Studies suggest that obesity is associated with migraine progression from an episodic into a chronic form. We discuss putative mechanisms to justify this relationship. Several of the inflammatory mediators that are increased in obese individuals are important in migraine pathophysiology, including interleukins and calcitonin gene-related peptide. Both migraine and obesity are prothrombotic states. Substances that are important in metabolic control are nociceptive at certain levels. Hypothalamic dysfunction in the orexin pathways seems to be a risk factor for both conditions. In addition, we discuss the importance of metabolic syndrome and autonomic dysfunction in modulating the obesity/migraine progression relationship.
ASJC Scopus subject areas
- Clinical Neurology
- Anesthesiology and Pain Medicine