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About Migraine

Migraine is a prevalent disabling neurological disease with attacks that can vary in intensity of pain and in associated symptoms, such as aura, nausea, photophobia and phonophobia1,2

 

Theories on the underlying cause of migraine have evolved with recent research and we now know more than ever about its pathophysiology. Regardless of the initial trigger of migraine, the headache is generally thought to involve the activation of the trigeminovascular system (TGVS), a catalyst for the release of vasoactive neuropeptides, such as calcitonin gene-related peptide (CGRP), that cause inflammation and vasodilation leading to head pain.3 Migraine aura has been attributed to cortical spreading depression (CSD), characterized by changes in blood flow and brain activity. Recent evidence also indicates that CSD plays a role in activation of the TGVS, leading to peripheral sensitization of the trigeminal nerve, followed by central sensitization.3

The role of CGRP

CGRP is a neuropeptide widely distributed in the nervous system, where it is thought to play a role in several processes, including vasodilation of cerebral and dural vessels, release of inflammatory mediators and transmission of nociceptive signals to the central nervous system.4,5


Several lines of evidence support the role of CGRP in migraine Specifically:6,7

• In the absence of triggers or during treatment, it has been noted that CGRP levels remain low in migraine sufferers.

• Elevations in serum and salivary CGRP have been observed in both spontaneous migraine attack and nitric oxide-induced attack.

• Intravenous CGRP can induce a migraine attack in a matter of hours in people who have had previous migraines but this effect was not observed in people who do not suffer from migraine.

 

References

  1. World Health Organization. Neurological disorders: public health challenges. 2006; World Health Organization, Geneva, Switzerland 

  2. International Headache Society. The International Classification of Headache Disorders, 3rd edition. Cephalgia 2018; 38(1): 1–211 

  3. Gasparini CF et al. Studies on the pathophysiology and genetic basis of migraine. Current Genomics 2013; 14(5): 300–315

  4. Durham PL. Calcitonin gene-related peptide (CGRP) and migraine. Headache 2006; 46 (Suppl 1): S3–S8

  5. Durham PL, Vause CV. CGRP receptor antagonists in the treatment of migraine. CNS Drugs 2010; 24(7): 539–548

  6. Raddant AC, Russo AF. Calcitonin gene-related peptide in migraine: intersection of peripheral inflammation and central modulation. Expert Rev Mol Med 2011; 13: e36

  7. Kaiser EA, Russo AF. CGRP and migraine: could PACAP play a role too? Neuropeptides 2013; 47(6): 451–461