Hypokalemic Paralysis Research Paper

Hypokalemic periodic paralysis is a rare, autosomal dominant channelopathy characterized by muscle weakness or paralysis with a matching fall in potassium levels in the blood (primarily due to defect in a voltage-gated calcium channel). In individuals with this mutation, attacks often begin in adolescence and are triggered by strenuous exercise followed by rest, high carbohydrate meals, meals with high sodium content, sudden changes in temperature, and even excitement, noise or flashing lights. Weakness may be mild and limited to certain muscle groups, or more severe full body paralysis. Attacks may last for a few hours or persist for several days. Recovery is usually sudden when it occurs, due to release of potassium from swollen muscles as they recover.
The CMAP (Compound Muscle Amplitude Potential) test, also called the exercise EMG or X-EMG, is diagnostic in 70–80% of cases when done correctly. Besides the patient history or a report of serum potassium low normal or low during an attack, the CMAP is the current standard for medical testing. Genetic diagnosis is often unreliable as only a few of the more common gene locations are tested, but even with more extensive testing 20–37% of people with a clinical diagnosis of hypokalemic periodic paralysis have no known mutation in the two known genes.[2] Standard EMG testing cannot diagnose a patient unless they are in a full blown attack at the time of testing. Provoking an attack with exercise and diet then trying oral potassium can be diagnostic, but also dangerous as this form of PP has an alternate form known as hyperkalemic periodic paralysis. The symptoms are almost the same, but the treatment is different. The old glucose insulin challenge is dangerous and risky to the point of being life threatening and should never be done when other options are so readily available[citation