1 Institute of Brain Science, National Yang-Ming University, Taipei, Taiwan.
2 Department of Neurology, Neurological Institute, Taipei Veterans General Hospital, Taipei, Taiwan.
Cephalalgia. 2018 Jun;38(7):1225-1236. doi: 10.1177/0333102417728751. Epub 2017 Aug 30.
Background The role of central pulsatile hemodynamics in the pathogenesis of white matter hyperintensities in migraine patients has not been clarified. Methods Sixty patients with migraine (20-50 years old; women, 68%) without overt vascular risk factors and 30 demographically-matched healthy controls were recruited prospectively. Cerebral white matter hyperintensities volume was determined by T1-weighted magnetic resonance imaging with CUBE-fluid-attenuated-inversion-recovery sequences. Central systolic blood pressure, carotid-femoral pulse wave velocity, and carotid augmentation index were measured by applanation tonometry. Carotid pulsatility index was derived from Doppler ultrasound carotid artery flow analysis. Results Compared to the controls, the migraine patients had higher white matter hyperintensities frequency (odds ratio, 2.75; p = 0.04) and greater mean white matter hyperintensities volume (0.174 vs. 0.049, cm, p = 0.04). Multivariable regression analysis showed that white matter hyperintensities volume in migraine patients was positively associated with central systolic blood pressure ( p = 0.04) and carotid-femoral pulse wave velocity ( p < 0.001), but negatively associated with carotid pulsatility index ( p = 0.04) after controlling for potential confounding factors. The interaction effects observed indicated that the influence of carotid-femoral pulse wave velocity ( p = 0.004) and central systolic blood pressure ( p = 0.03) on white matter hyperintensities formation was greater for the lower-carotid pulsatility index subgroup of migraine patients. White matter hyperintensities volume in migraine patients increased with decreasing carotid pulsatility index and with increasing central systolic blood pressure or carotid-femoral pulse wave velocity. Conclusions White matter hyperintensities are more common in patients with migraine than in healthy controls. Increased aortic stiffness or central systolic blood pressure in the presence of low intracranial artery resistance may predispose patients with migraine to white matter hyperintensities formation.
背景 偏头痛患者脑白质高信号(WMH)发病机制中心脉动血流动力学的作用尚不清楚。
方法 前瞻性招募 60 名偏头痛患者(20-50 岁;女性占 68%)和 30 名年龄匹配的健康对照者。采用 T1 加权磁共振成像 CUBE 液体衰减反转恢复序列确定脑白质高信号体积。应用平板压力测定法测量中心收缩压、颈股脉搏波速度和颈动脉增强指数。通过多普勒超声颈动脉血流分析得出颈动脉搏动指数。
结果 与对照组相比,偏头痛患者脑白质高信号的发生率更高(比值比 2.75;p=0.04),平均脑白质高信号体积更大(0.174 比 0.049,cm,p=0.04)。多变量回归分析显示,在偏头痛患者中,脑白质高信号体积与中心收缩压(p=0.04)和颈股脉搏波速度(p<0.001)呈正相关,但与颈动脉搏动指数呈负相关(p=0.04),在控制潜在混杂因素后。观察到的交互效应表明,对于颈动脉搏动指数较低的偏头痛患者亚组,颈股脉搏波速度(p=0.004)和中心收缩压(p=0.03)对脑白质高信号形成的影响更大。偏头痛患者的脑白质高信号体积随着颈动脉搏动指数的降低以及中心收缩压或颈股脉搏波速度的增加而增加。
结论 偏头痛患者的脑白质高信号比健康对照组更常见。颅内动脉阻力降低时主动脉僵硬度或中心收缩压升高可能使偏头痛患者易发生脑白质高信号形成。