The following is the summary of “Migraine attacks are of peripheral origin: the debate goes on” published in the January 2023 issue of Headache and Pain by Do, et al.
Despite migraine’s widespread prevalence, the pathophysiological mechanisms that trigger episodes are still poorly understood and a subject of scholarly controversy. Researchers identify directions for future research that may shed light on whether the problem originated in the periphery or the center, and we discuss the most compelling evidence in favor of each scenario.
The trigeminovascular system, which includes the trigeminal nerve and its axonal projections to the cerebral blood vessels, is thought to have a role in the etiology of migraine. There is no doubt that both peripheral and central mechanisms contribute to migraine pathophysiology; however, how the activation phase of an attack begins remains unclear. Sensitization of perivascular sensory afferents early on in a migraine attack is evidence supporting a peripheral origin of attacks, meaning that the onset of symptoms occurs outside of the blood-brain barrier. Prodromal symptoms, migraine aura, and early and ongoing activation of central nervous system components all point to a central origin for migraines.
Input from peripheral nociceptive receptors is required for pain transmission, and cerebral activity is essential for the experience of pain, suggesting that both peripheral and central mechanisms contribute to a migraine’s severity. Whether a peripheral or central location initiates a migraine attack has not been settled. In the near future, significant reasons needed to address this question may be provided by the increased focus on prodromal symptoms and on the constrion of a human model of migraine aura. There will be no final resolution to the discussion until then.