EXPLORING THE POSSIBLE LINK BETWEEN G6PD DEFICIENCY INDUCE MIGRAINE: A REVIEW
Tiwari Pratibha, PrernaTiwari, Chirag Desai* and Arindam Paul
ABSTRACT
Migraine is a prevalent neurological disorder characterized by recurrent headaches, often accompanied by nausea, photophobia, and phonophobia. Although its exact pathophysiology remains unclear, growing evidence suggests that oxidative stress plays a crucial role in its development. An imbalance between reactive oxygen species (ROS) and antioxidant defenses may contribute to the frequency and severity of migraine attacks. This review explores the potential association between Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency and migraine, highlighting oxidative stress as a common pathological mechanism. G6PD deficiency disrupts the pentose phosphate pathway, leading to reduced glutathione production and increased oxidative susceptibility. While primarily affecting erythrocytes, this heightened oxidative stress may extend to the brain, exacerbating neuroinflammation and migraine pathogenesis. Additionally, individuals with G6PD deficiency often exhibit elevated Red Cell Distribution Width (RDW), a marker of systemic inflammation, which has been implicated in migraine development. Persistent oxidative stress in migraine sufferers, even between attacks, promotes neuroinflammation and central pain sensitization. Given these overlapping mechanisms, it is hypothesized that G6PD deficiency could intensify migraine symptoms. Targeting oxidative stress through antioxidant-based interventions and personalized migraine management strategies may offer therapeutic benefits, particularly for individuals with G6PD deficiency. Further research is needed to elucidate this relationship and develop optimized treatment approaches.
Keywords: Migraine, G6PD deficiency, oxidative stress, neuroinflammation, pentose phosphate pathway, antioxidant therapy
[Full Text Article]
[Download Certificate]