Introduction: Enterovirus-D68 (EV68) is associated with acute flaccid myelitis (AFM) in children. Since August 2014, 120 pediatric AFM cases have occurred in the United States, coinciding with a nationwide EV68 endemic. Like poliovirus, EV68 induces limb paralysis through inflammation and destruction of anterior horn cells of the cervical spine. Objectives: To date, no medical intervention has altered the course of EV68-induced AFM. Of 120 recently described AFM cases, only 2 children have recovered full limb function. We report nerve transfers in 7 limbs of 6 patients as a potential treatment of EV68-induced AFM. Methods: We performed nerve transfers in 6 pediatric patients from 2 centers with sustained neuropathy following EV68-induced AFM. Postoperative outcomes included muscle strength, graded on the British Medical Research Council (BMRC) scale. Results: In all, 3/6 patients were male, with a mean age of 6.9 ± 5.3 years. All patients reported a viral prodrome prior to neurologic symptom onset, with an average latency time of 3.25 ± 2.5 days. In addition, 3/6 patients had bilateral upper extremity involvement, of which 2 developed quadriparesis that has since resolved, 2/6 had unilateral involvement on the right side, and 1/6 had unilateral involvement on the left. The mean delay in presentation for evaluation was 6.7 ± 2.2 months. Preoperative electrodiagnostic testing in all patients revealed abnormal motor but normal sensory function. In addition, 4/6 patients had magnetic resonance imaging that demonstrated T2 hyperintensity in the gray matter of the cervical spine. Also, 5/6 limbs were treated with proximal nerve transfers. One patient with proximal upper extremity involvement on the right side and distal involvement on the left side underwent bilateral nerve transfers. Transfers performed for shoulder abduction included the following: spinal accessory nerve to suprascapular nerve, contralateral C7 to the upper trunk with an interposition sural nerve graft, thoracodorsal to axillary nerve, medial pectoral branch to axillary nerve, and radial fascicular to axillary nerve. Transfers performed for elbow flexion included intercostals (2-4) to the musculocutaneous nerve and median fascicular to brachialis branch of the musculocutaneous nerve. Finally, transfers for wrist and finger flexion included brachialis to anterior interosseous nerve and side to side flexor digitorum profundus (FDP) transfers in the wrist. The mean follow-up time was 7.7 ± 2.0 months. Early results in the 3 patients demonstrated promising signs of recovery with contraction and even active motion with gravity eliminated for shoulder abduction, external rotation, and elbow flexion. Three patients with longer clinical follow-up improved from 0 for all functions to 2 to 3 for shoulder abduction, 2 for external rotation, and 3 to 4 for elbow flexion. At 6 months postoperatively, the one patient treated with distal nerve transfers demonstrated active flexor pollicis longus (FPL) and FDP pinch. Conclusion: We present early outcomes of a promising reconstructive technique for this emerging and devastating viral endemic. Detailed physical examination and preoperative electrodiagnostic testing is essential to determine available donor nerves, as traditional donors may not be available, necessitating custom solutions. Our patients presented late in the course of their disease; early recognition and identification of EVD68 may improve the outcome of nerve reconstruction for treating EV-D68-induced nerve palsy.
