Dysfunction of sensory nerves during attacks of hypokalemic periodic paralysis.
Reversible electrophysiologic abnormalities of sensory nerve function were found by chance in three patients with hypokalemic periodic paralysis, a disorder previously considered to affect the function of muscle membranes only. A formal, prospective study was therefore conducted. Serial nerve conduction studies were done in ten additional patients. Amplitude of sensory action potentials was significantly smaller during paralytic attacks, but did not differ from controls after normalization of serum potassium concentration. These apparently novel findings might be explained by previous electrodiagnostic studies either not involving the testing of sensory nerves at all, or not being repeated after recovery from an attack. Involvement of sensory nerves in hypokalemic periodic paralysis is suggested to arise through dorsal root ganglia having an incomplete blood-nerve barrier and sensory neurons being particularly vulnerable to derangements affecting nerve cell metabolism. Neuronal inexcitability is postulated to occur consequent upon possible inactivation of the sodium-potassium pump by the low concentration of extracellular potassium. In patients with acute areflexic limb weakness, the diagnosis of hypokalemic periodic paralysis should not be excluded by abnormal results of sensory nerve conduction studies.
Neurosciences Department, Rashid Hospital, Dubai, United Arab Emirates.
J S
JS
Inshasi
V P
VP
Jose
C A
CA
van der Merwe
R F
RF
Gledhill
D000328:Adult; D004562:Electrocardiography; D004594:Electrophysiology; D005260:Female; D006801:Humans; D007008:Hypokalemia / Q000097:blood / Q000503:physiopathology*; D008297:Male; D009431:Neural Conduction / Q000502:physiology; D009475:Neurons, Afferent / Q000502:physiology*; D010245:Paralyses, Familial Periodic / Q000097:blood / Q000503:physiopathology*; D011188:Potassium / Q000097:blood
D011188:Potassium