A migraine attack can last from hours to days. Migraine is a disorder that usually occurs as recurrent attacks. Also, hemiplegic migraine (migraine with motor weakness) is believed to be dominantly inherited. Mutations in three different ion channel genes, CACNA1A, SCN1A, and ATP1A2, are found to be causal in migraine disorders in family studies. Some migraine disorders are believed to be caused due to mutations in a single gene, while others are caused due to polymorphisms in many genes.

The genetic basis of migraines is complex. Sensitization also explains the throbbing quality of migraine pain, hyperalgesia, and worsening pain with coughing and sudden head movements. Sensitization in primary afferent neurons, the second-order neurons in the trigeminal nucleus caudalis, and higher-order neurons in the central nervous system play a role in migraine attacks. The process of neurons becoming increasingly sensitive to nociceptive and non-nociceptive stimulation is called sensitization. It is also involved in the vasodilatory component of neurogenic inflammation. It mediates pain transmission to the central nervous system from the intracranial vessels. CGRP is a neuropeptide that has a vasodilatory effect on the cerebral and the dural vessels. Serotonin is thought to be involved in the pathogenesis of migraines due to its direct action on the cranial vasculature and its role in central pain control pathways.Ĭalcitonin gene-related peptide (CGRP) plays an essential role in the pathogenesis of migraines. It could mediate by acting directly over the cranial vessels or in central pain control pathways, or by cortical projections of brainstem serotonergic nuclei. Most likely, serotonin levels are low between attacks because it may cause a deficiency in the serotonin pain inhibition system, therefore helping the activation of the trigeminal system. Serotonin, released from the brainstem serotonergic nuclei, may play a role in migraine however, the exact role of its mechanisms remains a matter of controversy. The convergence of these projections at the trigeminal nucleus caudalis explains the distribution of migraine pain that involves anterior and posterior regions of the head and the upper neck. Trigeminal ganglion stimulation leads to the release of vasoactive neuropeptides like substance P, neurokinin A, and calcitonin-gene-related peptide (CGRP), which in turn leads to neurogenic inflammation. The trigeminovascular system consists of sensory neurons originating from the trigeminal ganglion and upper cervical dorsal roots: these sensory neurons project to innervate large cerebral vessels, dura mater, and dial vessels. This activates the trigeminal afferents, which cause inflammatory changes in the meninges, leading to pain.Īctivation of the trigeminovascular system is also believed to be involved in the pathophysiology of migraine. Neuronal and glial depolarization spreading across the cerebral cortex is thought to cause the aura of the migraine. Multiple mechanisms are believed to be involved in the pathophysiology of migraines. Some of the precipitating factors for migraine headaches include: Withdrawn or exposure to several factors contribute to the development of migraine headaches. A retrospective study found that 76% of the patients reported triggers. Identifying these genes in an individual with migraines could predict the targeted prophylactic treatment. The risk of migraines in ill relatives is three times greater than that of relatives of non-ill subjects, but no inheritance pattern was identified. The genetic basis of migraine is complex, and it is uncertain which loci and genes are the ones implicated in the pathogenesis it may be based on more than one genetic source at different genomic locations acting in tandem with environmental factors to bring susceptibility and the characteristics of the disease in such individuals. This, in turn, activates trigeminal afferents, which cause inflammatory changes in the pain-sensitive meninges that generate the migraine headache through central and peripheral reflex mechanisms. It is believed that a primary neuronal dysfunction leads to a sequence of changes intracranially and extracranially, which causes migraines. The aura of migraine is thought to be due to neuronal and glial depolarization that spreads across the cerebral cortex. The exact etiology of various aspects of migraine is not completely understood.

Migraine with aura definition