Muscular Disorders in Hypothyroidism

Hypothyroidism impairs metabolism in the muscle fiber and decreases contractile force. Repair and replacement of myofibrillar proteins are defective because protein turnover is reduced. Slow muscle contraction and relaxation result from the diminished activity of myosin ATPase and from the impaired uptake of calcium by the sarcoplasmic reticulum. Reduced cardiac output results from -adrenergic hyposensitivity. The pathophysiology responsible for muscle cramps and muscle fiber enlargement is unknown. Deposition of mucopolysaccharides in muscle occurs inconsistently.

Symptoms and Signs

The primary clinical features are proximal weakness (including pronounced proximal leg muscle weakness and atrophy in some patients), fatigue, slowed movements, stiffness, myalgias, cramps, and, occasionally, enlarged muscles (especially the anterior compartment muscles of the leg). These features generally develop over weeks to months. Tendon reflexes are slowed, with relaxation of the Achilles tendon reflex being markedly prolonged. In about one third of hypothyroid patients, myoedema (mounding) lasting >= 5 seconds can be elicited by direct percussion of muscle. A similar response can occur in malnourished patients.

The severity of symptoms appears to relate more to the total duration of thyroid deficiency and to the percent elevation of the thyroid-stimulating hormone (TSH) level than to the absolute level of free thyroxine or TSH.

Muscle-related symptoms in hypothyroidism may be exacerbated by the use of cholesterol-lowering drugs, which require close monitoring in patients with thyroid deficiency.

Complications include carpal and tarsal tunnel syndromes and a distal, symmetric sensorimotor polyneuropathy. Rarely, marked fatigability of hip girdle and trunk muscles results from impaired neuromuscular transmission.

Diagnosis

The circulating thyroid hormone level is decreased, and (in primary hypothyroidism) the TSH level is elevated. Usually, muscle enzyme levels, especially CK levels, are increased several times the normal values.

Electrodiagnostic testing and muscle biopsy may be needed to rule out other disorders that resemble hypothyroid neuropathy and myopathy. Electromyographic findings may show no abnormality or both neurogenic and myopathic features. Occasionally, muscle membrane hyperirritability is evident. Findings on repetitive nerve stimulation mimic those of Eaton-Lambert syndrome. Electrodiagnostic studies may show compression neuropathies. Muscle biopsy results are usually normal; occasionally the proportion and size of type 2 muscle fibers are reduced.

Prognosis and Treatment

The long-term prognosis is good; however, patients with severe muscle wasting may never fully recover muscle strength and bulk.

Thyroid hormone must be replaced. Once the euthyroid state is achieved, serum CK levels return to normal. Control of muscle pain and fatigue significantly improves in some patients, even those in whom TSH levels are minimally elevated. Surgery rarely is needed to reverse symptoms related to median or tibial nerve compression.