MIGRAINE AND ANTIMIGRAINE DRUIGS

BY M.SARANYA

INTRODUCTION
Migraine is common and debilitating condition affecting 10-15% of people, Migraine is a mysterious disorder characterized by moderate to severe headaches, and nausea although the cause is not understood. which comes in attacks lasting 4-48 hours. It is about three times more common in women than in men.

Signs and symptoms

Migraine attack consist of an initial visual disturbance (the aura), in which a flickering pattern, followed by blind spot (a scintillating scotoma), progresses gradually across an area of the visual field. The visual disturbance is followed ,about 10 minutes later, by a severe throbbing headache, starting unilaterally. And often associated with nausea, vomiting ,sensitivity to light and sound, flashes of light ,vertigo, loose motions and other symptoms.

Two major types are

Migraine without aura( common migraine) involves migraine headaches that are not accompanied by an aura (visual disturbance). Migraine with aura (classical migraine )usually involves migraine headaches accompanied by an aura or other neurological symptoms. Two other varieties are Familial hemiplegic migraine and Sporadic hemiplegic migraine, Another variety is basilar-type migraine, where a headache and aura are accompanied by difficulty speaking, vertigo, ringing in ears, or a number of other brainstem-related symptoms, but not motor weakness.

Cause and Triggers

Cause The underlying cause of migraines is unknown. There are, however, many biological events that have been clinically associated with migraine. Triggers Migraines may be induced by triggers, with some reporting it as an influence in a minority of cases and others the majority. Many things have been labeled as triggers, however the strength and significance of these relationships are uncertain. Common triggers quoted are stress, hunger, and fatigue (these equally contribute to tension headaches).

Pathophysiology

Both vascular and neural influences cause migraines. stress triggers changes in the brain These changes cause serotonin and/or histamine to be released blood vessels constrict and dilate chemicals including substance P irritate nerves and blood vessels causing neurogenic inflammation and pain.

Cont..

The Vascular theory holds that initial vasoconstriction or shutting of blood through carotid arterio -venous anastomoses produces cerebral ischaemia and starts the attack. The neurogenic theory considers it to be a spreading depression of cortical electrical activity followed by vascular phenomena.

Postulated pathogenesis of migraine

Peripheral mechanisms

5-HT receptor 5-HT Vascular endothelium

NO

5-HT (-) Antagonists

Dilatation of extracerebral vessels 5-HT1D(-) agonists sensitisation of sensory nerve 5-HT(-) agonists

sensory nerve discharge

Release of mediators (prostaglandins,kinins,etc) Neuropeptide release (CGRP,SP) NASIDS (-) Neuroinflammation

aura and pain

Central mechanism
sensory nerve discharge

(-)

5-HT1D agonist

central pain sensitisation Unknown factors spreading depression aura & pain

Antimagraine drugs
Mild:

Simple analgesics (e.g. aspirin,paracetamol,with or without metoclopramide to hasten absorption ) NSAIDs or their combinations (+antiemetic) Moderate: NSAIDs combinations /ergot alkaloids / sumatriptan (+antiemetic)

Severe Ergot alkaloids/

Prophylaxis

Tricyclic antidepressants (e.g. amitriptyline). Clonidine, an alpha2-adrenoceptor agonist. Calcium channel blockers : (e.g.Flunarizine, Dihydropyridines, verapamil)

Reference
Goodman & Gilman's-manual of pharmacology and therepuetics Essentials of medical pharmacologyKD Tripathi. www.wikipedia.com