MIGRAINE HEADACHE ANTONIA C CHALMERS, MD. PREVALENCE Migraine is the most prevalent neurological...
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Transcript of MIGRAINE HEADACHE ANTONIA C CHALMERS, MD. PREVALENCE Migraine is the most prevalent neurological...
MIGRAIN
E HEADACHE
AN
TO
NI A
C C
HA
L ME
RS
, M
D
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)