PDF(Pubmed)
Abstract：
Limited clinical evidence is available regarding the potential effectiveness of anti-CGRP monoclonal antibodies for the preventive treatment of migraine with aura.
This observational study involved a series of migraine patients affected by either migraine with or without aura, who were investigated for any changes in their frequencies and their migraine aura attack characteristics observed during treatment with anti-CGRP Mabs over a 1-year period.
Twelve migraine patients were included, seven of whom were treated with erenumab, 2 with fremanezumab, and 3 with galcanezumab. Clinical data were collected at baseline, which were defined as 3 months prior to the initiation of treatment, and thereafter at each trimester, over the 1-year treatment period. The parameters included the number of headache and migraine days/month, the frequency of aura episodes, the number of days with acute drug intakes/month, and the scores from the migraine disability status scale (MIDAS), and the Headache Impact Test 6 (HIT-6).
Anti-CGRP Mbs antibodies induced significant decreases in mean headache and migraine without aura days per month, the number of days with medication intake, as well as MIDAS and HIT-6 scores (p < 0.0001). In contrast, the anti-CGRP Mab treatment did not appear to impact the frequency of migraine with aura attacks but seemed to reduce both the intensity and the duration of headache phases of migraine aura. Furthermore, some migraine patients referred to having aura attacks without headache over the course of the treatment period.
Based on the above findings, we hypothesize that anti-CGRP Mabs did not influence neuronal and vascular events related to cortical spreading depression (CSD) which is considered the pathophysiological substrate of aura. Conversely, these antibodies are able to counteract, via their peripheral mechanisms of action, the sensitization of the trigemino-vascular pathway which is triggered by CSD. This aforementioned might explain why in our patients, migraine aura attacks remained unchanged in their frequencies, but the headache phases were either reduced or absent.
This observational study involved a series of migraine patients affected by either migraine with or without aura, who were investigated for any changes in their frequencies and their migraine aura attack characteristics observed during treatment with anti-CGRP Mabs over a 1-year period.
Twelve migraine patients were included, seven of whom were treated with erenumab, 2 with fremanezumab, and 3 with galcanezumab. Clinical data were collected at baseline, which were defined as 3 months prior to the initiation of treatment, and thereafter at each trimester, over the 1-year treatment period. The parameters included the number of headache and migraine days/month, the frequency of aura episodes, the number of days with acute drug intakes/month, and the scores from the migraine disability status scale (MIDAS), and the Headache Impact Test 6 (HIT-6).
Anti-CGRP Mbs antibodies induced significant decreases in mean headache and migraine without aura days per month, the number of days with medication intake, as well as MIDAS and HIT-6 scores (p < 0.0001). In contrast, the anti-CGRP Mab treatment did not appear to impact the frequency of migraine with aura attacks but seemed to reduce both the intensity and the duration of headache phases of migraine aura. Furthermore, some migraine patients referred to having aura attacks without headache over the course of the treatment period.
Based on the above findings, we hypothesize that anti-CGRP Mabs did not influence neuronal and vascular events related to cortical spreading depression (CSD) which is considered the pathophysiological substrate of aura. Conversely, these antibodies are able to counteract, via their peripheral mechanisms of action, the sensitization of the trigemino-vascular pathway which is triggered by CSD. This aforementioned might explain why in our patients, migraine aura attacks remained unchanged in their frequencies, but the headache phases were either reduced or absent.
摘要：
背景：关于抗CGRP单克隆抗体用于预防先兆偏头痛的潜在有效性的临床证据有限。
目的：这项观察性研究涉及一系列偏头痛患者，无论有无先兆，在使用抗CGRPMab治疗1年期间，对他们的频率和偏头痛先兆发作特征进行了调查。
方法：纳入12例偏头痛患者，其中7人接受了erenumab治疗，2与Fremanezumab，和3与galcanezumab。在基线时收集临床数据，定义为治疗开始前3个月，然后在每三个月，在1年的治疗期间。参数包括头痛和偏头痛天数/月，先兆事件的频率，急性药物摄入天数/月，和偏头痛残疾状况量表(MIDAS)的评分，和头痛冲击测试6（HIT-6）。
结果：抗CGRPMbs抗体诱导平均头痛和偏头痛每月无先兆天数显著减少，服用药物的天数，以及MIDAS和HIT-6评分（p<0.0001）。相比之下,抗CGRPMab治疗似乎并未影响先兆偏头痛发作的频率,但似乎可降低先兆偏头痛头痛期的强度和持续时间.此外，一些偏头痛患者提到在治疗期间有先兆发作而没有头痛。
结论：基于上述发现，我们假设抗CGRP单克隆抗体不影响与皮质扩散抑制(CSD)相关的神经元和血管事件,CSD被认为是先兆的病理生理基础.相反，这些抗体能够抵消，通过它们的外围作用机制，CSD引发的三叉神经血管通路的敏化。前面提到的这可能解释了为什么在我们的病人中，偏头痛先兆发作的频率保持不变，但头痛阶段减少或不存在。
目的：这项观察性研究涉及一系列偏头痛患者，无论有无先兆，在使用抗CGRPMab治疗1年期间，对他们的频率和偏头痛先兆发作特征进行了调查。
方法：纳入12例偏头痛患者，其中7人接受了erenumab治疗，2与Fremanezumab，和3与galcanezumab。在基线时收集临床数据，定义为治疗开始前3个月，然后在每三个月，在1年的治疗期间。参数包括头痛和偏头痛天数/月，先兆事件的频率，急性药物摄入天数/月，和偏头痛残疾状况量表(MIDAS)的评分，和头痛冲击测试6（HIT-6）。
结果：抗CGRPMbs抗体诱导平均头痛和偏头痛每月无先兆天数显著减少，服用药物的天数，以及MIDAS和HIT-6评分（p<0.0001）。相比之下,抗CGRPMab治疗似乎并未影响先兆偏头痛发作的频率,但似乎可降低先兆偏头痛头痛期的强度和持续时间.此外，一些偏头痛患者提到在治疗期间有先兆发作而没有头痛。
结论：基于上述发现，我们假设抗CGRP单克隆抗体不影响与皮质扩散抑制(CSD)相关的神经元和血管事件,CSD被认为是先兆的病理生理基础.相反，这些抗体能够抵消，通过它们的外围作用机制，CSD引发的三叉神经血管通路的敏化。前面提到的这可能解释了为什么在我们的病人中，偏头痛先兆发作的频率保持不变，但头痛阶段减少或不存在。
