Pain sensitivity and clinical progression in Parkinson's disease
Identifieur interne : 000210 ( Main/Exploration ); précédent : 000209; suivant : 000211Pain sensitivity and clinical progression in Parkinson's disease
Auteurs : Veit Mylius [Allemagne, France] ; Juliane Brebbermann [Allemagne] ; Helena Dohmann [Allemagne] ; Isabel Engau [Allemagne] ; Wolfgang H. Oertel [Allemagne] ; Jens C. Möller [Allemagne, Suisse, France]Source :
- Movement Disorders [ 0885-3185 ] ; 2011-10.
English descriptors
- KwdEn :
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. © 2011 Movement Disorder Society
Url:
DOI: 10.1002/mds.23825
Affiliations:
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Le document en format XML
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<front><div type="abstract" xml:lang="en">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. © 2011 Movement Disorder Society</div>
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