MIGRAINE & MIGRAINE MANAGEMENT: A REVIEW

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ABOUT AUTHORS
Muthyala Nagavamsidhar*1, Qadrie ZL.2, Suman A.1
*1 Department of Pharmacy Practice,
Pratishta Institute of Pharmaceutical Sciences,
Suryapet, Hyderabad, Telangana, India

nagavamsi.muthyala@gmail.com

ABSTRACT:  Pain is defined as an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage. The WHO has rated migraine amongst the top 20 most disabling life time conditions. Migraine is a pervasive and debilitating, chronic neurological painful disorder, affecting from 15% to 29% of the general population. It is the second most common cause of headache characterized by recurrent episodes of headache and associated symptoms i.e. nausea, sensitivity to light and noise that typically last from 4 to 72 hours which is divided into four phases. Migraine is well explained with three hypothesis i.e., vascular, platelet, central nervous system. It affects people of all groups, sexes, races and social classes around the globe. Migraine can occur due to various trigger factors and can be managed with both pharmacological and non-pharmacological treatment.

Reference Id: PHARMATUTOR-ART-2580

PharmaTutor (Print-ISSN: 2394 - 6679; e-ISSN: 2347 - 7881)

Volume 6, Issue 4

Received On: 05/02/2018; Accepted On: 12/02/2018; Published On: 01/04/2018

How to cite this article: Muthyala N, Qadrie ZL, Suman A; Migraine & Migraine Management: A Review; PharmaTutor; 2018; 6(4); 8-17; http://dx.doi.org/10.29161/PT.v6.i4.2018.8

INTRODUCTION
Migraine is a pervasive and debilitating, chronic neurological painful disorder, affecting from 15% to 29% of the general population (10% of adult population in United States) (Alvin et. al. 1979). Migraine is the second most common cause of headache characterized by recurrent episodes of headache and associated symptoms i.e., nausea, sensitivity to light and noise that typically last from 4 to 72 hours. Pain management of migraine includes both non-pharmacological and pharmacologic methods for acute episodes and prophylaxis. Pain is defined as an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage (Terry J. Baumann,2005). Pain is a dynamic complex process which is generally classified in  terms of nociceptive and neuropathic pathways, migraine pain is a neuropathic pathways which is quiet different from nociceptive pain which is sustained by abnormal processing of sensory input by peripheral or CNS, a large number neuropathic pain syndromes exist and clinically ,they are often difficult to treat (pasero et al ,1999)  patients presents  with spontaneous pain transmissions often described as tingling, burning, shockline or shooting, exaggerated painful response to normally non-noxious stimuli (Allodynia) (pasero et al 1999,Elliott,1994)or painful repoint to noxious stimuli (hyperalgesia).

On an average a migraineur experiences around 13 attacks per year which may vary from person to person. The WHO has rated migraine amongst the top 20 most disabling life time conditions. It affects people of all groups, sexes, races and social classes around the globe. Migraine can occur due to various trigger factors like stress, emotions, environmental factors, genetic factors, diet, sleep disturbances hormonal factors (menstruation, oral contraceptives) (migraine.org.uk/triggers).

PATHOPHYSIOLOGY:
According to vascular hypothesis proposed by Harold Wolff in 1938, the migraine aura is caused by intracerebral arterial vasoconstrictions that is followed by reactive extra-cranial vasodilatation and associated headache. Migraine without aura is a neurobiological disorder (J Olesen et al,2004) and pain is believed to result from activity within trigeminal nucleus results in release of vasoactive neuropeptides, particularly calcitonin gene-related peptide (CGRP), Neurokinin A, and substance P, from perivascular axons. The released neuropeptides interact with dural blood vessels to promote vasodilatation and dural plasma extravasations, resulting in perivascular inflammation. Orthodromic conduction alone trigeminovascular fibres transmits pain impulses to the trigeminal nucleus caudalis where the information is relayed further to higher cortical pain centres (www.hartp.neurology.ucla.edu).

Migraine genes identified by studying families with familial hemiplegic migraine (FHM) which involves gene mutations CACNA1A of calcium voltage gated (50%) and SCN1A of Na+/K+ ATPase (20%). Data also support a role for dopamine in pathophysiology of certain sub types of migraine which induces stimulation so dopaminergic antagonists show effective therapeutic agents against migraine. Pharmacological data supports the serotonin (5-HT) as antimigraine therapy (Peter J Goadsby et al,2005). Coming to platelet hypothesis, which involves abnormal platelet activation with relevant characteristics like:
a. They do not adhere to one another unless precipitated;
b. Certain stimuli (catecholamines, thromboxane A2 and ADP.
c. Once aggregates form; they release a portion of contents (eg. Serotonin, adenosine and its phosphate derivatives).

Prostaglandin produced by platelets (thromboxane A2) and vascular endothelium (prostacyclin) produces vasoconstriction and vasodilatation (Deshmukh 1977, Meyer). This platelet hyperaggregability forms micro-emboli that lodge in microvasculature release their contents cause changes in vasomotor tone which induce tissue response leading to migraine pain. Platelets which is a primary blood source of serotonin where a rapid decline in plasma levels occur in initiation and during migraine attack which is indicated with increase in metabolite of serotonin, urinary 5-hydroxyindoleacetic acid which indicate serotonin release during migraine attackswhere as this does not occur in other headache types and not a reaction to pain, stress and vomiting (Rydzewski 1978, Saito et al 1987). Serotonin enhance sensitivity to pain receptors leading to vacular permeability where pain producing substance release at site leading to inflammatory response in migraine attacks (Glover et al, 1982), according to central nervous system hypothesis it is a disturbance with secondary vasomotor changes in CNS, it is initiation of neurologic symptoms occurs primarily in cerebral cortex and progressed gradually with cerebral depression (Olesen ,1985). Migraine attacks can be precipitated centrally with psychological stress, fatigue excitation of neural pathways by environmental stimuli (i.e., Noise, Glare).

From above discussion it is evident that no complete satisfying description of pathologic events associated with migraine exists. Migraine is general classified by International Headache Society shown below in flowchart (Olesen et al, 2004, ihs.org).

Headache Chart

Flow-chart 1: Based on IHS Classifications, Types of Migraine

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