School of Medical Sciences (Neuroscience), Brain and Mind Centre, University of Sydney, Camperdown, NSW, 2050, Australia.
Baker Heart and Diabetes Institute, Melbourne, VIC, 3004, Australia.
J Headache Pain. 2022 Jan 15;23(1):9. doi: 10.1186/s10194-021-01381-w.
The precise underlying mechanisms of migraine remain unknown. Although we have previously shown acute orofacial pain evoked changes within the brainstem of individuals with migraine, we do not know if these brainstem alterations are driven by changes in higher cortical regions. The aim of this investigation is to extend our previous investigation to determine if higher brain centers display altered activation patterns and connectivity in migraineurs during acute orofacial noxious stimuli.
Functional magnetic resonance imaging was performed in 29 healthy controls and 25 migraineurs during the interictal and immediately (within 24-h) prior to migraine phases. We assessed activation of higher cortical areas during noxious orofacial heat stimulation using a thermode device and assessed whole scan and pain-related changes in connectivity.
Despite similar overall pain intensity ratings between all three groups, migraineurs in the group immediately prior to migraine displayed greater activation of the ipsilateral nucleus accumbens, the contralateral ventrolateral prefrontal cortex and two clusters in the dorsolateral prefrontal cortex (dlPFC). Reduced whole scan dlPFC [Z + 44] connectivity with cortical/subcortical and brainstem regions involved in pain modulation such as the putamen and primary motor cortex was demonstrated in migraineurs. Pain-related changes in connectivity of the dlPFC and the hypothalamus immediately prior to migraine was also found to be reduced with brainstem pain modulatory areas such as the rostral ventromedial medulla and dorsolateral pons.
These data reveal that the modulation of brainstem pain modulatory areas by higher cortical regions may be aberrant during pain and these alterations in this descending pain modulatory pathway manifests exclusively prior to the development of a migraine attack.
偏头痛的确切潜在机制尚不清楚。尽管我们之前已经表明,偏头痛患者的脑干中会出现急性口面部疼痛诱发的变化,但我们不知道这些脑干变化是否是由皮质区域的变化引起的。本研究旨在扩展我们之前的研究,以确定偏头痛患者在急性口面部有害刺激期间,大脑高级中枢是否显示出改变的激活模式和连接。
在间歇期和偏头痛发作前 24 小时内,对 29 名健康对照者和 25 名偏头痛患者进行功能磁共振成像。我们使用热模设备评估了有害的口面部热刺激期间大脑高级区域的激活情况,并评估了全扫描和与疼痛相关的连接变化。
尽管所有三组的总体疼痛强度评分相似,但在偏头痛发作前组的偏头痛患者中,同侧伏隔核、对侧腹外侧前额叶皮层和前额叶背外侧皮层的两个簇的激活增加。偏头痛患者的全扫描背外侧前额叶皮层[Z+44]与涉及疼痛调节的皮质/皮质下和脑干区域的连接减少,如壳核和初级运动皮层。还发现,偏头痛发作前,背外侧前额叶皮层和下丘脑的连接与脑干疼痛调节区域(如腹侧吻端延髓和背外侧脑桥)的疼痛相关变化也减少。
这些数据表明,大脑高级区域对脑干疼痛调节区域的调节可能在疼痛期间异常,这种下行疼痛调节通路的改变仅在偏头痛发作前表现出来。