PATHOLOGY OF MIGRAINE

Migraine is characterized by an aura of variable duration that may involve nausea, vomiting, visual scotomas or even hemianopsia, and speech abnormalities, the aura is followed by a severe throbbing unilateral headache that lasts for a few hours 1-2 days. Migraine involves the trigeminal nerve distribution to intracranial arteries. These nerves release peptide neurotransmitters, especially calcitonin gene-related peptide.

The mechanical stretching caused by this perivascular edema may be the immediate cause of activation of pain nerve endings in the dura. The onset of headache can also be associated with a marked increase in amplitude of temporal artery pulsations.

CURRENT TREATMENT AND THEIR MECHANISM OF ACTION

1. Triptans - are first line therapy for acute server migraine, they are selective agonist for 5HT1D and 5HT1B. They have a vasoconstriction action which prevents vasodilation and stretching of the pain endings.
2. Ergot alkaloids – activates 5-HT1D and 5-HT1B receptors on presynaptic trigeminal nerve endings to inhibit the release of vasodilating peptides. Its effect include agonist, partial agonist and antagonist action at alpha adrenoceptors and serotonin receptors and agonist or partial agonist actions at CNS dopamine receptors.
3. Nonsteroidal anti-inflammatory analgesic agents – helpful in treating migraine pain
4. Beta-adrenoceptor blockers and Calcium channel blockers – are migraine prophylaxis
5. Tricyclic antidepressants - activates 5-HT1D and 5-HT1B
6. SSRIs
7. Anti-seizures – suppresses excessive firing of these nerve endings
8. Anticonvulsants valproic acid and topiramate – it has some prophylactic efficacy in migraine.