Migraine pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Migraines are believed to be a neurovascular disorder[1][2] with evidence supporting its mechanisms starting within the brain and then spreading to the blood vessels.[3] Migraine begins by neuronal changes leading to the activation of the brainstem and diencephalic nuclei and subsequent dilatation of the large cranial and proximal intracranial vessels.[1] Some researchers feel neuronal mechanisms play a greater role,[4] while others feel blood vessels play the key role.[5] Others feel both are likely important.[6] High levels of the neurotransmitter serotonin, also known as 5-hydroxytryptamine, are believed to be involved.[3]
Pathophysiology
Aura
Cortical spreading depression or spreading depression of Leão is bursts of neuronal activity followed by a period of inactivity, which is seen in those with migraines with an aura.[7] There are a number of explanations for its occurrence including activation of NMDA receptors leading to calcium entering the cell.[7] After the burst of activity the blood flow to the cerebral cortex in the area affected is decreased for two to six hours.[7] It is believed that when depolarization travels down the underside of the brain, nerves that sense pain in the head and neck are triggered.[7]
Shown below is an image depicting cortical spreading depression which is the underlying pathophysiology of aura.
Pain
The exact mechanism of the head pain which occurs during a migraine is unknown.[8] Some evidence supports a primary role for central nervous system structures (such as the brainstem and diencephalon)[9] while other data support the role peripheral activation (such as via the sensory nerves that surround blood vessels of the head and neck).[8] The potential candidate vessels include dural arteries, pial arteries and extracranial arteries such as those of the scalp.[8] The role of vasodilatation of the extracranial arteries, in particular, is believed to be significant.[10]
References
- ↑ 1.0 1.1 Goadsby PJ, Lipton RB, Ferrari MD (2002). "Migraine--current understanding and treatment". N Engl J Med. 346 (4): 257–70. doi:10.1056/NEJMra010917. PMID 11807151.
- ↑ Bartleson JD, Cutrer FM (May 2010). "Migraine update. Diagnosis and treatment". Minn Med. 93 (5): 36–41. PMID 20572569.
- ↑ 3.0 3.1 The Headaches Chp. 29, Pg. 276
- ↑ Goadsby, PJ (January 2009). "The vascular theory of migraine – a great story wrecked by the facts". Brain : a journal of neurology. 132 (Pt 1): 6–7. doi:10.1093/brain/awn321. PMID 19098031.
- ↑ Brennan, KC (June 2010). "An update on the blood vessel in migraine". Current Opinion in Neurology. 23 (3): 266–74. doi:10.1097/WCO.0b013e32833821c1. PMID 20216215. Unknown parameter
|coauthors=ignored (help) - ↑ Dodick, DW (April 2008). "Examining the essence of migraine – is it the blood vessel or the brain? A debate". Headache. 48 (4): 661–7. doi:10.1111/j.1526-4610.2008.01079.x. PMID 18377395.
- ↑ 7.0 7.1 7.2 7.3 The Headaches, Chp. 28, pp. 269–72
- ↑ 8.0 8.1 8.2 Olesen, J (July 2009). "Origin of pain in migraine: evidence for peripheral sensitization". Lancet neurology. 8 (7): 679–90. doi:10.1016/S1474-4422(09)70090-0. PMID 19539239. Unknown parameter
|coauthors=ignored (help) - ↑ Akerman, S (2011-09-20). "Diencephalic and brainstem mechanisms in migraine". Nature Reviews Neuroscience. 12 (10): 570–84. doi:10.1038/nrn3057. PMID 21931334. Unknown parameter
|coauthors=ignored (help) - ↑ Shevel, E (March 2011). "The extracranial vascular theory of migraine – a great story confirmed by the facts". Headache. 51 (3): 409–17. doi:10.1111/j.1526-4610.2011.01844.x. PMID 21352215.