Headache in Calcified Neurocysticercosis: Emerging Insights into an Inflammation-Driven Phenotype

Calcified neurocysticercosis (NCC), traditionally considered an inert marker of past infection, is increasingly recognized as a clinically meaningful condition associated with migraine-like headaches. Evidence from population-based cohorts, clinical series, and imaging studies consistently shows that individuals with calcified NCC have a higher prevalence and severity of headache than those without lesions. Prospective neuroimaging demonstrates that intermittent perilesional inflammation, including edema and blood-brain barrier disruption, can activate migraine-generating pathways, with calcitonin gene-related peptide-mediated trigeminovascular sensitization emerging as a key mechanism. These findings challenge the assumption that calcified lesions are clinically irrelevant and instead, support the concept of a distinct inflammation-driven headache phenotype. Recognizing this entity has important implications for diagnosis, counseling, and therapeutic decision-making, particularly in endemic regions where calcifications are common and often dismissed as incidental. Calcified NCC also provides a unique human model for understanding how focal neuroinflammation shapes headache susceptibility.