Impact of perilesional edema on severity of migraine in patients with calcified neurocysticercosis: A prospective evaluation.

Objectives: Recent research has sparked increasing interest in the role of neuroinflammation in the pathogenesis of migraine. We hypothesize that perilesional edema, an imaging marker of inflammation caused by an immune response in the brain parenchyma surrounding calcified neurocysticercosis (NCC), may influence migraine pathophysiology. This study was designed to explore the potential impact of perilesional edema on migraine severity and treatment response.

Background: Cranial imaging of patients with primary headache may sometimes reveal calcified lesions indicative of calcified NCC. These lesions were once considered incidental and harmless findings. However, recent studies have shown that such calcifications are more frequently associated with headaches. Some research suggests that patients with calcified brain lesions experience more frequent and severe migraine compared to those without these lesions, though the pathophysiology underlying this association remains unclear.

Methods: This single-center, prospective cohort study was conducted at King George Medical University, India, from September 2022 to September 2024. A total of 80 patients with migraine with calcified NCC were enrolled. Cranial magnetic resonance imaging with contrast was used to detect perilesional edema. Patients were divided into two groups based on the presence (Group A) or absence (Group B) of perilesional edema. Both groups were assessed for migraine frequency, severity, and disability using standard scales. They were treated with standard migraine therapy and followed up for 3 months. Statistical analysis was performed to compare migraine characteristics, treatment responses, and disability between the two groups.

Results: Perilesional edema was observed in six of the 80 patients (7.5%). At presentation, Group A (those with perilesional edema) experienced more frequent migraine, with a mean (standard deviation [SD]) of 22.5 (4.4) days/month, compared to Group B (those without perilesional edema), which averaged 8.2 (2.7) days/month. The headaches in Group A were also more severe, as indicated by higher median visual analog scale scores (median [interquartile range, IQR] in Group A of 10.0 [8.5-10.0] and 7 [7.0-8.0] in Group B, p < 0.001). Disability scores were significantly higher in Group A, with higher median scores on the Migraine Disability Assessment Scale (median [IQR] score in Group A of 43 [40.5-48.5] and 21.5 [17.0-26.3] in Group B, p < 0.001) and six-item Headache Impact Test (median [IQR] score in Group A of 66 [64.25-71.23] and 57 [54.8-62.0] in Group B, p < 0.001) scales. Although both groups showed improvement over 3 months of treatment, Group A continued to experience greater migraine severity. In Group A, the mean (SD) headache frequency was 22.5 (4.4) at presentation, 14.0 (1.6) at 30 days, 10.7 (1.6) at 60 days, and 9.2 (2.0) at 90 days (p < 0.001). Similarly, in Group B, headache frequency decreased over time, with a mean (SD) of 8.2 (2.7) at presentation, 3.8 (1.7) at 30 days, 2.3 (1.0) at 60 days, and 1.9 (1.0) at 90 days (p < 0.001). After 30 days, there was a significant reduction in the use of abortive medications, with more patients in Group B (56/74 [76%]) showing a favorable response compared to Group A (2/6 [33%]; p = 0.046; odds ratio 0.16, 95% confidence interval 0.03-0.95).

Conclusions: Our study found that among patients with migraine with calcified NCC, those with perilesional edema experienced more severe and harder-to-treat migraine compared to those without perilesional edema. These findings suggest that perilesional edema may influence the underlying mechanisms of migraine, leading to more severe migraine episodes.