Abstract

Delayed onset muscle soreness (DOMS) is a subacute pain state arising 24–48 hours after a bout of unaccustomed eccentric muscle contractions. Functional magnetic resonance imaging (fMRI) was used to examine the patterns of cortical activation arising during DOMS-related pain in the quadriceps muscle of healthy volunteers evoked by either voluntary contraction or physical stimulation. The painful movement or physical stimulation of the DOMS-affected thigh disclosed widespread activation in the primary somatosensory and motor (S1, M1) cortices, stretching far beyond the corresponding areas somatotopically related to contraction or physical stimulation of the thigh; activation also included a large area within the cingulate cortex encompassing posteroanterior regions and the cingulate motor area. Pain-related activations were also found in premotor (M2) areas, bilateral in the insular cortex and the thalamic nuclei. In contrast, movement of a DOMS-affected limb led also to activation in the ipsilateral anterior cerebellum, while DOMS-related pain evoked by physical stimulation devoid of limb movement did not.

Highlights

  • Functional magnetic resonance imaging has revealed several aspects on how acute and chronic pain is processed in the human brain

  • Electrical stimulation, injection of hypertonic saline or acid phosphate buffer have been used in conjunction with event-related functional magnetic resonance imaging and positron emission tomography (PET) to study the supraspinal processing of muscle pain [2,13,14,15,16,17]

  • Psychophysical ratings and painfulness of the stimulus To quantify the pain, all subjects had to rate the pain perceived during contraction and physical stimulation of the sore quadriceps before the Functional magnetic resonance imaging (fMRI) measurement

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Summary

Introduction

Functional magnetic resonance imaging (fMRI) has revealed several aspects on how acute and chronic pain is processed in the human brain. Evoking pain results in unwanted activation of nonnociceptive nerve and muscle fibers and muscle twitches and limb movement may accompany the stimulation and adulterate functional brain imaging [7,8]. Another frequently used model consists in the injection of chemicals into the muscle tissue, such as hypertonic saline, acid phosphate buffer, bradykinin or glutamate; these substances induce cramp like diffuse pain mimicking the chronic pain observed by patients. Electrical stimulation, injection of hypertonic saline or acid phosphate buffer have been used in conjunction with event-related functional magnetic resonance imaging (fMRI) and positron emission tomography (PET) to study the supraspinal processing of muscle pain [2,13,14,15,16,17]

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