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Pain. 2015 Apr;156(4):666-74. doi: 10.1097/j.pain.0000000000000096.

Disinhibition of the primary somatosensory cortex in patients with fibromyalgia.

Author information

1
aMEG Center, Department of Neurosurgery, Seoul National University Hospital, Seoul, South Korea bNeuroscience Research Institute, Seoul National University Medical Research Center, Seoul, South Korea cDepartment of Rehabilitation, Radboud University Medical Center, Nijmegen, the Netherlands dSensory Organ Research Institute, Seoul National University Medical Research Center, Seoul, South Korea eDepartment of Brain and Cognitive Sciences, Seoul National University College of Natural Sciences, Seoul, South Korea fDivision of Rheumatology, Department of Internal Medicine, Eulji University School of Medicine, Eulji General Hospital, Seoul, South Korea gDivision of Rheumatology, Department of Internal Medicine, Seoul National University College of Medicine, Seoul, South Korea hDepartment of Internal Medicine, Hallym University College of Medicine, Chuncheon, South Korea iDivision of Rheumatology, Department of Internal Medicine, Hallym University Sacred Heart Hospital, Anyang, South Korea.

Abstract

Fibromyalgia (FM) is a chronic widespread pain condition linked to central sensitization. Altered excitability of sensorimotor cortex has been proposed as an underlying pathology of FM. This study aimed to investigate intracortical excitability of the primary somatosensory cortex (S1) and its potential role in clinical pain in patients with FM. Somatosensory evoked magnetic fields were recorded in 17 right-handed females with FM and 21 age-, sex-, and handedness-matched healthy control subjects. Paired-pulse median nerve stimulation was delivered to the left and right wrist. We assessed the peak-to-peak amplitudes of the N20m-P35m and peak amplitude of each N20m and P35m component. Paired-pulse suppression (PPS) of the second response was quantified as the ratio of the amplitudes of the second to the first response. Patients with FM displayed significantly higher PPS ratio for the N20m-P35m in both hemispheres, indicating reduced intracortical inhibition in the S1. Notably, PPS ratio for the P35m was higher in patients with FM than in healthy controls, whereas no differences were apparent in PPS ratio for the N20m in both hemispheres. For both the N20m-P35m and the P35m in the left hemisphere, PPS ratios were positively associated with the sensory pain on the short-form McGill Pain Questionnaire. This study demonstrated that intracortical inhibition in the S1 is compromised bilaterally in patients with FM, and the extent of disinhibition can be closely associated with increased clinical pain. Our results suggest that changes of intracortical inhibition of the S1 may contribute to the pathophysiology of FM pain.

PMID:
25630027
DOI:
10.1097/j.pain.0000000000000096
[Indexed for MEDLINE]

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