Headache Centre, Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Naples, Italy.
Advanced MRI Neuroimaging Centre, Department of Advanced Medical and Surgical Sciences, University of Campania "Luigi Vanvitelli", Naples, Italy.
J Headache Pain. 2024 Oct 15;25(1):180. doi: 10.1186/s10194-024-01885-1.
Although neuroimaging investigations have consistently demonstrated that "hyperresponsive" and "hyperconnected" visual cortices may represent the functional substrate of cortical spreading depolarization in patients with migraine with aura, the mechanisms which underpin the brain "tendency" to ignite the cortical spreading depolarization and, consequently, aura phenomenon are still matter of debate. Considering that triggers able to induce aura phenomenon constrain brain to increase global (such as physical activity, stressors and sleep abnormalities) or local (such as bright light visual stimulations) energy demand, a vascular supply unable to satisfy the increased energy requirement could be hypothesized in these patients.
Twenty-three patients with migraine with aura, 25 patients with migraine without aura and 20 healthy controls underwent a 3-Tesla MRI study. Cerebral blood flow and local functional connectivity (regional homogeneity) maps were obtained and registered to the MNI space where 100 cortical regions were derived using a functional local-global normative parcellation. A surrogate estimate of the regional neurovascular coupling for each subject was obtained at each parcel from the correlation coefficient between the z-scored ReHo map and the z-scored cerebral blood flow maps.
A significantly higher regional cerebral blood flow across the visual cortex of both hemispheres (i.e. fusiform and lingual gyri) was detected in migraine with aura patients when compared to patients with migraine without aura (p < 0.05, corrected for multiple comparisons). Concomitantly, a significantly reduced neurovascular coupling (p < 0.05, false discovery rate corrected) in the primary visual cortex parcel (VIS-4) of the large-scale visual network was observed in the left hemisphere of patients with migraine with aura (0.23±0.03), compared to both patients with migraine without aura (0.32±0.05) and healthy controls (0.29±0.05).
Visual cortex neurovascular "decoupling" might represent the "link" between the exposure to trigger factors and aura phenomenon ignition. While physiological vascular oversupply may compensate neurovascular demand-supply at rest, it becomes inadequate in case of increased energy demand (e.g. when patients face with trigger factors) paving the way to the aura phenomenon ignition in patients with migraine with aura. Whether preventive treatments may exert their therapeutic activity on migraine with aura restoring the energy demands and cerebral blood flow trade-off within the visual network should be further investigated.
尽管神经影像学研究一致表明，“超反应性”和“超连接性”的视觉皮层可能代表偏头痛伴先兆患者皮质扩散性抑制的功能基础，但支持大脑“倾向”引发皮质扩散性抑制进而引发先兆现象的机制仍存在争议。鉴于能够引发先兆现象的触发因素迫使大脑增加全局（如体力活动、应激和睡眠异常）或局部（如强光视觉刺激）的能量需求，在这些患者中，可能存在血管供应无法满足增加的能量需求的假设。
23 例偏头痛伴先兆患者、25 例偏头痛无先兆患者和 20 例健康对照者接受了 3T MRI 研究。获得脑血流和局部功能连接（局部一致性）图，并将其注册到 MNI 空间，使用功能局部-全局规范分割方法得出 100 个皮质区。从 z 分数 ReHo 图与 z 分数脑血流图之间的相关系数，获得每个被试每个区的局部神经血管耦合的替代估计值。
与偏头痛无先兆患者相比，偏头痛伴先兆患者双侧半球（即梭状回和舌回）视觉皮层的区域脑血流显著增加（p<0.05，多重比较校正）。同时，在偏头痛伴先兆患者的左侧半球，大尺度视觉网络的初级视觉皮层区（VIS-4）的神经血管耦合显著降低（p<0.05，假发现率校正）（0.23±0.03），与偏头痛无先兆患者（0.32±0.05）和健康对照组（0.29±0.05）相比。
视觉皮层神经血管“解耦”可能是暴露于触发因素与先兆现象点火之间的“联系”。虽然生理性血管过度供应可能在休息时补偿神经血管供需，但在能量需求增加时（例如当患者面临触发因素时），这种供应就变得不足，从而为偏头痛伴先兆患者的先兆现象点火铺平道路。预防性治疗是否可以通过恢复视觉网络内的能量需求和脑血流平衡来发挥其治疗偏头痛伴先兆的作用，还需要进一步研究。
