Veränderungen des Schmerzerlebens im klinischen Verlauf des Morbus Parkinson

In dieser Studie sollte gezeigt werden, inwieweit sich objektive Schmerz-schwellen und subjektives Schmerzerleben im Laufe der Parkinson-Krankheit verändern und auf welcher Ebene der Schmerzverarbeitung sich diese Veränderungen manifestieren. Dazu wurden 29 Parkinson-Patienten und 27 gesunde Kontrol...

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Bibliographische Detailangaben
1. Verfasser: Brebbermann, Juliane
Beteiligte: Mylius, V. (PD Dr.) (BetreuerIn (Doktorarbeit))
Format: Dissertation
Sprache:Deutsch
Veröffentlicht: Philipps-Universität Marburg 2013
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Pain sensitivity in Parkinson’s disease (PD) is known to be altered in a L-dopa-dependant 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, this study aimed to detect how far experimental pain sensivity and spinal nociception are changing in the course of the disease. For this purpose, 29 PD patients and 27 healthy control persons were tested in regard to their heat and electrical pain thresholds. In addition, the nociception flexion reflex (NFR) threshold was assessed as a marker of spinal nociception. To exclude confounding factors (e.g. depression, dementia, anxiety and pain of other origin), all participants completed a selection of questionnaires whose requirements had to be fulfilled to participate in the study. The severity of disease was classified by using the well-established Unified Parkinson Disease Rating Scale (UPDRS) motor score under their usual medication (“on” state). Based on this score, the patients were divided into three severity groups for further analysis. The electrophysiological investigation of the pain and NFR thresholds took place in the morning between 6 and 9 a.m. in the medication-defined “off” state. Data provided evidence for a preserved spinal nociception and pain sensitivity in the early state of Parkinson’s disease. Following increased spinal nociception, also electrical and heat pain thresholds decreased in the course of disease. These findings support the assumption that PD-related pain might arise because of modified spinal nociception, which increases in the course of the disease. Regarding current studies, central and peripheric mechanisms are also considered to influence pain perception. The central dopaminergic and noradrenergic system as well as the descending inhibitory control system likely affect pain processing in PD. Also cutaneous denervation is supposed to be responsible for the sensory deficit of PD patients.