Neurovascular-immune mediator dynamics in migraine: State-dependent effects of caffeine
Khasawneh RR, Almahasneh FA, Abu-El-Rub E, Aljariri H, Kasasbeh A, Almazari RA
Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 0 citas
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- Diseño
- Ensayo controlado aleatorizado (indexado por PubMed)
- Estudiado en
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- Resultado principal
- Solo mecanismos
Quién lo pagó
- Financiación
- Financiación no declarada
Publicación
- Publicado
- 2026-06-08 · Neurol Sci · vol. 47 · número 7
- Editorial
- Springer Science+Business Media
- Citado
- 0 citas · más que el 42% de estudios similares · 0.0× el promedio de su campo
- Referencias
- 26 trabajos
- Acceso
- De pago
- Áreas de investigación
- Migraine and Headache Studies · Pain Mechanisms and Treatments · Neuropeptides and Animal Physiology
- Palabras clave
- migraine, caffeine, calcitonin gene-related peptide, nitric oxide, endothelin-1, interleukin-6, TNF-α, neuroinflammation, trigeminovascular system, ictal phase, interictal period, vasoconstriction, individual variability in response, migraine pathophysiology
- MeSH
- humans, nitric oxide, caffeine, endothelin-1, tumor necrosis factor-alpha, calcitonin gene-related peptide, central nervous system stimulants, interleukin-6, cross-over studies, double-blind method, adult, female, male, migraine disorders, young adult
6 autores
- Ramada R. Khasawneh🇯🇴 · autor de correspondenciaYarmouk University
- Fatimah A. Almahasneh🇯🇴Yarmouk University
- Ejlal M. Abu-El-Rub🇯🇴Yarmouk University
- Heba Aljariri🇯🇴Yarmouk University
- Amani Kasasbeh🇯🇴Yarmouk University
- Rawan A. Almazari🇯🇴Yarmouk University
Resumen
El texto original del estudio, en el idioma en que se publicó.
Background
Migraine is a complex neurovascular disorder involving interactions between trigeminovascular, endothelial, and neuroimmune pathways. Dysregulation of key mediators-calcitonin gene-related peptide (CGRP), nitric oxide (NO), endothelin-1, interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α)-is central to its pathophysiology. However, their phase-dependent dynamics and acute responsiveness to caffeine remain unclear. This study evaluated phase-specific alterations in these mediators and their intra-individual response to caffeine.
Methods
A total of 327 participants (174 migraine patients and 153 healthy controls) were included. Migraine patients were assessed across interictal and ictal phases using a within-subject design. During ictal attacks, participants underwent a randomized, double-blind, placebo-controlled crossover intervention with 200 mg caffeine or placebo. Blood samples were collected at baseline (T0) and 60 min post-intervention (T1). Mediators were measured using ELISA and analyzed with linear mixed-effects models.
Results
CGRP, NO, IL-6, and TNF-α were significantly elevated during migraine, particularly in the ictal phase, while endothelin-1 was reduced. Caffeine significantly decreased CGRP and NO levels and increased endothelin-1 compared with placebo. IL-6 and TNF-α showed modest reductions. Responses varied between individuals, with greater effects observed in those with higher baseline levels.
Conclusions
Migraine is characterized by dynamic, phase-dependent neurovascular and inflammatory alterations. Acute caffeine administration modulates key mediators, promoting a shift toward a more vasoconstrictive vascular balance and reduced trigeminovascular activation. These effects are influenced by baseline mediator levels, highlighting the importance of state-dependent responsiveness. The findings emphasize the need for temporally sensitive and individualized approaches in understanding migraine pathophysiology and therapeutic modulation.
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