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Related Experiment Video

Updated: May 18, 2026

Swimming Induced Paralysis to Assess Dopamine Signaling in Caenorhabditis elegans

Swimming Induced Paralysis to Assess Dopamine Signaling in Caenorhabditis elegans

Published on: April 3, 2019

Secondary hypokalaemic paralysis.

Ankush Gupta¹, Vibhu Narain Khanna, Imran Rizvi

¹Department of Medical, Military Hospital Jodhpur, Jodhpur, Rajasthan, India. drankushgupta@gmail.com

BMJ Case Reports

|October 5, 2012

Summary

This case study shows how electrocardiogram (ECG) findings of hypokalemia (low potassium) can guide treatment for acute flaccid quadriplegia, even when lab tests are inconclusive.

Area of Science:

Neurology
Cardiology
Internal Medicine

Background:

Acute flaccid quadriplegia is a critical neurological condition requiring prompt diagnosis.
Metabolic disturbances, such as electrolyte imbalances, can precipitate neurological symptoms.
Hypokalemia can manifest with significant neuromuscular and cardiac effects.

Observation:

A 28-year-old male presented with acute, ascending, bilateral, symmetrical, areflexic motor paralysis.
History included fever, vomiting, chloroquine use, and intravenous dextrose administration.
Initial laboratory results showed metabolic alkalosis with normal serum potassium levels.

Findings:

Electrocardiogram (ECG) revealed characteristic changes indicative of hypokalemia.
Despite normal serum potassium levels, ECG findings guided the diagnosis and management.

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The patient's condition improved successfully following management based on ECG findings.

Implications:

Highlights the critical role of ECG in diagnosing hypokalemia, especially when serum levels are misleading.
Emphasizes the importance of considering ECG in the workup of acute flaccid quadriplegia.
Underscores the potential for iatrogenic causes of electrolyte disturbances and paralysis.