Department of Neurology, King George Medical University, Lucknow, Uttar Pradesh, India.
Department of Neurology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India.
Am J Trop Med Hyg. 2022 Oct 10;107(6):1190-1195. doi: 10.4269/ajtmh.22-0335. Print 2022 Dec 14.
Recently, inflammation and free-radical release has been described in the surrounding brain parenchyma of seemingly inert calcified lesions of neurocysticercosis. These free radicals can induce migraine by stimulating calcitonin gene-related peptide release. This stipulated mechanism led us to hypothesize that calcified neurocysticercosis may increase migraine severity. This case-control study included patients (migraine with calcified neurocysticercosis) and control subjects (migraine without calcified neurocysticercosis) in a 1:1 ratio. Headache frequency, visual analog scale (VAS) score, and Migraine Disability Assessment (MIDAS) score were assessed at baseline and at the end of 3 months. To compare treatment responsiveness between patients and control subjects, we treated both groups identically so that difference in treatment would not confound the results. Each group comprised 78 patients. Baseline headache frequency (11.3 ± 3.3 versus 7.9 ± 3.4), VAS score (7.5 ± 1.1 versus 6.0 ± 1.2), and MIDAS score (15 ± 7.6 versus 9.6 ± 4.5) were significantly greater in patients than control subjects. Interestingly, the change from baseline to the end of 3 months in headache frequency (6.0 ± 1.7 versus 2.8 ± 1.4), VAS score (2.6 ± 0.02 versus 1.4 ± 0.01), and MIDAS score (8.3 ± 5.0 versus 3.6 ± 2.0) were significantly greater in patients than control subjects. Our study emphasizes that calcified lesions of neurocysticercosis are not inert, and cause an increase in the frequency and severity of migraine attacks. Interestingly, these patients also showed a better response to treatment with amitriptyline, possibly resulting from its anti-inflammatory action. Further studies are warranted to explore possible inflammatory mechanisms in calcified neurocysticercosis, which influences migraine physiology.
最近，在看似惰性的囊虫性脑囊尾蚴钙化病灶的周围脑组织中，已经描述了炎症和自由基释放。这些自由基可以通过刺激降钙素基因相关肽的释放来诱发偏头痛。这个规定的机制使我们假设钙化性脑囊虫病可能会增加偏头痛的严重程度。这项病例对照研究包括患者（钙化性脑囊虫病伴偏头痛）和对照组（无钙化性脑囊虫病伴偏头痛），比例为 1:1。在基线和 3 个月结束时评估头痛频率、视觉模拟量表（VAS）评分和偏头痛残疾评估（MIDAS）评分。为了比较患者和对照组之间的治疗反应，我们对两组进行了相同的治疗，以避免治疗差异影响结果。每组包括 78 名患者。基线时头痛频率（11.3±3.3 比 7.9±3.4）、VAS 评分（7.5±1.1 比 6.0±1.2）和 MIDAS 评分（15±7.6 比 9.6±4.5）在患者中显著高于对照组。有趣的是，从基线到 3 个月结束时，头痛频率（6.0±1.7 比 2.8±1.4）、VAS 评分（2.6±0.02 比 1.4±0.01）和 MIDAS 评分（8.3±5.0 比 3.6±2.0）在患者中显著大于对照组。我们的研究强调，神经囊尾蚴病的钙化病灶并非惰性，会导致偏头痛发作的频率和严重程度增加。有趣的是，这些患者对阿米替林的治疗反应也更好，这可能是由于其抗炎作用。需要进一步的研究来探索钙化性神经囊尾蚴病中可能的炎症机制，这会影响偏头痛的生理。
