Metabolic Syndrome in Migraine Patients: Recent Findings and Treatment Approach

Abstract

The neurovascular theory explains migraine to be a result of complex pathophysiological changes leading to activation of trigeminal nociceptors by several inflammatory mediators. Different classes of drugs have been used to control migraine where specific class of drugs inhibit only specific mediators while sparing others, resulting into suboptimal treatment response. Migraine is also reported by a significant proportion of patients suffering with various metabolic syndrome related conditions. The chronic inflammation caused by metabolic disruptions has been the leading cause that contributes in inducing and worsening migraine attacks. Treating these patients for conditions such as obesity and insulin resistance has resulted in significant improvement in alleviating migraine episodes. These findings provide opportunities to devise a comprehensive migraine treatment regimen that combines pharmacotherapy with metabolic corrections, lifestyle changes and diet therapy to achieve improved treatment outcome. Metabolic Syndrome in Migraine Patients Migraine and Current Treatment OptionsMigraine is the third most prevalent neurological disorder worldwide. As per the latest estimate, US have 38 million migraine patients, with women comprising 85% of them [1]. It is more debilitating than a simple headache due to associated 'aura' like conditions that includes nausea, photophobia or phonophobia. The pathophysiological basis of migraine has been explained in terms of neurological changes originating from hypothalamus and brainstem and spreading to central trigeminovascular neurons where consequent inflammatory pathways release various inflammatory mediators including histamine, prostaglandins, leukotrienes, cytokines and tryptase [2]. These mediators act on pain nociceptors of trigeminovascular system inducing headache. While neurological theory has gained more support recently, vascular theory was once considered as the root cause of the migraine. As per vascular theory, abnormal vasodilation of cranial blood vessels results into release of pain mediators which activate pain nociceptors located on trigeminal nerves that closely follow cranial blood vessels [3]. More recently, research is focused on CGRP as pain mediator. CGRP is a prominent neuropeptide expressed in 35-50% of neurons in the trigeminal ganglia and exert vasodilation effect [4].