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Reversible electrophysiological abnormalities in acute secondary hyperkalemic paralysis
Karkal R Naik1, Aralikatte O Saroja, Mallikarjun S Khanpet
1Department of Neurology, KLE University's Jawaharlal Nehru Medical College and KLES Dr. Prabhakar Kore Hospital and MRC, Nehrunagar, Belgaum, India.
Annals of Indian Academy of Neurology
|January 26, 2013
Summary
Secondary hyperkalemic paralysis can cause acute flaccid paralysis, mimicking Guillain Barré syndrome (GBS). Electrophysiological findings in this case showed demyelination, highlighting diagnostic challenges.
Area of Science:
- Neurology
- Clinical Electrophysiology
Background:
- Secondary hyperkalemic paralysis (SHP) presents with acute neuromuscular paralysis, clinically resembling Guillain Barré syndrome (GBS).
- While SHP's clinical features are documented, electrophysiological evaluations during paralysis are rarely reported.
- Electrophysiological studies in SHP have previously suggested demyelinating features.
Observation:
- A middle-aged man presented with rapidly reversible acute quadriplegia.
- The patient's condition was diagnosed as secondary hyperkalemic paralysis.
Findings:
- Nerve conduction studies revealed electrophysiological abnormalities.
- These abnormalities mimicked demyelinating neuropathies, similar to GBS.
Implications:
- The findings underscore the diagnostic challenges posed by SHP due to its mimicry of GBS.
- Electrophysiological evaluation is crucial for differentiating SHP from other causes of acute flaccid paralysis.
- This case highlights the importance of considering hyperkalemia in the differential diagnosis of acute paralysis.
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