Thyrotoxic periodic paralysis (TPP) is a rare condition featuring attacks of muscle weakness in the presence of hyperthyroidism (overactivity of the thyroid gland).

[1] The condition has been linked with genetic mutations in genes that code for certain ion channels that transport electrolytes (sodium and potassium) across cell membranes.

[3] The abnormality in the channel is thought to lead to shifts of potassium into cells, under conditions of high thyroxine (thyroid hormone) levels, usually with an additional precipitant.

Treatment of the low levels of potassium in the blood, followed by correction of the hyperthyroidism, leads to complete resolution of the attacks.

[1][2][5] On neurological examination during an attack, flaccid weakness of the limbs is noted; reflexes are usually diminished, but the sensory system is unaffected.

[5] Attacks may be brought on by physical exertion, drinking alcohol, or eating food high in carbohydrates or salt.

[1] Of people with TPP, 33% from various populations were demonstrated to have mutations in KCNJ18, the gene coding for Kir2.6, an inward-rectifier potassium ion channel.

[2] The muscle weakness and increased risk of irregular heart beat in TPP result from markedly reduced levels of potassium in the bloodstream.

These are normal in the other forms, and in thyrotoxicosis the levels of thyroxine and triiodothyronine are elevated, with resultant suppression of TSH production by the pituitary gland.

[6] In the acute phase of an attack, administration of potassium will quickly restore muscle strength and prevent complications.

Subsequent attacks may be prevented by avoiding known precipitants, such as high salt or carbohydrate intake, until the thyroid disease has been adequately treated.

[1][2] TPP occurs predominantly in males of Chinese, Japanese, Vietnamese, Filipino, and Korean descent,[1] as well as Thais,[3] with much lower rates in people of other ethnicities.

[1][2] After several case reports in the 18th and 19th centuries, periodic paralysis was first described in full by the German neurologist Karl Friedrich Otto Westphal (1833–1890) in 1885.

[9][10] The first English-language report, in 1931, originated from Dunlap and Kepler, physicians at the Mayo Clinic; they described the condition in a patient with features of Graves' disease.