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Mitochondria, magnesium and migraine

K M Welch¹, N M Ramadan

¹Department of Neurology, K-11 Henry Ford Hospital and Health Sciences Center, Detroit, MI 48202, USA.

Journal of the Neurological Sciences

|December 1, 1995

Summary

Migraine attacks may stem from brain energy metabolism issues, specifically disordered mitochondrial function and low magnesium levels. These metabolic changes between attacks create neuronal instability, increasing migraine susceptibility.

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Area of Science:

Biochemistry
Neuroscience
Mitochondrial Biology

Background:

Migraine is a debilitating neurological disorder.
Evidence suggests mitochondrial dysfunction in migraine patients.
Reduced intracellular free magnesium is observed in migraine sufferers.

Purpose of the Study:

To review the evidence for mitochondrial oxidative phosphorylation and magnesium level disturbances in migraine.
To propose a mechanism linking metabolic shifts to migraine susceptibility.

Main Methods:

Literature review of studies on mitochondrial function and magnesium levels in migraine.
Analysis of metabolic changes in brain and body tissue.

Main Results:

Disordered mitochondrial oxidative phosphorylation is evident in migraine sufferers.
Reduced intracellular free magnesium is consistently found in migraine patients.
These metabolic alterations occur both between and during migraine attacks.

Conclusions:

Metabolic shifts, including impaired mitochondrial function and low magnesium, contribute to neuronal instability.
This instability between attacks enhances susceptibility to developing a migraine attack.
Targeting mitochondrial function and magnesium levels may offer novel therapeutic strategies for migraine.

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