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February 1, 1919


JAMA. 1919;72(5):348-349. doi:10.1001/jama.1919.02610050030015

When a motor nerve is severed, the muscle which it supplies enters into a state of inaction, so far as its usual contractile function is concerned, and muscular atrophy gradually ensues. Ultimately the nerve may regenerate so that a functional connection with its muscles again becomes restored. Obviously it would be of enormous physiologic advantage if the intervening muscular atrophy could be wholly or in part averted. Attempts at a successful therapy to prevent the disaster that follows the nerve injury and may be termed denervated muscle atrophy have not been wanting. The earliest efforts were based on the disuse theory—the belief that the wasting of the denervated muscle is due to the lack of exercise. Three quarters of a century ago in an experimental study of the problem, John Reid undertook to supply the supposedly needed activity by inducing contraction in denervated muscle by means of electrical stimulation; likewise

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