Migraine is a common neurological disorder. It is characterized by recurrent attacks of pulsatile headaches. Data achieved through familial hemiplegic migraine suggest that; mutations in channel proteins can lead dysregulation of calcium and sodium levels and hyperexcitability in nervous system. Even though, genetic tendencies can be responsible for migraine, accumulating data show that many metabolic or environmental factors can also trigger migraine attacks and its severity. Calcitonin gene-related peptide, nitric oxide, adipokines, neuropeptides, amino acids, and cytokines are all molecules shown to be involved both in migraine and obesity pathogenesis. In this paper, we take the metabolic approach to the problem and review the possible mechanisms take part in the pathogenesis of migraine to explore its relationship with obesity and inflammation.
Dildar Konukoglu and Eda Merve Kurtulus