Movement Disorders (revue)

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Pain Sensitivity and Clinical Progression in Parkinson's Disease

Identifieur interne : 002944 ( PascalFrancis/Curation ); précédent : 002943; suivant : 002945

Pain Sensitivity and Clinical Progression in Parkinson's Disease

Auteurs : Veit Mylius [Allemagne] ; Juliane Brebbermann [Allemagne] ; Helena Dohmann [Allemagne] ; Isabel Engau [Allemagne] ; Wolfgang H. Oertel [Allemagne] ; Jens C. Möller [Allemagne, Suisse]

Source :

RBID : Pascal:11-0481759

Descripteurs français

English descriptors

Abstract

Pain sensitivity in Parkinson's disease is known to be altered in an L-dopa-dependent manner with increased spinal nociception and experimental pain perception in the medication-defined "off" state. As Parkinson's disease-related pain can be an early symptom in Parkinson's disease, the present study aimed to investigate experimental pain sensitivity and spinal nociception during clinical progression. The nociceptive flexion reflex as a marker of spinal nociception as well as electrical and heat pain thresholds were assessed during the medication-defined "off" state in 29 patients with Parkinson's disease divided into 3 severity groups (according to their Unified Parkinson's Disease Rating Scale motor score) and compared with 27 healthy elderly subjects. Parkinson's disease-related pain was also quantified. Data provided evidence that spinal nociception and pain sensitivity are preserved during the early phase of Parkinson's disease. Following increased spinal nociception (F1,36 = 6.838, P = .013), experimental thermal and electrical pain sensitivity were augmented during the course of Parkinson's disease (F1,34 = 5.397, P = .014; F1,34 = 6.038, P = 0.053), whereas spinal nociception further increased (F1,34 = 5.397, P <.001). Increased experimental pain sensitivity was observed in patients exhibiting Parkinson's disease-related pain. Spinal alterations either on the local level or induced by diminished dopaminergic descending inhibition probably led to increased pain sensitivity in later stages. Because Parkinson's disease-related pain is correlated with experimental pain sensitivity these 2 observations likely reflect a causal relation.
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A08 01  1  ENG  @1 Pain Sensitivity and Clinical Progression in Parkinson's Disease
A11 01  1    @1 MYLIUS (Veit)
A11 02  1    @1 BREBBERMANN (Juliane)
A11 03  1    @1 DOHMANN (Helena)
A11 04  1    @1 ENGAU (Isabel)
A11 05  1    @1 OERTEL (Wolfgang H.)
A11 06  1    @1 MÖLLER (Jens C.)
A14 01      @1 Department of Neurology, Philipps University @2 Marburg @3 DEU @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 4 aut. @Z 5 aut. @Z 6 aut.
A14 02      @1 Paediatric Clinic Siegen @2 Siegen @3 DEU @Z 4 aut.
A14 03      @1 Neurocentro della Svizzera Italiana, Ente Ospedaliero Cantonale @2 Lugano @3 CHE @Z 6 aut.
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A44       @0 0000 @1 © 2011 INIST-CNRS. All rights reserved.
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C01 01    ENG  @0 Pain sensitivity in Parkinson's disease is known to be altered in an L-dopa-dependent manner with increased spinal nociception and experimental pain perception in the medication-defined "off" state. As Parkinson's disease-related pain can be an early symptom in Parkinson's disease, the present study aimed to investigate experimental pain sensitivity and spinal nociception during clinical progression. The nociceptive flexion reflex as a marker of spinal nociception as well as electrical and heat pain thresholds were assessed during the medication-defined "off" state in 29 patients with Parkinson's disease divided into 3 severity groups (according to their Unified Parkinson's Disease Rating Scale motor score) and compared with 27 healthy elderly subjects. Parkinson's disease-related pain was also quantified. Data provided evidence that spinal nociception and pain sensitivity are preserved during the early phase of Parkinson's disease. Following increased spinal nociception (F1,36 = 6.838, P = .013), experimental thermal and electrical pain sensitivity were augmented during the course of Parkinson's disease (F1,34 = 5.397, P = .014; F1,34 = 6.038, P = 0.053), whereas spinal nociception further increased (F1,34 = 5.397, P <.001). Increased experimental pain sensitivity was observed in patients exhibiting Parkinson's disease-related pain. Spinal alterations either on the local level or induced by diminished dopaminergic descending inhibition probably led to increased pain sensitivity in later stages. Because Parkinson's disease-related pain is correlated with experimental pain sensitivity these 2 observations likely reflect a causal relation.
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 @5 02
C03 02  X  ENG  @0 Nervous system diseases @5 02
C03 02  X  SPA  @0 Sistema nervioso patología @5 02
C03 03  X  FRE  @0 Sensibilité douleur @5 09
C03 03  X  ENG  @0 Pain sensitivity @5 09
C03 03  X  SPA  @0 Sensibilidad dolor @5 09
C03 04  X  FRE  @0 Diagnostic @5 10
C03 04  X  ENG  @0 Diagnosis @5 10
C03 04  X  SPA  @0 Diagnóstico @5 10
C03 05  X  FRE  @0 Réflexe flexion @5 11
C03 05  X  ENG  @0 Flexion reflex @5 11
C03 05  X  SPA  @0 Reflejo flexión @5 11
C03 06  X  FRE  @0 Douleur @5 12
C03 06  X  ENG  @0 Pain @5 12
C03 06  X  SPA  @0 Dolor @5 12
C03 07  X  FRE  @0 Perception @5 13
C03 07  X  ENG  @0 Perception @5 13
C03 07  X  SPA  @0 Percepción @5 13
C07 01  X  FRE  @0 Pathologie de l'encéphale @5 37
C07 01  X  ENG  @0 Cerebral disorder @5 37
C07 01  X  SPA  @0 Encéfalo patología @5 37
C07 02  X  FRE  @0 Syndrome extrapyramidal @5 38
C07 02  X  ENG  @0 Extrapyramidal syndrome @5 38
C07 02  X  SPA  @0 Extrapiramidal síndrome @5 38
C07 03  X  FRE  @0 Maladie dégénérative @5 39
C07 03  X  ENG  @0 Degenerative disease @5 39
C07 03  X  SPA  @0 Enfermedad degenerativa @5 39
C07 04  X  FRE  @0 Pathologie du système nerveux central @5 40
C07 04  X  ENG  @0 Central nervous system disease @5 40
C07 04  X  SPA  @0 Sistema nervosio central patología @5 40
N21       @1 332
N44 01      @1 OTO
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Pascal:11-0481759

Le document en format XML

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<div type="abstract" xml:lang="en">Pain sensitivity in Parkinson's disease is known to be altered in an
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-dopa-dependent manner with increased spinal nociception and experimental pain perception in the medication-defined "off" state. As Parkinson's disease-related pain can be an early symptom in Parkinson's disease, the present study aimed to investigate experimental pain sensitivity and spinal nociception during clinical progression. The nociceptive flexion reflex as a marker of spinal nociception as well as electrical and heat pain thresholds were assessed during the medication-defined "off" state in 29 patients with Parkinson's disease divided into 3 severity groups (according to their Unified Parkinson's Disease Rating Scale motor score) and compared with 27 healthy elderly subjects. Parkinson's disease-related pain was also quantified. Data provided evidence that spinal nociception and pain sensitivity are preserved during the early phase of Parkinson's disease. Following increased spinal nociception (F
<sub>1,36</sub>
= 6.838, P = .013), experimental thermal and electrical pain sensitivity were augmented during the course of Parkinson's disease (F
<sub>1,34</sub>
= 5.397, P = .014; F
<sub>1,34</sub>
= 6.038, P = 0.053), whereas spinal nociception further increased (F
<sub>1,34</sub>
= 5.397, P <.001). Increased experimental pain sensitivity was observed in patients exhibiting Parkinson's disease-related pain. Spinal alterations either on the local level or induced by diminished dopaminergic descending inhibition probably led to increased pain sensitivity in later stages. Because Parkinson's disease-related pain is correlated with experimental pain sensitivity these 2 observations likely reflect a causal relation.</div>
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<sub>L</sub>
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<sub>1,36</sub>
= 6.838, P = .013), experimental thermal and electrical pain sensitivity were augmented during the course of Parkinson's disease (F
<sub>1,34</sub>
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<sub>1,34</sub>
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<sub>1,34</sub>
= 5.397, P <.001). Increased experimental pain sensitivity was observed in patients exhibiting Parkinson's disease-related pain. Spinal alterations either on the local level or induced by diminished dopaminergic descending inhibition probably led to increased pain sensitivity in later stages. Because Parkinson's disease-related pain is correlated with experimental pain sensitivity these 2 observations likely reflect a causal relation.</s0>
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<s0>Maladie de Parkinson</s0>
<s2>NM</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG">
<s0>Parkinson disease</s0>
<s2>NM</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA">
<s0>Parkinson enfermedad</s0>
<s2>NM</s2>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE">
<s0>Pathologie du système nerveux</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG">
<s0>Nervous system diseases</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA">
<s0>Sistema nervioso patología</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE">
<s0>Sensibilité douleur</s0>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG">
<s0>Pain sensitivity</s0>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA">
<s0>Sensibilidad dolor</s0>
<s5>09</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE">
<s0>Diagnostic</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG">
<s0>Diagnosis</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA">
<s0>Diagnóstico</s0>
<s5>10</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE">
<s0>Réflexe flexion</s0>
<s5>11</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG">
<s0>Flexion reflex</s0>
<s5>11</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA">
<s0>Reflejo flexión</s0>
<s5>11</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE">
<s0>Douleur</s0>
<s5>12</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG">
<s0>Pain</s0>
<s5>12</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA">
<s0>Dolor</s0>
<s5>12</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE">
<s0>Perception</s0>
<s5>13</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG">
<s0>Perception</s0>
<s5>13</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA">
<s0>Percepción</s0>
<s5>13</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE">
<s0>Pathologie de l'encéphale</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG">
<s0>Cerebral disorder</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA">
<s0>Encéfalo patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE">
<s0>Syndrome extrapyramidal</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG">
<s0>Extrapyramidal syndrome</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA">
<s0>Extrapiramidal síndrome</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE">
<s0>Maladie dégénérative</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG">
<s0>Degenerative disease</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA">
<s0>Enfermedad degenerativa</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Pathologie du système nerveux central</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>
<fN21>
<s1>332</s1>
</fN21>
<fN44 i1="01">
<s1>OTO</s1>
</fN44>
<fN82>
<s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
</record>

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