Annals of Indian Academy of Neurology
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CASE REPORT
Year : 2012  |  Volume : 15  |  Issue : 4  |  Page : 339-343

Reversible electrophysiological abnormalities in acute secondary hyperkalemic paralysis


1 Department of Neurology, KLE University's Jawaharlal Nehru Medical College and KLES Dr. Prabhakar Kore Hospital and MRC, Nehrunagar, Belgaum, India
2 Department of Nephrology, KLE University's Jawaharlal Nehru Medical College and KLES Dr. Prabhakar Kore Hospital and MRC, Nehrunagar, Belgaum, India

Correspondence Address:
Karkal R Naik
Department of Neurology, KLE University's Jawaharlal Nehru Medical College and KLES Dr. Prabhakar Kore Hospital and MRC, Nehrunagar, Belgaum-590010
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0972-2327.104354

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Hyperkalemia manifests clinically with acute neuromuscular paralysis, which can simulate Guillain Barré syndrome (GBS) and other causes of acute flaccid paralysis. Primary hyperkalemic paralysis occurs from genetic defects in the sodium channel, and secondary hyperkalemic paralysis (SHP) from diverse causes including renal dysfunction, potassium retaining drugs, Addison's disease, etc. Clinical characteristics of SHP have been addressed in a number of publications. However, electrophysiological evaluations of these patients during neuromuscular paralysis are infrequently reported and have demonstrated features of demyelination. The clinical features and electrophysiological abnormalities in secondary hyperkalemia mimic GBS, and pose diagnostic challenges. We report the findings of nerve conduction studies in a middle-aged man who was admitted with rapidly reversible acute quadriplegia resulting from secondary hyperkalemic paralysis.


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