¶ Migraine is a chronic neurological disorder characterized by attacks of moderate or severe headache and reversible neurological and systemic symptoms.
Accordingly with Dodik (2018), the following mechanisms are involved in each phase:
¶ Premonitory phase
The premonitory phase is the earliest stage of a migraine attack and it starts in the CNS, with activation in the posterior and lateral regions of the hypothalamus and adjacent midbrain ventral tegmentum. Migraine is commonly triggered by alterations in homoeostasis (eg, changes in sleep–wake cycles, missed meals).
¶ Aura
Cortical spreading depression (CSD) is thought to be the underlying physiological cause of the aura. CSD is an extreme depolarization of glial and neuronal cell membranes that results in disruption of ionic gradients, a rise in extracellular potassium concentrations, release of glutamate, and a transient increase followed by a decrease in cerebral blood flow. The spread of a CSD wave across neural tissue occurs at a rate of 2–6 mm/min—similar to the progression of the fortification spectra and cerebral oligaemia seen on cerebral blood flow imaging during aura in human beings.
¶ Headache
The headache phase of migraine is due to activation of trigeminal sensory pathways that innervate pain-sensitive intracranial structures, including the eye, dura mater, large cerebral and pial blood vessels, and the dural venous sinuses. These structures are supplied by a plexus of largely unmyelinated fibers that project from the ophthalmic division of the trigeminal nerve and the upper cervical spinal roots. These peripheral trigeminal sensory afferents converge and synapse on second-order neurons in the trigeminal cervical complex.
Neuropeptides are implicated in trigeminal activation, and calcitonin gene-related peptide in particular has become a promising target of therapeutic intervention for migraine.
¶ Postdrome
The final phase of migraine is the postdrome, the period of time from the resolution of headache symptoms until return to baseline following a migraine. People often report neuropsychiatric, sensory, gastrointestinal, and general symptoms during this time, which can limit activity. (Qubty, 2020)
¶ Anatomical sites involved (Charles, 2018)
¶ References
Charles A. The pathophysiology of migraine: implications for clinical management. Lancet Neurol. 2018 Feb;17(2):174-182. doi: 10.1016/S1474-4422(17)30435-0. Epub 2017 Dec 8. PMID: 29229375.
Dodick DW. Migraine. Lancet. 2018 Mar 31;391(10127):1315-1330. doi: 10.1016/S0140-6736(18)30478-1. Epub 2018 Mar 6. PMID: 29523342.
Qubty W, Patniyot I. Migraine Pathophysiology. Pediatr Neurol. 2020 Jun;107:1-6. doi: 10.1016/j.pediatrneurol.2019.12.014. Epub 2020 Feb 4. PMID: 32192818.