Magnesium is a mineral that acts as an electrolyte in the body, which means it carries an electrical charge when dissolved in fluids like blood. This electrolyte is involved in over 300 metabolic reactions, playing a broad but often overlooked role in the body’s overall function. A significant drop in the concentration of magnesium in the blood, a condition known as hypomagnesemia, can lead to severe neurological complications. While many people experience mild symptoms from low magnesium, a severe deficiency can indeed disrupt the normal electrical stability of the brain, leading to unprovoked seizures. Hypomagnesemia is defined as a serum magnesium level below the normal range, typically considered to be under 1.8 milligrams per deciliter (mg/dL).
Magnesium’s Role in Neurological Function
Magnesium’s primary function within the nervous system is to act as a natural stabilizer for nerve cell membranes. It helps regulate the flow of ions—charged particles like sodium, potassium, and calcium—across the neuronal membrane. This regulation is essential for maintaining a stable electrical charge, which prevents nerve cells from firing uncontrollably. The magnesium ion suppresses chemical signal transmission by binding to voltage-dependent calcium channels at the ends of nerve cells. This action dampens the release of neurotransmitters at the synapse. Without sufficient magnesium, the nervous system loses its natural brake, leading to neuronal hyperexcitability and making neurons more prone to excessive electrical discharges.
How Low Magnesium Causes Seizures
The direct link between low magnesium and seizure activity involves the N-methyl-D-aspartate (NMDA) receptor, a specific protein channel on nerve cells. Under normal conditions, the magnesium ion acts as a physical plug within the NMDA receptor channel, preventing the flow of ions, particularly calcium, into the neuron. When magnesium levels drop significantly, this plug is removed. Without the magnesium block, NMDA receptors become excessively sensitive to glutamate, the brain’s primary excitatory neurotransmitter. This results in an excessive and prolonged influx of calcium ions into the neuron. This massive surge of calcium overexcites the nerve cell, triggering the rapid, uncontrolled electrical firing characteristic of a seizure. This process, known as excitotoxicity, explains how severe hypomagnesemia directly causes convulsions.
Symptoms and Causes of Low Magnesium
Symptoms of hypomagnesemia are primarily related to the neuromuscular and cardiovascular systems. Early signs include fatigue, weakness, and decreased appetite. As the deficiency worsens, patients may experience muscle irritability, manifesting as twitching, tremors, and painful muscle cramps (tetany). Personality changes, such as apathy, confusion, or delirium, can also occur. Seizures and convulsions are signs of severe hypomagnesemia, often occurring when serum levels fall below 1.25 mg/dL. Hypomagnesemia usually results from excessive loss or reduced absorption, rather than inadequate dietary intake.
Primary Causes of Hypomagnesemia
Hypomagnesemia is typically caused by:
- Chronic alcohol use, which impairs nutrient absorption and increases magnesium excretion.
- Gastrointestinal disorders, such as chronic diarrhea, Celiac disease, or inflammatory bowel disease, which reduce absorption.
- Proton pump inhibitors (PPIs) used for acid reflux.
- Various types of diuretics, which increase the loss of magnesium through urination.
Diagnosis and Treatment
Diagnosing low magnesium begins with a blood test to measure the serum magnesium concentration, typically ranging between 1.8 and 2.2 mg/dL. A low level clearly indicates hypomagnesemia, though a normal blood level does not guarantee sufficient body stores since most magnesium is stored in cells and bones. Magnesium levels are routinely checked alongside other electrolytes during a seizure workup. Treatment depends on the severity of the deficiency and symptoms. Mild, asymptomatic cases are often corrected with oral supplements and dietary adjustments. When a patient presents with severe symptoms, such as an active seizure, cardiac arrhythmias, or tetany, immediate intravenous (IV) magnesium replacement is necessary. The goal of acute treatment is to quickly raise the concentration to a safe level to eliminate seizure activity. The underlying cause of the loss must also be identified and addressed to prevent recurrence.