Boska M D, Welch K M A, Barker P B, Nelson J A, Schultz L
Department of Neurology, Henry Ford Hospital, Detroit, MI, USA.
Neurology. 2002 Apr 23;58(8):1227-33. doi: 10.1212/wnl.58.8.1227.
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.
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 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.
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.
先前对偏头痛患者进行的单体素（31）P MRS 初步研究表明，能量代谢紊乱或镁离子（Mg(2+)）缺乏可能是偏头痛患者神经组织兴奋性过高的原因。这些研究通过多层（31）P MR 波谱成像扩展到包括多个脑区和更多患者。
使用 3-T 扫描仪，在发作间期对有先兆偏头痛（MWA）、无先兆偏头痛（MwoA）和偏瘫性偏头痛患者进行（31）P MRS 成像研究。
将结果与无头痛的健康对照受试者的结果进行比较。在 MwoA 中，大多数脑区的磷酸二酯浓度[PDE]持续升高，后脑的[Mg(2+)]有升高趋势。在 MWA 中，前脑区域的磷酸肌酸浓度（[PCr]）略有降低，在切片 1 后部观察到[Mg(2+)]有降低趋势，但磷酸单酯浓度[PME]、[PDE]、无机磷酸盐浓度（[Pi]）或 pH 没有一致变化。在偏瘫性偏头痛患者中，[PCr]有降低趋势，且[Mg(2+)]显著低于对照受试者的后脑区域。趋势分析显示，随着神经症状严重程度增加，后脑区域的脑[Mg(2+)]和[PDE]显著降低。
总体而言，结果支持能量代谢无实质性或一致性异常，但据推测镁离子稳态紊乱可能导致大脑皮层兴奋性过高以及与神经症状相关的偏头痛综合征的发病机制。相比之下，无神经先兆的偏头痛患者可能在[Mg(2+)]和膜磷脂方面表现出代偿性变化，以抵消皮层兴奋性。
