Role of magnesium in the pathogenesis and treatment of migraine

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Date: Mar. 2009
From: Expert Review of Neurotherapeutics(Vol. 9, Issue 3)
Publisher: Expert Reviews Ltd.
Document Type: Report
Length: 9,446 words

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Author(s): Christina Sun-Edelstein [[dagger]] 1 , Alexander Mauskop 2


headache; intracellular magnesium; ionized magnesium; magnesium; magnesium deficiency; migraine; migraine pathogenesis; serum magnesium

Magnesium is a vital intracellular element that is involved in numerous cellular functions. Deficiencies in magnesium may play an important role in the pathogenesis of migraine headaches, by promoting cortical spreading depression (CSD), alteration of neurotransmitter release and the hyperaggregation of platelets. Given this multifaceted role of magnesium in migraine, the use of magnesium in both acute and preventive headache treatment has been studied as a potentially simple, inexpensive, safe and well-tolerated option.

Role of magnesium in human physiology

Magnesium is an essential cation that plays a critical role in a multitude of physiological processes, owing to its central role in normal ATP function and glucose metabolism. It is also necessary for the proper functioning of several ATPases, such as the Na+ /K+ ATPase, which controls the Na+ pump. It has powerful membrane-stabilizing properties that are important for the insertion of proteins and the formation of phospholipids [1] . It also contributes significantly to skeletal and cardiac muscle function in that it is vital to cellular cytoskeleton contraction and at the myoneural junction. Magnesium is absorbed through intestinal epithelial channels via a nonvitamin D-dependent process, and reabsorbed with calcium in the thick ascending limb of the kidneys and also by means of specific magnesium transport channels in the distal tubule. [2] . Magnesium homeostasis is maintained by the Ca2+ /Mg2+ sensing receptor (CASR) [3] , which is located in the parathyroid hormone (PTH)-secreting cells of the parathyroid glands and in the nephron segments that are involved in renal calcium and magnesium reabsorption. CASR acts by sensing levels of ionized calcium and magnesium, then regulating these levels by controlling PTH secretion [4,5] . Less than 2% of the total body magnesium is in the measurable, extracellular space and, therefore, the levels found on routine blood testing do not reflect true total body stores [6] . It is the second most abundant intracellular cation, with 31% of total body magnesium located intracellularly and 67% in the bone.

Hypomagnesemia is common: an epidemiological study evaluating an unselected population group of approximately 16,000 people in Germany found that its prevalence (Mg serum level below 0.76 mmol/l) was approximately 14.5%, with higher frequencies observed in females and outpatients [7] . It may be due to decreased intake, decreased gastrointestinal absorption or diarrhea, increased urinary losses, genetic factors [8] or any combination of these causes. Deficits in magnesium can also be seen in any chronic medical illness, including cardiovascular disease, diabetes, preeclampsia, eclampsia, sickle cell disease and chronic alcoholism [9] . Low magnesium has also been noted in patients with end-stage renal disease who suffer from hemodialysis headache [10] . Clinical symptoms include apathy, depression, delirium, seizures, paresthesias, tremors, general weakness, premenstrual syndrome, cold extremities, leg and foot cramps and ventricular arrythmias. Hypomagnesemia frequently occurs in conjunction with other electrolyte abnormalities, such as hypokalemia, hyponatremia, hypocalcemia and hypophosphatemia [11] . Since serum levels do not accurately reflect total body stores...

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Gale Document Number: GALE|A224275915