Muscular pain is the most frequent kind of nondystonic pain associated with Parkinson's disease (PD). It might be related not only to peripheral factors but also to an abnormal nociceptive input processing in the central nervous system. To test this hypothesis, we recorded CO2 laserevoked potentials (LEPs) in response to shoulder stimulation (skin over deltoid muscle) in 11 hemiparkinsonian PD patients complaining of muscular pain in the shoulder (ipsilateral to motor symptoms) and compared the results with those obtained in 12 pain-free PD patients with hemiparkinson and in 11 normal subjects. N2/P2 LEP, which is thought to originate from the cingulate cortex and insula, was significantly lower in amplitude in both groups of PD patients than in controls, regardless of the clinically affected body side. In both groups of PD patients, no significant correlation was observed between the severity of motor symptoms and N2/P2 amplitude abnormalities. In PD patients with muscular pain, the N2/P2 amplitude obtained following stimulation of the painful shoulder was significantly reduced compared with that obtained in response to nonpainful shoulder stimulation and compared with the values obtained in pain-free PD patients. No significant correlation was observed between the intensity of muscular pain and N2/P2 amplitude abnormalities in this group of PD patients. These results suggest abnormal nociceptive input processing in PD, which appears to be independent of clinical expression of parkinsonian motor signs. These alterations are more evident in the presence of muscular pain.

Muscular pain in Parkinson's disease and nociceptive processing assessed with CO2 laser-evoked potentials

Defazio, G;
2010-01-01

Abstract

Muscular pain is the most frequent kind of nondystonic pain associated with Parkinson's disease (PD). It might be related not only to peripheral factors but also to an abnormal nociceptive input processing in the central nervous system. To test this hypothesis, we recorded CO2 laserevoked potentials (LEPs) in response to shoulder stimulation (skin over deltoid muscle) in 11 hemiparkinsonian PD patients complaining of muscular pain in the shoulder (ipsilateral to motor symptoms) and compared the results with those obtained in 12 pain-free PD patients with hemiparkinson and in 11 normal subjects. N2/P2 LEP, which is thought to originate from the cingulate cortex and insula, was significantly lower in amplitude in both groups of PD patients than in controls, regardless of the clinically affected body side. In both groups of PD patients, no significant correlation was observed between the severity of motor symptoms and N2/P2 amplitude abnormalities. In PD patients with muscular pain, the N2/P2 amplitude obtained following stimulation of the painful shoulder was significantly reduced compared with that obtained in response to nonpainful shoulder stimulation and compared with the values obtained in pain-free PD patients. No significant correlation was observed between the intensity of muscular pain and N2/P2 amplitude abnormalities in this group of PD patients. These results suggest abnormal nociceptive input processing in PD, which appears to be independent of clinical expression of parkinsonian motor signs. These alterations are more evident in the presence of muscular pain.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11584/235070
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