Trudell RG, Kaiser KK, Griggs RC: Acetazolamide-responsive myotonia congenita. Neurology 37:488, 1987.
Tyler FH, Stephens FE, Gunn FD, Perkoff GT: Studies on disorders of muscle: VII. Clinical manifestations and inheritance of a type of periodic paralysis without hypopotassemia. J Clin Invest 30:492, 1951.
Valli G, Barbieri S, Stefano C, et al: Syndromes of abnormal muscular activity: Overlap between continuous muscle fiber activity and the stiff-man syndrome. J Neurol Neurosurg Psychiatry 46:241, 1983.
Vernino S, Lennon VA: Ion channel and striational antibodies define a continuum of autoimmune neuromuscular hyperexcitability. Muscle Nerve 26:702, 2002.
Viets HR: A historical review of myasthenia gravis from 1672 to 1900. JAMA 153:1273, 1953.
Vincent A, Newsom-Davis J: Acetylcholine receptor antibody as a diagnostic test for myasthenia gravis: Results in 153 validated cases and 2967 diagnostic assays. J Neurol Neurosurg Psychiatry 48:1246, 1985.
Vincent A, Newsom-Davis J, Martin V: Antiacetylcholine receptor antibodies in d-penicillamine associated myasthenia gravis. Lancet 1:1254, 1978.
Vincent A, Wray D (eds): Neuromuscular Transmission. Basic and Applied Aspects. New York, Manchester Press, 1990.
Vorgerd M, Ricker K, Ziemssen W, et al: A sporadic case of rippling muscle disease caused by a de novo caveolin-3 mutation. Neurology 57:2273, 2001.
Walker MB: Treatment of myasthenia gravis with physostigmine. Lancet 1:1200, 1934.
Weinberg DH, Rizzo JF, Hayes MT, et al: Ocular myasthenia gravis: Predictive value of single-fiber electromyography. Muscle Nerve 22:1222, 1999.
Witte AS, Cornblath DR, Parry GJ, et al: Azathioprine in the treatment of myasthenia gravis. Ann Neurol 15:602, 1984.
Wolfe GI, Kaminski HJ, Aban IB, et al: Randomized trial of thymectomy in myasthenia gravis. N Engl J Med 375:511, 2016.
Yazaki K, Kuribayashi T, Yamamura Y, et al: Hypokalemic myopathy associated with a 17α-hydroxylase deficiency: A case report. Neurology 32:94, 1982.
Figure 46-1. A. Endplate from a patient with myasthenia gravis. The terminal axon contains abundant presynaptic vesicles, but the postsynaptic folds are wide and there are few secondary folds. The loose junctional sarcoplasm is filled with microtubules and ribosomes. The synaptic cleft (asterisk) is widened. (From Santa et al by permission.) B. Normal endplate for comparison. (Courtesy of Dr. A.G. Engel.)
Chapter  46    Disorders of the Neuromuscular Junction, Myotonias, and Persistent Muscle Fiber Activity
Anxiety Disorders, Hysteria, and