Electrical Stimulation Improves Repair of Nerve Injury
Abstract & Commentary
Source: Zealear DL, et al. J Neurophysiol. 2002;87:2195-2199.
At present, medical insurers will not cover facial nerve electrical stimulation for the treatment of Bell’s palsy. Recent evidence in rodents suggests it may be beneficial and, thus, warrants further attention. The evidence is not all in, especially in the facial nerve, and very little has been undertaken in the motor vagus nerve.
Both the posterior cricoarytenoid muscle (PCA), a vocal cord abductor, and the thyroarytenoid muscle (TA), a vocal cord adductor, are innervated by the recurrent laryngeal nerve. Injury to this nerve commonly results in aberrant reinnervation whereby adductor nerve fibers enter the abductor muscle, resulting in functional laryngeal paralysis. Might continuous electrical stimulation of either muscle enhance correct reinnervation by its native nerve fibers?
Eight canines underwent electrode implantation of their PCA muscles for continuous electrical stimulation and recording of the electromyographic (EMG) activity, both spontaneous and evoked. Resection and reanastomosis of the right recurrent laryngeal nerve was performed and continuous electrical stimulation over an 11- month period was administered to 4 dogs, with the 4 remaining animals serving as nonstimulated controls. Correct PCA reinnervation was assessed by measuring maximal vocal cord opening, both spontaneously and in response to CO2 enhanced respiratory drive. Aberrant reinnervation was assessed by evaluating reflex vocal cord activity, both in response to saline application to the vocal cord mucosa, and by electrically stimulating the internal branch of the superior laryngeal nerve. Both of these normally reflexly close the glottis by stimulating the TA. Physiologic assessments were performed monthly. Two-tailed, unpaired Student’s t-test provided statistical analysis.
Appropriate reinervation was significantly enhanced (P < 0.0064) and aberrant innervation inhibited (P < 0.0084) by continuous stimulation of the PCA muscle. A nonsignificant (P < 0.113) trend to increased magnitude of PCA reinnervation was also seen. Continuous stimulation, for reasons yet to be elucidated, appears to foster correct reconnection of nerve to muscle.
Commentary
Brief electrical stimulation of injured motor nerves promotes their reinnervation into muscle (Al-Majed AA, et al. J Neurosci. 2000;20:2602-2608). Following resection and reanastomosis of rat femoral nerve, continuous electrical stimulation of injured nerve at 20 Hz, for 1 hour to 2 weeks, shortened the time necessary for motor reinnervation from 10 weeks (with no electrical stimulation) to 3 weeks. Although the mechanism of this benefit is uncertain, it may be via enhanced production of neurotrophic factors (Al-Majed AA, et al. Eur J Neurosci. 2000;12:4381-4390). Electrical stimulation was applied to the femoral nerve, again following unilateral femoral nerve resection and repair. Using semiquantitative in situ hybridization to measure mRNA expression of brain-derived neurotrophic factor (BDNF) and its receptor, tyrosine kinase B (trkB), electrical stimulation for 1 hour increased BDNF and trkB mRNA by 3- and 2-fold, respectively, within 8 hours, and by 6- and 4-fold, respectively, by 2 days. Sham stimulation resulted in no such increase. Alternatively, protein absorption may be altered by a change in the electric field of extracellular matrix molecules engendered by the electric stimulation, thereby increasing neurite extension (Kotwal A, Schmidt CE. Biomaterials. 2001;22:1055-1064). —Michael Rubin
Dr. Rubin, Professor of Clinical Neurology, New York Presbyterian Hospital-Cornell Campus, is Assistant Editor of Neurology Alert.
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