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Central nervous system magnesium deficiency.

W F Langley¹, D Mann

¹Holy Cross Hospital, Fort Lauderdale, Fla.

Archives of Internal Medicine

|March 1, 1991

Summary

This summary is machine-generated.

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Magnesium (Mg++) is vital for central nervous system function, with low levels causing neurologic dysfunction. Bone magnesium (Mg++) dynamics and parathyroid gland activity significantly impact brain Mg++ levels and neurological health.

Area of Science:

Neurology
Biochemistry
Endocrinology

Background:

Magnesium (Mg++) is essential for central nervous system (CNS) function, with critical levels required to prevent neurological dysfunction.
The parathyroid gland regulates calcium and magnesium (Mg++) homeostasis, influencing Mg++ levels in the CNS, extracellular fluid, and bone.
Skeletal magnesium (Mg++) stores are dynamic and can be rapidly depleted, particularly when parathyroid gland activity is altered.

Observation:

The interchange of magnesium (Mg++) between cerebrospinal fluid, extracellular fluid, and bone is more rapid than previously understood.
Hypertrophied parathyroid glands associated with skeletal Mg++ depletion can lead to decreased CNS Mg++ levels.
Increased serum calcium can activate the skeletal buffer system, potentially lowering CNS Mg++.

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Findings:

Prolonged parathyroid gland inhibition and extreme skeletal Mg++ depletion can result in severe neurological symptoms, including seizures, coma, and death.
External stimuli like noise and excitement can precipitate neurological symptoms in Mg++-deficient individuals, mirroring findings in animal models.
Acute CNS demyelinating syndromes may share similarities with reactive CNS Mg++ deficiency.

Implications:

Understanding the dynamic relationship between bone Mg++, parathyroid function, and CNS Mg++ is crucial for diagnosing and treating neurological disorders.
Therapeutic strategies targeting magnesium (Mg++) levels may be beneficial for certain neurological conditions, including CNS demyelinating syndromes.
Further research into Mg++'s role in neurological function and its regulation by the parathyroid gland is warranted.