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Myopathies can occur in the setting of a variety of systemic diseases. Previous chapters have discussed inflammatory myopathies that can occur in the setting of connective tissue diseases (e.g., systemic lupus erythematosus, mixed connective tissue disease, Sjögren syndrome, and rheumatoid arthritis) and systemic infections (e.g., HIV). Myopathies occurring as complications of medications (toxic myopathies) are also dealt with elsewhere in the book. In this chapter, we will focus on myopathies related to endocrine disturbances, electrolyte imbalance, nutritional deficiency, and amyloidosis. We also discuss some other less well-defined syndromes such as fibromyalgia.


Myopathies can complicate various endocrinopathies.1,2 In this section, we review myopathies associated with thyroid, parathyroid, adrenal, pituitary, and pancreatic disorders.


Both hyperthyroidism and hypothyroidism can be associated with myopathy. In addition, polyneuropathy and neuromuscular junction disorders can occur with dysthyroid states and these need to be differentiated from one another.


Clinical Features

The mean age of onset of thyrotoxicosis is in the fifth decade. The severity of the myopathy does not necessarily relate to the severity of the thyrotoxicosis. Muscle symptoms usually appear several months after the onset of other clinical symptoms associated with mild hyperthyroidism.3 Interestingly, thyrotoxicosis is more common in females; however, thyrotoxic myopathy occurs more commonly in men. Anywhere from 61% to 82% of patients with thyrotoxicosis have some degree of detectable weakness on examination, but only about 5% of patients with thyrotoxicosis present with muscle weakness as their chief complaint.1,35

Thyrotoxic myopathy is characterized by proximal muscle weakness and atrophy.27 Some individuals have severe shoulder-girdle atrophy and scapular winging.2 Distal extremity weakness can be the predominant feature in approximately 20% of patients.4 Myalgias and fatigue are common. Some patients develop dysphagia, dysphonia, and respiratory distress due to involvement of bulbar, esophageal–pharyngeal muscles, and ventilatory muscles.8,9 Weakness of extraocular muscles and proptosis occur in the setting of Graves’ disease but the sphincters are spared in hyperthyroidism. Rarely, rhabdomyolysis with myoglobinuria can develop in severe thyrotoxicosis.10

Muscle stretch tendon reflexes are often brisk. In addition, fasciculations and myokymia are occasionally seen which probably reflects thyrotoxicosis-induced irritability of anterior horn cells or peripheral nerves.1113 Peripheral neuropathy in hyperthyroidism is quite rare, but a demyelinating polyneuropathy has been reported.11

Other manifestations of hyperthyroidism include nervousness, anxiety, psychosis, tremor, increased perspiration, heat intolerance, palpitations, insomnia, diarrhea, increased appetite, and weight loss. Common signs include goiter, tachycardia, atrial fibrillation, widened pulse pressure, as well as warm, thin, and moist skin.

Myasthenia gravis can develop in association with Graves’ disease. It can be a challenge distinguishing which neuromuscular symptoms are related to Graves’ disease ...

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