  X  SPA  @0 Parkinson enfermedad @2 NM @5 01
C03 02  X  FRE  @0 Pathologie du système nerveux périphérique @5 02
C03 02  X  ENG  @0 Peripheral nerve disease @5 02
C03 02  X  SPA  @0 Nervio periférico patología @5 02
C03 03  X  FRE  @0 Pathologie du système nerveux @5 03
C03 03  X  ENG  @0 Nervous system diseases @5 03
C03 03  X  SPA  @0 Sistema nervioso patología @5 03
C03 04  X  FRE  @0 Neuropathie @5 09
C03 04  X  ENG  @0 Neuropathy @5 09
C03 04  X  SPA  @0 Neuropatía @5 09
C03 05  X  FRE  @0 Complication @5 10
C03 05  X  ENG  @0 Complication @5 10
C03 05  X  SPA  @0 Complicación @5 10
C03 06  X  FRE  @0 Lévodopa @2 NK @2 FR @5 11
C03 06  X  ENG  @0 Levodopa @2 NK @2 FR @5 11
C03 06  X  SPA  @0 Levodopa @2 NK @2 FR @5 11
C03 07  X  FRE  @0 Homocystéine @2 NK @2 FR @5 12
C03 07  X  ENG  @0 Homocystein @2 NK @2 FR @5 12
C03 07  X  SPA  @0 Homocisteína @2 NK @2 FR @5 12
C03 08  X  FRE  @0 Acide méthylmalonique @5 13
C03 08  X  ENG  @0 Methylmalonic acid @5 13
C03 08  X  SPA  @0 Metilmalónico ácido @5 13
C07 01  X  FRE  @0 Pathologie de l'encéphale @5 38
C07 01  X  ENG  @0 Cerebral disorder @5 38
C07 01  X  SPA  @0 Encéfalo patología @5 38
C07 02  X  FRE  @0 Syndrome extrapyramidal @5 39
C07 02  X  ENG  @0 Extrapyramidal syndrome @5 39
C07 02  X  SPA  @0 Extrapiramidal síndrome @5 39
C07 03  X  FRE  @0 Maladie dégénérative @5 40
C07 03  X  ENG  @0 Degenerative disease @5 40
C07 03  X  SPA  @0 Enfermedad degenerativa @5 40
C07 04  X  FRE  @0 Pathologie du système nerveux central @5 41
C07 04  X  ENG  @0 Central nervous system disease @5 41
C07 04  X  SPA  @0 Sistema nervosio central patología @5 41
N21       @1 343
N44 01      @1 OTO
N82       @1 OTO

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Pascal:08-0522196

Le document en format XML

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<div type="abstract" xml:lang="en">The presence and potential etiologies of peripheral neuropathy (PN) in patients with Parkinson's Disease (PD) is unknown. We examined for presence of PN in patients with PD. From a PD patient population of 500 patients screened for features of symptomatic PN, patients were further selected for clinical, electrophysiological, and laboratory studies related to PN. This PD patient population with idiopathic PN (PD-IPN) was compared to a group of PD patients without PN (PD-only), and a large group of patients without PD with idiopathic PN (IPN) for abnormalities in Cbl, fasting homocysteine (Hcy), and fasting methylmalonic acid (MMA) levels. PD-IPN and IPN patients identified with abnormalities in Cbl, Hcy, or MMA levels were treated with intramuscular Cbl for 1 to 2 years. Of 49 PD patients with symptomatic PN, 34 patients (69%) had PD-IPN, and 32/34 (94%) had abnormal Hcy or MMA levels as compared to 26/258 (10%) of IPN patients. Cumulative lifetime L-dopa dosage and fasting MMA levels were associated with PN severity. Cbl therapy led to improvements in Hcy and MMA levels in all groups, and PN in PD-IPN patients stabilized during therapy. PN in PD patients may be associated with iatrogenic Cbl metabolic abnormalities. Alternatively PN may be a peripheral nervous system manifestation of PD.</div>
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<s0>The presence and potential etiologies of peripheral neuropathy (PN) in patients with Parkinson's Disease (PD) is unknown. We examined for presence of PN in patients with PD. From a PD patient population of 500 patients screened for features of symptomatic PN, patients were further selected for clinical, electrophysiological, and laboratory studies related to PN. This PD patient population with idiopathic PN (PD-IPN) was compared to a group of PD patients without PN (PD-only), and a large group of patients without PD with idiopathic PN (IPN) for abnormalities in Cbl, fasting homocysteine (Hcy), and fasting methylmalonic acid (MMA) levels. PD-IPN and IPN patients identified with abnormalities in Cbl, Hcy, or MMA levels were treated with intramuscular Cbl for 1 to 2 years. Of 49 PD patients with symptomatic PN, 34 patients (69%) had PD-IPN, and 32/34 (94%) had abnormal Hcy or MMA levels as compared to 26/258 (10%) of IPN patients. Cumulative lifetime L-dopa dosage and fasting MMA levels were associated with PN severity. Cbl therapy led to improvements in Hcy and MMA levels in all groups, and PN in PD-IPN patients stabilized during therapy. PN in PD patients may be associated with iatrogenic Cbl metabolic abnormalities. Alternatively PN may be a peripheral nervous system manifestation of PD.</s0>
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</fC03>
<fC03 i1="08" i2="X" l="FRE">
<s0>Acide méthylmalonique</s0>
<s5>13</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG">
<s0>Methylmalonic acid</s0>
<s5>13</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA">
<s0>Metilmalónico ácido</s0>
<s5>13</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE">
<s0>Pathologie de l'encéphale</s0>
<s5>38</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG">
<s0>Cerebral disorder</s0>
<s5>38</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA">
<s0>Encéfalo patología</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE">
<s0>Syndrome extrapyramidal</s0>
<s5>39</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG">
<s0>Extrapyramidal syndrome</s0>
<s5>39</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA">
<s0>Extrapiramidal síndrome</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE">
<s0>Maladie dégénérative</s0>
<s5>40</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG">
<s0>Degenerative disease</s0>
<s5>40</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA">
<s0>Enfermedad degenerativa</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Pathologie du système nerveux central</s0>
<s5>41</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Central nervous system disease</s0>
<s5>41</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Sistema nervosio central patología</s0>
<s5>41</s5>
</fC07>
<fN21>
<s1>343</s1>
</fN21>
<fN44 i1="01">
<s1>OTO</s1>
</fN44>
<fN82>
<s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
</record>

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