In 1924, Walshe1 first reported that intramuscular injection of diluted procaine reduced muscle rigidity in a patient with postencephalitic parkinsonism. Its mechanism of action was attributed to blockade of muscle afferents because the muscle motor response elicited by electric stimulation was unchanged. Since then, this method of treating muscle hyperactivity has been ignored because of its transient action. Recently we revived this muscle afferent block (MAB) by intramuscularly injecting 0.5% lidocaine together with 100% ethanol in a 10:1 volume ratio.2,3 The mixture is expected to work as a short-latency, long-duration anesthetic because ethanol in a 5 to 10% concentration is a long-acting sodium channel blocker.4 In addition to writer’s cramp2 and oromandibular dystonia,3 it is used for treating cervical dystonia.5 In MAB, the solution is not directly injected to the nerve or the motor point but is diffused into the whole muscle. It is technically easier and carries less risk of unexpected palsy or sensory deficits than the conventional nerve block with ethanol or phenol. Because the diluted anesthetic preferentially affects small-diameter fibers, such as …