Periodic paralysis corresponds to a group of neuromuscular disorders that occur due to the affection of the ion channels of the skeletal muscle. The authors of this article decided to group the forms of periodic paralysis according to the concomitant serum potassium levels: hyperkalaemic periodic paralysis, normokalaemic periodic paralysis and hypokalaemic periodic paralysis. Clinically, periodic hypokalaemic paralysis is characterized by the sudden and transient appearance of muscle weakness, usually proximal and symmetrical, starting in the lower limbs and progressing to the upper limbs. Acute episodes may be preceded by a prodromal period consisting of myalgias and muscle spasms. The duration of episodes of paralysis varies from case to case, and may last a few minutes or several days. Most have a spontaneous resolution, however, in severe potassium depletion, acute tetraparesis is more marked and may culminate in tetraplegia and death from respiratory muscle failure and/or fatal arrhythmias. The cardinal laboratory manifestation is a serum potassium of less than 3.5 mmol/L, although it is usually much lower. Most cases of periodic paralysis are hereditary, although there are secondary causes of periodic paralysis. These conceptually occur by any changes in the transcellular distribution of potassium, absorption, or elimination (renal or extra-renal). In this article, we perform a review of the published literature to date of secondary causes of periodic hypokalaemic paralysis.