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Thyrotoxic paroxysmal myoplegia

Thyrotoxic paroxysmal myoplegia is a complication of thyrotoxicosis, manifested in recurrent attacks of paralysis, increasing with the use of thyroidin and disappearing with the treatment of thyrotoxicosis.

There are acute and chronic forms of the disease. The latter are often detected upon careful examination in the form of local atrophies and weakening of tendon reflexes. Well-known constant complaints of patients with thyrotoxicosis of muscle weakness.

The combination of thyrotoxicosis and myasthenia was repeatedly described. At the same time, myotonia (the pathogenetic antipode of myasthenia), as a rule, is accompanied by hypothyroidism.

The pathogenesis of thyrotoxic paroxysmal myasthenia is not clear. Along with ideas about the peripheral effect of thyroid hormones on muscle tissue, there are also ideas about the central-nervous origin of these disorders. The basis of muscle lesions in thyrotoxicosis is the damage to the motor nerve cells and, therefore, thyrotoxic myopathy is neural amyotrophy (DI Friedberg). Potassium ions are of great importance in the pathogenesis of the disease. It was shown that the level of potassium in the blood serum during an attack drops to 11–9 mg%. Taking potassium can stop paralysis.

Some evidence suggests a connection with the disease of the hypothalamus.

The clinical picture (signs and symptoms). In this condition, paralysis of the muscles of the limbs and trunk suddenly occurs, the muscles of the neck and face are rarely affected. Attacks of immobility occur most often at night or during the day at rest. Paralysis sluggish, decreased muscle tone, tendon reflexes disappear. Electric excitability is violated, even its complete loss occurs. The attack of myoplegia is accompanied by the following vegetative manifestations: arterial hypotension, bradycardia, expansion of the heart, an increase in the size of paralyzed muscles, drooling, thirst, nausea, and a feeling of heat. With severe seizures, creatinuria appears. Attacks last from several hours to several days. Outside of an attack, no abnormalities in the muscular system are detected in patients.

Symptomatic treatment .