Studies in thyrotoxic periodic paralysis

Abstract

A new case of thyrotoxic periodic paralysis (TPP) is described. Prior to treatment by subtotal thyroidectomy, paralysis was induced by a variety of measures which acutely decreased the serum potassium concentration. The magnitude of the potassium ion shifts was not consistent with the degree of clinical paralysis, nor did the serum potassium concentrations rise as the clinical attacks cleared. Hypokalemia was not, therefore, the sole cause of paralysis. Aldosterone excretion seemed to be normal. EMG studies revealed that the paralytic attacks were caused by an acute myopathy, and the muscle biopsy showed a prominent vacuolar myopathy during paralysis. The vacuoles developed from the sarcoplasmic reticulum (SR) and were absent or much less notable between attacks. Glycogen masses, degenerative changes and other microscopic findings seem to be secondary phenomena; some degree of vacuolization is the only consistent histologic finding in all cases studied thus far. A small but significant increase of the muscle water content in an affected muscle was found in the present case during induced paralysis. Although it is tempting to attribute paralysis to SR distension by fluid, this mechanism of paralysis in TPP is unproven and may also be a secondary phenomenon. The EMG studies indicated a depression of sarcolemmal excitability during paralysis, which should be investigated when possible in the future by means of microelectrode recording of the muscle membrane potential. A systemic factor appears to trigger paralysis in TPP. The only endocrine abnormality is hyperthyroidism and the attacks recur after thyroid treatment if an excess of hormone is administered. The level of circulating hormone should be studied in future cases in relationship to spontaneous and induced paralytic attacks.