Changes in oxidative stress and inflammation biomarkers in the pathogenesis of migraine: possible relationships with lipid metabolism.

INTRODUCTION

Migraine is a common neurological disease that limits daily life. Researchers have proposed various mechanisms in the pathogenesis of migraine, including vascular dysfunction, neurogenic inflammation, oxidative stress, and stimulation of the trigeminovascular system. Studies consistently demonstrate the impact of oxidative stress and neurogenic inflammation on lipid metabolism. Although causality cannot be definitively established, several studies suggest that migraine may be associated with alterations in lipid metabolism, potentially resulting in an atherogenic lipid profile. This study aimed to investigate the status of oxidative stress and inflammation during the interictal phase of migraine and explore their potential impact on lipid metabolism.

METHODS

The Neurology outpatient clinic included fifty-seven migraine patients and thirty control cases. Migraine diagnosis and classification were made according to the International Classification of Headache Disorders (ICHD-3), with clear categorization into episodic or chronic migraine and migraine with aura (MWA) or without aura (MWoA). Serum levels of malondialdehyde (MDA, a marker of lipid peroxidation), glutathione (GSH, an antioxidant), NOD-like receptor family pyrin domain containing 3 (NLRP3, an inflammasome component), and nuclear factor kappa B (NF-κB, a proinflammatory transcription factor), as well as lipid parameters and headache characteristics, were assessed. CRP levels were measured via standard turbidimetric method; MDA and GSH were determined using spectrophotometric methods; NLRP3 and NF-κB were analyzed using ELISA kits per manufacturer protocols.

RESULTS

In migraine patients, MDA and CRP levels significantly increased, while GSH and NLRP3 levels significantly decreased (p < 0.05). Subgroup analysis revealed that CRP and NLRP3 levels were significantly different between MWA and MWoA groups. Additionally, LDL levels were higher in patients with MWA.

CONCLUSIONS

This study demonstrates a statistically significant association between elevated oxidative stress (increased MDA, decreased GSH), altered inflammatory response (elevated CRP, reduced NLRP3), and migraine. Differences between MWA and MWoA suggest subtype-specific pathophysiological mechanisms. Although this study supports a potential link between oxidative stress, inflammation, and lipid metabolism in migraine, they do not establish causality. These biomarkers may represent targets for future diagnostic and therapeutic strategies.