Abstract
The success of devices delivering functional electrical stimulation (FES) has been hindered by complications related to implants including skin breakdown and subsequent wound dehiscence. Our hypothesis was that a vascularized muscle flap along the dorsal surface of an epimysial electrode would prevent skin breakdown during FES therapy to treat atrophy of the gastrocnemius muscle during peripheral nerve injury. Resection of a tibial nerve segment with subsequent electrode implantation on the dorsal surfaces of the gastrocnemius muscle was performed on ten Lewis rats. In five rats, the biceps femoris (BF) muscle was dissected and placed along the dorsal surface of the electrode (Flap group). The other five animals did not undergo flap placement (No Flap group). All animals were treated with daily FES therapy for 2 weeks and degree of immune response and skin breakdown were evaluated. The postoperative course of one animal in the No Flap group was complicated by complete wound dehiscence requiring euthanasia of the animal on postoperative day 4. The remaining 4 No Flap animals showed evidence of ulceration at the implant by postoperative day 7. The 5 animals in the Flap group did not have ulcerative lesions. Excised tissue at postoperative day 14 examined by histology and in vivo Imaging System (IVIS) showed decreased implant-induced inflammation in the Flap group. Expression of specific markers for local foreign body response were also decreased in the Flap group.
Highlights
During a peripheral nerve injury, the denervated skeletal muscle undergoes an inevitable course of atrophy leading to the muscle being replaced by fibrous connective tissue and fat
By increasing myogenic precursor cell proliferation and facilitating fusion with mature myofibers, functional electrical stimulation (FES) improves the regenerative capacity of skeletal muscle [18, 19]
Our hypothesis was that a vascularized muscle flap along the dorsal surface of an epimysial electrode would prevent skin breakdown leading to wound dehiscence during FES therapy to treat atrophy of the gastrocnemius muscle during acute peripheral nerve injury while the nerve is being regenerated
Summary
During a peripheral nerve injury, the denervated skeletal muscle undergoes an inevitable course of atrophy leading to the muscle being replaced by fibrous connective tissue and fat. Devices delivering functional electrical stimulation (FES) have been developed to prevent muscle atrophy and enhance functional recovery during peripheral nerve injury [4, 5]. Electrical stimulation of the proximal nerve stump accelerates nerve outgrowth across the injury site but the distal denervated muscles for extended periods of time become atrophied, diminishing the potential for optimal functional recovery [6,7,8,9,10]. Direct electrical stimulation of the denervated muscle may reduce muscle atrophy and increase the number of functional motor units available for recovery [4, 11,12,13,14,15]. By increasing myogenic precursor cell proliferation and facilitating fusion with mature myofibers, FES improves the regenerative capacity of skeletal muscle [18, 19]
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