A migraine headache is a neurovascular disorder often initiated by a trigger and characterized by a headache, which 20% of the time is preceded by a visual aura. The headache may be accompanied by a variety of multiple organ system symptoms, such as allodynia, nausea, vomiting and urinary frequency. There are various types of migraine, the diagnostic criteria for which have been established by the International Headache Society.77 The types of migraine are divided into two groups: migraine without aura ("common migraine") and migraine with aura ("classic migraine"). Further subdivisions include migraine with typical aura with or without headache, familial hemiplegic migraine, sporadic hemiplegic migraine, basilar type migraine, and retinal migraine.77 Treatment of migraines encompasses a wide variety of xenobiotics and can be broadly classified as prophylactic or abortive therapies (Table 51–1).
Table 51–1. Xenobiotics Used in Migraine Treatment |Favorite Table|Download (.pdf)
Table 51–1. Xenobiotics Used in Migraine Treatment
|β adrenergic antagonists||Acetaminophen|
|Butterbur root||Antiemetics: metoclopramide, ondansetron, prochlorperazine|
|Calcium channel blockers||Aspirin|
|MAO inhibitors||Valproic acid|
|Onabotulinumtoxin/A (Botox A)|
|Selective serotonin reuptake inhibitors|
The initiation of migraines is not fully understood, but likely involves genetic abnormalities in central nervous system (CNS) ion channels that predispose sufferers to specific triggers. Patients with familial hemiplegic migraine, an autosomal dominant disorder, have missense mutations in the α1 subunit of brain specific P/Q voltage gated calcium channels resulting in altered function of these channels. During migraines, the upper brainstem has increased blood flow and is implicated as a "migraine generator." After activation, a wave of cortical depression spreads across the cortex from a caudal to rostral fashion followed by a spreading wave of oligemia, which can produce the auras that occur in 20% of migraineurs.23,34,83 Current theories suggest that this spreading wave occurs in patients who do not experience visual auras and spares the visual cortex.
Cephalagia begins during vasoconstriction prior to vasodilation unlike previous vascular theory suggested prior to cerebral blood flow studies. Antidromic activation of the afferent neurons of the ophthalmic division of the trigeminal nerve and branches of the C1 and C2 nerves (first order neurons) located on dural arteries at the base of the brain releases inflammatory neuropeptides such as calcitoningene related polypeptide, VIP ...