When Stress Becomes Pain: Hpa Axis Dysregulation and the Neurobiology of Migraine

Migraine is considered to be the most disabling neurological disorder involving sensitization to light and sound accompanied by nausea and/or vomiting, and the marking feature of migraine is a pulsating headache lasting between 4–72 hours. Emerging evidence presents migraine as a disorder that is linked with allostatic load. This review aims at examining how HPA-axis dysfunction has a role to play in the chronicification of migraine via the neuro-inflammatory pathways and evaluates the potential of non-pharmacological, stress-focused interventions. Literature points that individuals with chronic migraine pain frequently show altered levels of basal cortisol, disrupted diurnal rhythms and blunted cortisol awakening responses alongside elevated cytokines like interleukin‑6 and tumor necrosis factor‑α. The changes in the immune system lead to activation of microglial and central sensitization in the pain-processing circuit, reducing the threshold for migraine attacks and continuing with a self-perpetuating cycle of pain and stress. The initial data suggest that mindfulness programs, yoga, cognitive therapies, and relaxation training may influence HPA Axis activity and inflammatory activities in the body, though the findings remain mixed, and the mechanisms behind it are still not fully understood. Overall, the present evidence supports a meaningful link between HPA-axis dysregulation, neuro inflammation, and migraine chronicity, shedding light upon the need for integrated, biomarker-informed trials of non- pharmacological interventions.