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Contrasts in cortical magnesium, phospholipid and energy metabolism between migraine syndromes

From the Departments of Neurology (Drs. Boska, Welch, and Barker, and J.A. Nelson) and Biostatistics (Dr. Schultz), Henry Ford Hospital, Detroit, MI.

Address correspondence and reprint requests to M.D. Boska, Department of Radiology, University of Nebraska Medical Center, 981045 NE Medical Center, Omaha, NE 68198.

Background: Previous single voxel ³¹P MRS pilot studies of migraine patients have suggested that disordered energy metabolism or Mg²⁺ deficiencies may be responsible for hyperexcitability of neuronal tissue in migraine patients. These studies were extended to include multiple brain regions and larger numbers of patients by multislice ³¹P MR spectroscopic imaging.

Methods: Migraine with aura (MWA), migraine without aura (MwoA), and hemiplegic migraine patients were studied between attacks by ³¹P MRS imaging using a 3-T scanner.

Results: Results were compared with those in healthy control subjects without headache. In MwoA, consistent increases in phosphodiester concentration [PDE] were measured in most brain regions, with a trend toward increase in [Mg²⁺] in posterior brain. In MWA, phosphocreatine concentration ([PCr]) was decreased to a minor degree in anterior brain regions and a trend toward decreased [Mg²⁺] was observed in posterior slice 1, but no consistent changes were found in phosphomonoester concentration [PME], [PDE], inorganic phosphate concentration ([Pi]), or pH. In hemiplegic migraine patients, [PCr] had a tendency to be lower, and [Mg²⁺] was significantly lower than in the posterior brain regions of control subjects. Trend analysis showed a significant decrease of brain [Mg²⁺] and [PDE] in posterior brain regions with increasing severity of neurologic symptoms.

Conclusions: Overall, the results support no substantial or consistent abnormalities of energy metabolism, but it is hypothesized that disturbances in magnesium ion homeostasis may contribute to brain cortex hyperexcitability and the pathogenesis of migraine syndromes associated with neurologic symptoms. In contrast, migraine patients without a neurologic aura may exhibit compensatory changes in [Mg²⁺] and membrane phospholipids that counteract cortical excitability.

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