Migraine and Anti Migraine Druigs

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    MIGRAINE ANDANTIMIGRAINE DRUIGS

    BY

    M.SARANYA

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    INTRODUCTION

    Migraine is common anddebilitating condition affecting 10-15% ofpeople, Migraine is a mysterious

    disorder characterized by moderate tosevere headaches, and nausea althoughthe cause is not understood. which

    comes in attacks lasting 4-48 hours. It isabout three times more common inwomen than in men.

    http://en.wikipedia.org/wiki/Headachehttp://en.wikipedia.org/wiki/Nauseahttp://en.wikipedia.org/wiki/Nauseahttp://en.wikipedia.org/wiki/Headache
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    Signs and symptoms

    Migraine attack consist of an initial visualdisturbance (the aura), in which a flickeringpattern, followed by blind spot (a scintillatingscotoma), progresses gradually across anarea of the visual field.

    The visual disturbance is followed ,about 10minutes later, by a severe throbbingheadache, starting unilaterally.

    And often associated with nausea, vomiting,sensitivity to light and sound, flashes of light,vertigo, loose motions and other symptoms.

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    Two major types are

    Migraine without aura(common migraine) involvesmigraine headaches that are not accompanied by anaura (visual disturbance).

    Migraine with aura(classical migraine )usually

    involves migraine headaches accompanied by an auraor other neurological symptoms.

    Two other varieties are Familial hemiplegic migraineand Sporadic hemiplegic migraine, Another variety isbasilar-type migraine, where a headache and aura areaccompanied by difficulty speaking, vertigo, ringing inears, or a number of other brainstem-relatedsymptoms, but not motor weakness.

    http://en.wikipedia.org/wiki/Familial_hemiplegic_migrainehttp://en.wikipedia.org/wiki/Sporadic_hemiplegic_migrainehttp://en.wikipedia.org/wiki/Basilarhttp://en.wikipedia.org/wiki/Dysarthriahttp://en.wikipedia.org/wiki/Vertigo_%28medical%29http://en.wikipedia.org/wiki/Tinnitushttp://en.wikipedia.org/wiki/Tinnitushttp://en.wikipedia.org/wiki/Tinnitushttp://en.wikipedia.org/wiki/Tinnitushttp://en.wikipedia.org/wiki/Vertigo_%28medical%29http://en.wikipedia.org/wiki/Dysarthriahttp://en.wikipedia.org/wiki/Basilarhttp://en.wikipedia.org/wiki/Sporadic_hemiplegic_migrainehttp://en.wikipedia.org/wiki/Familial_hemiplegic_migraine
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    Cause and Triggers

    Cause The underlying cause of migraines is unknown. There

    are, however, many biological events that have beenclinically associated with migraine.

    Triggers Migraines may be induced by triggers, with some

    reporting it as an influence in a minority of cases andothers the majority.

    Many things have been labeled as triggers, however

    the strength and significance of these relationships areuncertain. Common triggers quoted are stress,hunger, and fatigue (these equally contribute totension headaches).

    http://en.wikipedia.org/wiki/Tension_headacheshttp://en.wikipedia.org/wiki/Tension_headaches
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    Pathophysiology

    Both vascular and neural influences causemigraines.

    stress triggers changes in the brain

    These changes cause serotonin and/orhistamine to be released

    blood vessels constrict and dilate

    chemicals including substance P irritatenerves and blood vessels causing neurogenicinflammation and pain.

    http://en.wikipedia.org/wiki/Neurogenic_inflammationhttp://en.wikipedia.org/wiki/Neurogenic_inflammationhttp://en.wikipedia.org/wiki/Neurogenic_inflammationhttp://en.wikipedia.org/wiki/Neurogenic_inflammation
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    Cont..

    The Vascular theory holds that initialvasoconstriction or shutting of blood throughcarotid arterio -venous anastomoses produces

    cerebral ischaemia and starts the attack. The neurogenic theory considers it to be a

    spreading depression of cortical electricalactivity followed by vascular phenomena.

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    Postulated pathogenesis of migraine

    Peripheral mechanisms

    5-HT Dilatation of

    receptor extracerebral vessels

    5-HT Vascular NO 5-HT1D(-) sensory nerve

    endothelium agonists discharge

    sensitisation of

    5-HT (-) sensory nerve

    Antagonists 5-HT(-)

    agonists

    Release of mediators

    (prostaglandins,kinins,etc) Neuropeptide release

    (CGRP,SP)

    NASIDS (-)

    Neuroinflammation aura and pain

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    Central mechanism

    sensory nerve discharge

    (-)5-HT1D agonist

    central pain sensitisationUnknown factors aura & painspreading depression

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    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)

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    Severe

    Ergot alkaloids/

    Prophylaxis

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    Tricyclic antidepressants (e.g.amitriptyline).

    Clonidine, an alpha2-adrenoceptoragonist.

    Calcium channel blockers :(e.g.Flunarizine, Dihydropyridines,verapamil)

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    Reference

    Goodman & Gilman's-manual ofpharmacology and therepuetics

    Essentials of medical pharmacology-KD Tripathi.

    www.wikipedia.com

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