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Myxedema, Pseudomyotonia, and Myotonia Congenita

Leonard W. Jarcho; Frank H. Tyler
AMA Arch Intern Med. 1958;102(3):357-366. doi:10.1001/archinte.1958.00030010357003.
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For the student of neuromuscular disorders, the thyroid gland poses several unsolved problems. Thus, hyperthyroidism has been shown to be associated with myopathy and ophthalmoplegia and may be related in some manner to myasthenia gravis and periodic paralysis.1 Similarly, the concurrence of hypothyroidism and muscle dysfunction has been noted repeatedly.2 Again, certain questions have arisen concerning the part played by thyroid hypofunction in myotonia. Five principal types of association are at issue.

A majority of patients with evident myxedema will show a delay in the relaxation of muscle after deep tendon reflexes are elicited. The phenomenon has been termed pseudomyotonia. Lambert3 demonstrated that the delay includes all phases of the tendon reflex, but only the slowing of relaxation is obvious clinically. Hormone replacement sufficient to correct the basal metabolic rate and the clinical signs of myxedema eradicates the pseudomyotonia. While the nature of the disturbance in muscle function is not


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