Periodic paralysis and the sodium-potassium pump

Ann Neurol. 1982 Jun;11(6):547-52. doi: 10.1002/ana.410110602.


Analysis of the pathophysiology of hypokalemic paralysis, as it occurs in barium poisoning, chronic potassium deficiency, and thyrotoxicosis, suggests that these disorders may have a similar mechanism. An increased ratio of muscle sodium permeability to potassium permeability reduces the ionic diffusion potential, while the resting membrane potential is sustained by an increase of Na-K pump electrogenesis. The result is that potassium entry (the sum of active and passive influx) exceeds potassium efflux; this causes a large shift of extracellular potassium into muscle until the Na-K pump turns off, leading to depolarization and paralysis. The primary defect in familial hypokalemic periodic paralysis, as in the example of barium poisoning, may be a marked reduction of muscle permeability to potassium.

MeSH terms

  • Animals
  • Anura
  • Barium / poisoning
  • Chronic Disease
  • Dogs
  • Humans
  • Hyperthyroidism / complications
  • Ion Channels / physiology*
  • Paralysis / chemically induced
  • Paralysis / etiology
  • Paralysis / genetics
  • Paralysis / physiopathology*
  • Periodicity*
  • Potassium Deficiency / complications
  • Rats


  • Ion Channels
  • Barium