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PREVALENCEMigraine is the most prevalent neurological

disorder.

More than 80 million people suffer migraine headaches in US and Europe

28 million people in the US older than age 12

21 million females , 7 million males

The ratio of female to male is 3:1

Migraine Prevalence peaks between 35 and 45

Migraine is so common that 1 in 4 households has one with migraine

There seems to be a genetic predisposition

DEFINITION

Migraine headache is a result of specific changes within the brain.

Migraine is a complex disorder characterized by recurring headaches, often unilateral. Headaches can be associated with visual or sensory aura. The aura often precede the head pain but may occur during or after the head pain.

Migraine is most common among women and has a genetic component.

A variety of environmental and behavioral factors may precipitate migraine attacks in persons with a predisposition to migraine

MIGRAINE TRIGGERSHormonal

Stress

Excessive or insufficient sleep

Medications : BCP, vasodilators

Smoking

Exposure to bright lights and strong odors

Head trauma

Weather changes

Motion sickness

Fasting or skipping meals

Certain foods and preservatives : chocolate, nitrates, aged cheeses, MSG

Alcohol

Lack of exercise

PATHOPHYSIOLOGY OF MIGRAINE

Neurovascular theory : -neurogenic process with secondary

changes in cerebral perfusion associated with a sterile neurogenic inflammation

-At baseline, a migraineur who is not having any headache has a state of neuronal hyperexcitability in the cerebral cortex. This explains the susceptibility of the migrainous brain to headaches.

PATHOPHYSIOLOGY OF MIGRAINE

Cortical spreading depression ( CSD):- Oligemia : CSD of Leao: wave of neuronal excitation in

the cortical gray matter that spreads from the site of origin at the rate of 2-6 mm/min. This is responsible for the aura. This in turn, activates the trigeminal fibers, causing the headache phase.

- Trigeminovascular system (TVS) : Activation of the TVS by CSD stimulates the release of pain generating substances such as Calcitonin gene related peptide, substance P, vasoactive intestinal peptides, and Neurokinin A. This leads to sterile inflammation, vasodilatation and protein extravasation producing pain.

SEROTONIN AND MIGRAINE

Serotonin receptors ( 5hydroxytryptamine [ 5HT] ) is the most important receptor in headache pathway. 5HT 1D receptors are present in the trigeminal sensory neurons and 5HT1 B on smooth muscle cells in meningeal vessels and coronary vessels . The Triptans are selective 5 HT1B/D agonists and prevent the release of neuropeptides and block neurotransmission.

SIGNS AND SYMPTOMS

HEAD PAIN:Throbbing or pulsating pain, moderate to severe

Pain aggravated by activity and movement

Pain often unilateral but can be bilateral or global : 50% unilateral and 40% bilateral

Headache lasts for 4-72 hours in adults and 2-48 hours in children

Systemic symptoms often present: light/noise sensitivity, nausea/vomiting , lightheadedness

1/3 of patients experience an aura

MIGRAINE AURA

May precede or accompany the headache phase or may occur in isolation

Usually develops over 5-20 minutes and last less than 60 minutes

Most commonly visual but can be sensory , motor or combination of these

Visual aura can be positive or negative

The most common positive visual aura is the scintillating scotoma, an arc of absent vision with shimmering zigzag border

DIAGNOSIS: ICHD II CRITERIA FOR MIGRAINE WO AURA

Must have had at least 5 headache attacks that lasted for 4-72 hours with at least 2 of the following characteristics:

- Unilateral location

- Pulsating Quality

- Moderate to severe pain intensity

- Aggravated by routine activity

In addition, during the headache phase, the patient must have at least 1 of the following:

- Nausea and/or vomiting

- Photophobia and/or phonophobia

- Headaches cannot be attributed to another disorder

H E A D A C H E C L A S S I F I C AT I O N C O M M I T T E E O F T H E I N T E R N AT I O N A L H E A D A C H E S O C I E T Y

MIGRAINE VARIANTS

Childhood periodic syndromes

Late life migrainous accompaniments

Basilar Migraine

Hemiplegic Migraine

Retinal Migraine

HIS CLASSIFICATION : ICHD-2

Primary headache

-symptoms based

-tools now available to help measure/monitor patient disability

Secondary headache

-etiology based

Red flags can help separate the diagnosses

SECONDARY HEADACHES RED FLAGS“SSNOOP”Systemic symptoms (fever, weight loss)

Secondary risk factors: underlying disease ( HIV, systemic illness, cancer)

Neurologic symptoms or abnormal signs (confusion, impaired alertness , or consciousness)

Onset : sudden, abrupt, or split second ( first, worst)

Older: new onset and progressive headache, especially in the middle age >50( giant cell arteritis)

Previous headache history or headache progression: pattern change, first headache or different (change in attack frequency, severity, or clinical features)

DIAGNOSTIC TESTS

Selection of laboratory/imaging studies to rule out conditions other than migraine headache is determine by the clinical presentation and examination.

Sed rate and CRP for patients above 50 years of age to ro temporal arteritis

Neuroimaging is not necessary is patients with a history of recurrent migraine headaches and a normal neurological examination

DIAGNOSTIC TESTING: CT AND MRI

In patients with migraine, neither CT nor MRI is warranted except in cases with :

-recent substantial change in headache pattern

-history of seizures

-focal neurological symptoms or signs

-red flags

Consensus expert opinion

-MRI is more sensitive

MANAGEMENT OF MIGRAINE

Acute or abortive treatment with the goal of return to function. Early intervention is essential.

Preventive treatment with the goal of preventing more attacks

ACUTE VS PREVENTIVE THERAPY

Acute ( Abortive)

Taken after attack has begun to relieve pain and disability and stop progression

Preventive

Taken daily to reduce attack frequency severity and duration

Patients taking preventive medication can also use acute medication

MANAGEMENT

Acute/abortive medications:Selective serotonin receptor agonists: Triptans

Ergot alkaloids i.e. ergots, dihydroergotamine ( DHE)

Analgesics

Nonsteroidal Anti-infammatory drugs (NSAIDS)

Combination products

Anti emetics

ACUTE THERAPIES FOR MIGRAINE

Specific :

Ergotamine or dihydroergotamine

Triptans: Sumatriptan, Rizatriptan, Zomitriptan, Almotriptan, Eletriptan, Naratriptan and Frovatriptan

Non specific:

pain killers (non narcotics, narcotics, combination medications ), anti emetics

CONSIDERATIONS FOR PREVENTIVE TXHeadaches cause major disruption in patient’s

lifestyle, with significant disability that lasts 3 or more days

Prolonged and frequent headaches. More than 1 headache per week.

Abortive therapy fails/ineffective, contraindicated or is overused

Symptomatic medications are contraindicated or ineffective

Use of abortive medications more than 2x per week

Migraine variants such as hemiplegic migraine

*Preventive treatment reduces the progression to more frequent and more severe headaches and improves responsiveness to abortive treatment.

PRINCIPLES OF PREVENTIVE DRUG TX

Start with low dose and increase slowly

Need adequate trial ( 2-3 months)

Avoid drug overuse and interfering drugs

Evaluate therapy

-use migraine calendar/diary

-consider taper or stop if HA well controlled

Take co existing conditions into account

-determine contraindications (eg, pregnancy) to minimize potential risks

MANAGEMENT

Preventive treatment-anti epileptic drugs: Topiramate, sodium valproate

-beta blockers: propranolol, metoprolol, timolol

-Tricyclic antidepressants

-Calcium Channel blockers

-Selective serotonin reuptake inhibitors (SSRI)

-NSAIDs

-Botulinum toxin

-non pharmacologic : biofeedback, avoid triggers, exercise

MIGRAINE COMORBIDITY MAY ASSIST WITH SELECTION OF PREVENTIVE AGENT

Comorbidity Agent

Anxiety SSRI/SNRI, AED

Bipolar AED, SSRI/SNRI

Depression TCA

Epilepsy AED

Insomnia TCA

MVP B blocker

Raynaud Calcium blocker

MANAGEMENT

Alternative medicine

-reduction of migraine triggers ( eg, stress, certain foods, lack of sleep, hunger, fatigue )

-non pharmacologic therapy: biofeedback, cognitive-behavioral therapy

-integrative medicine ; butterbur, riboflavin 400mg, magnesium 400mg, feverfew, coenzyme Q10

SYNDROME OF MEDICATION OVERUSE HEADACHE (MOH)

Also maybe known as rebound headache

Occurs in patients with preexisting migraine/pain

Pattern of headaches and overuse of analgesics and other drugs in critical monthly doses and frequencies

Prevention limit frequency and dose of meds

Treatment refractory to otherwise appropriate therapy

-withdrawal therapy

-restriction of monthly doses for acute treatment

PRINCIPLES OF MOH THERAPY

Taper medications most likely causing MOH/rebound headache

Substitute acute medications that do not cause MOH/rebound headache

Consider synergistic combination therapy

Cautions:

Opiate and barbiturate abstinence syndrome

Increasing headache during withdrawal period

SUMMARY

Migraine headache is a brain disorder manifested with recurring headaches associated with systemic symptoms. Pain is often unilateral . It is very common in young women. There are triggers which should be managed.

There was a number of acute therapies both specific and non specific, that are used to lessen the severity o the headache. Timing is crucial, especially when using acute medications like the Triptans. Early use of Triptans results in better outcomes, less recurrence , and fewer adverse events.

There are preventive medications to be used when acute therapy fails, are contraindicated or the headaches are prolonged or too frequent.

References:

1 Silberstein SD, Holland S, Freitag F et al . Evidence based guideline update : Pharmacologic treatment for episodic migraine prevention in adults. Report of Quality Standards Subcommittee of the American Academy of Neurology and the American Headache Society. Neurology 2012;78:1337-1345.

2 Holland S, Siberstein SD, Freitag F et al . Evidence based guideline update: NSIDs and other complementary treatments for episodic migraine prevention in adults. Report of Quality Standards Subcommittee of the American Academy of Neurology and the American Headache Society. Neurology 2012;78:1346-1353.

3. Headache Classification Subcommittee of the International Headache Society. The international Classification of Headache Disorders, 2nd edition. Cephalagia 2004;24(suppl): S1-S6.

4. International headache Society . HIS classification ICHD-II:Migraine . Available at http://ihs-classification.org .

5. Chalwla, J, Lutsep HL. Migraine headaches . Medscape. Available at http://www.medscape.com.

6. May A, Goadsby PJ. The trigeminovascular system in humans: Pathophysiologic implications for primary headache syndromes of the neural influences on the cerebral circulation. J Cereb Blood Flow Metabolism. Feb 1999;19(2):115-27. ( Medline).

7. Cutrer FM, Charles A. The neurogenic basis of migraine. Headaches . Oct 2008;48 (9):1411-4. (Medline).

8 . Waeber C, moskowitz MA. Therapeutic implications of central and peripheral neurologic mechanisms in migraine. Neurology. October28 2003;61 (8 suppl 4):S9-20.(medline).

9 Silberstein SD, Freitag FG. Preventive treatment of migraine . Neurology.2003;60(7):S38-44.

10. Bigal ME, Lipton RB. Excessive acute migraine medication use and migraine progression. Neurology. Nov 25 2008;71(22):1821-8 (Medline)

11. Dowson AJ, Matthew NT, Pascual J. Review of clinical trials using early intervention with oral triptans for migraine management . Intl J Clin Pract. Jun 2006;60(6):698-706. ( Medline)