According to a story from sciencedaily.com, recent research has revealed the mechanism that causes hypokalemic periodic paralysis, a rare condition that causes patients to experience sudden, severe muscle weakness. The condition is caused by a hole that appears in a certain membrane protein which allows for ions of sodium to move across cell membranes. This discovery could help provide a basis for the development of new treatments for hypokalemic periodic paralysis.
About Hypokalemic Periodic Paralysis
Hypokalemic periodic paralysis is a condition in which a low concentration of potassium in the blood can trigger paralysis, or profound and sudden muscle weakness. There are several different mutations that can trigger the condition to appear. Hypokalemic periodic paralysis often appears as brief episodes of paralysis. These attacks can be triggered by a variety of different events. They often appear soon after waking, particularly after sleep following extensive, strenuous exercise. Meals high in carbohydrates and sodium, loud noises, excitement, flashes of light, cold temperatures, or abrupt temperature changes can all trigger an attack of hypokalemic periodic paralysis. Weakness can vary from quite mild to profound, fully body paralysis. They often begin in adolescence and can last anywhere from several days to a couple of hours. To learn more about hypokalemic periodic paralysis, click here.
The research that helped lead to this discovery examined muscle cell behavior at the atomic level. In normal conditions, muscle cells have different charges, or changes in ions, across their cell membranes, which are regulated by ion “pumps” that allow ions to pass in and out of a cell. A critical example is the sodium-potassium pump. This pump causes potassium levels to be higher within the cell while the sodium concentration is higher outside.
This arrangement maintains transmembrane voltage, which is necessary for muscles to contract. Under typical conditions, the voltage sensor has to separate chambers that do not connect, but a person with hypokalemic periodic paralysis has these two chambers joined together. This connection creates a route through which ions can escape. This causes the difference in charge, or polarization, within the cell membranes to disappear, leading to the loss of transmembrane voltage.
With the discovery of this new mechanism, drug developers will have a new target for designing the next treatment for hypokalemic periodic paralysis.