Hypokalemic periodic paralysis (HypoPP) is an autosomal dominant channelopathy most commonly caused by mutations in the CACNA1S gene (calcium channel, type 1 — 60%) or SCN4A gene (sodium channel — 20%). The mutant ion channels create an anomalous 'gating pore current' that allows cation leak when the membrane is hyperpolarized by low extracellular potassium. This depolarizes the resting membrane potential of skeletal muscle fibers, inactivating normal sodium channels and rendering the muscle inexcitable — resulting in flaccid paralysis. Episodes are triggered by factors that lower serum potassium: high-carbohydrate meals (insulin drives K+ intracellularly), rest after vigorous exercise (catecholamine-mediated cellular K+ uptake), stress, cold, and medications (beta-agonists, insulin, corticosteroids). Unlike hyperkalemic periodic paralysis, HypoPP attacks are longer (hours to days vs minutes to hours), more severe, myotonia is ABSENT between attacks, and serum potassium is LOW during episodes (<3.5 mEq/L, often <3.0). Thyrotoxic periodic paralysis (TPP) is an acquired form seen almost exclusively in Asian men with hyperthyroidism — the mechanism involves thyroid hormone-enhanced Na-K-ATPase activity driving excessive potassium intracellularly. TPP resolves with treatment of hyperthyroidism. Diagnosis is confirmed by genetic...