Hindlimb muscle atrophy occurs from peripheral nerve damage in a rat neuropathic pain model

The purpose of this study was to examine the effect of neuropathic pain produced by peripheral nerve damage on mass, myofibrillar protein content, and cross-sectional areas of Type I and II fibers of rat hindlimb muscles.

Adult male Sprague-Dawley rats were assigned to one of three groups: a pain group (n = 10) that underwent ligation and cut of the left L5 spinal nerve, a sham group (n = 10) that underwent a sham cut procedure, or a control group (n = 10) that underwent no procedures. The withdrawal threshold test was done to assess pain threshold on each of Days 1-7 and 14. Activity, body weight, and food intake were measured daily for 2 weeks. At 15 days, rats were anesthetized and the bilateral soleus, plantaris, and gastrocnemius muscles dissected.

At 15 days post-ligation, the pain group had significant decreases in total dietary intake, body weight, activity, and muscle weight as compared to sham and control animals. Muscle weight and cross-sectional area of Type II fiber of the ipsilateral soleus, plantaris, and gastrocnemius muscles decreased as did myofibrillar protein content of the ipsilateral plantaris and gastrocnemius muscles. Muscle weight of the contralateral gastrocnemius muscle decreased, as did myofibrillar protein content and cross-sectional area of Type II fiber of the contralateral plantaris muscle.

Hindlimb muscle atrophy occurs in both ipsilateral and contralateral sides following induction of neuropathic pain by unilateral peripheral nerve damage. Muscle changes of the ipsilateral side are more pronounced than those of the contralateral side.