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

Abstract

Neurology. 2002;58:1227‐1233. BACKGROUND: Previous single voxel (31)P MRS pilot studies of migraine patients have suggested that disordered energy metabolism or Mg(2+) 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 (31)P MR spectroscopic imaging. METHODS: Migraine with aura (MWA), migraine without aura (MwoA), and hemiplegic migraine patients were studied between attacks by (31)P 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 [Mg(2+)] in posterior brain. In MWA, phosphocreatine concentration ([PCr]) was decreased to a minor degree in anterior brain regions and a trend toward decreased [Mg(2+)] 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 [Mg(2+)] was significantly lower than in the posterior brain regions of control subjects. Trend analysis showed a significant decrease of brain [Mg(2+)] 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 [Mg(2+)] and membrane phospholipids that counteract cortical excitability. Comment: If the theory of hyperexcitability of migraine brain is correct, basic scientists will need to find clear markers for the neuronal abnormalities that underlie this excitability. Using their techniques, these researchers could not find such markers. SJT

1H-MRS of brain metabolites in migraine without aura: absolute quantification using the phantom replacement technique

“…Most of these studies suggested a metabolic disturbance in the brain of MwA patients and, to a lesser extent, of MwoA patients, which is evident even in the interictal period [10][11][12][13][14][15][16][17][18]. In MwoA, 1 H-MRS has only been performed following visual stimulation and using relative quantification.…”

“…One hypothesis is that migraine is a disorder that might be caused by the concurrence of two pathophysiological components: excessive cortical activation due to lack of habituation during repetitive stimulation as well as a decreased brain mitochondrial energy reserve [8,9]. In the last 20 years several magnetic resonance spectroscopy (MRS) studies, in particular phosphorus magnetic resonance spectroscopy ( 31 P-MRS), suggested an energy disturbance in the brain of migraine patients during interictal periods [10][11][12][13][14][15][16][17][18]. Recent studies emphasized more on proton magnetic resonance spectroscopy ( 1 H-MRS) with a lot of heterogenous, sometimes contradictory, results (Table 1).…”

Transcranial direct current stimulation in the prophylactic treatment of migraine based on interictal visual cortex excitability abnormalities: A pilot randomized controlled trial

“…It has been suggested that it could be the expression of a reduced inhibition consequent upon GABAergic system deficiency in occipital cortex [29,30]. Furthermore, insufficient glutamatergic function [31], mutations in the presynaptic calcium [32], low brain magnesium levels [33] and an abnormal mitochondrial energy metabolism [34][35][36] may also be involved.…”

Role of neuroimaging in our understanding of the pathogenesis of primary headaches

“…MRS studies have shown low phosphocreatine, high adenosine 5'-diphosphate, and low phosphocreatine:Pi ratios in patients with migraine. These findings have raised the question of whether there is a subset of migraine patients with mitochondrial energy defect [35].…”