Magnesium Treatment in Acute Stroke

Magnesium plays multiple roles in the normal function of our bodies. Early studies using rats and mice showed that if given at high concentrations, magnesium can decrease the area of the brain that is permanently lost as a result of a stroke. The results of these animal studies were so promising that a Phase II clinical trial was performed to test the safety of magnesium in the treatment of human stroke. Magnesium passed the safety test and since January of 2005 it is being tested in a Phase III clinical trial known as the FAST-MAG trial. The trial is well under way, completing 25% of its enrollment in April 2007.

But how does magnesium protect the injured brain? The response to a lack of oxygen and nutrients (i.e., ischemia) by the brain includes a local release of chemicals which can damage brain cells, even beyond the damage that can be expected by ischemia alone. Perhaps the most harmful of these chemicals is glutamate, an aminoacid used in very low amounts by brain cells to communicate with each other. During a stroke, however, the massive amount of glutamate released produces a flood of calcium inside brain cells which in turn causes them to die prematurely. Magnesium is thought to have the ability to prevent glutamate from causing this flood calcium in the cells, thus protecting them from premature death.

If magnesium infusion is found to be an effective approach for the treatment of acute stroke, it would be a much needed addition to the current armamentarium of medical therapies for acute stroke. Currently, less than 10% of stroke patients can benefit from tissue plasminogen activator (TPA) infusions partly because of the 3 hour limit after the onset of stroke symptoms in which it can be used, and partly because it is contraindicated in hemorrhagic strokes. The completion of the FAST-MAG trial will reveal whether magnesium should, or should not, become a standard medication for the treatment of acute stroke.

Recommended reading: The Basics of Stroke Treatment