Neurological lectures...Migraine

Treating Migraines Professor Yasser Metwally www.yassermetwally.com

World prevalence of migraine
1-year prevalence rates
Population-based studies
IHS criteria (or modified)
USA 12% Chile 7% Japan 8% Italy 16% Denmark 10% France 8% † Switzerland 13% Rasmussen and Olesen (1994); Rasmussen (1995); Lipton et al ( 1994); Lavados and Tenhamm (1997); Sakai and Igarashi (1997) † Prevalence measured over a few years

Prevalence of migraine by sex and age 30 25 20 15 10 5 0 20 30 40 50 60 70 80 100 Migraine prevalence (%) Age (years) Lipton and Stewart (1993) The American Migraine Study ( n =2479 migraine sufferers) Females Males

Diagnosis of migraine
Diagnosis depends on patient history
No specific tests or clinical markers for migraine
Cady (1999); Warshaw et al (1998)
Positive diagnosis if attack history fulfils IHS criteria for migraine
Other pointers include:
family history of migraine
age of onset <45
presence of aura
menstrual association
Organic disease must be excluded

Migraine Criteria
 5 attacks lasting 4 – 72 h
 2 of the following 4
Unilateral
Pulsating
Moderate or severe intensity
Aggravation by routine physical activity
 1 of the following
Nausea and/or vomiting
Photophobia and phonophobia
Not attributable to another disorder

SULTANS: two from column A, one from column B
evere
ni
ateral
hrobbing
Ctivity worsens
ausea
Lite and sound ensitivity
S U T A L N S

What is migraine?
Migraine without aura (MO)
Migraine with aura (MA) Headache Classification Committee of IHS (1988)
At least five attacks fulfilling these criteria:
Headache lasting 4–72 h
(2–48 h in children)
At least two attacks fulfilling these criteria:
At least three of the following:
one or more fully reversible aura symptoms
gradually developing or sequential aura symptoms
no one aura symptom lasts longer than 1 h
headache shortly follows or accompanies aura
Accompanied by at least one of:
nausea
vomiting
photophobia and/or phonophobia
No evidence of organic disease
With at least two of:
unilateral location
pulsating quality
moderate/severe intensity
aggravated by activity
No evidence of organic disease

Clinical features of migraine Sleepy Anorexia nausea Vomiting yawning Phonophobia Photophobia Phonophobia Photophobia Osmophobia Osmophobia Vomiting Deep sleep Headache III IV Headache Resolution Blau (1992) I II Normal Prodromes Aura Normal Appetite Awake/sleep Light tolerance Smell Noise Fluid balance Craving Tired yawning Heightened perception Fluid retention V Postdromes Normal Limited Light tolerance Noise Smell Fluid balance Tired Feeling high or low Diuresis Appetite Awake/sleep food tolerance Normal

IMPORTANT DIAGNOSTIC CONSIDERATIONS Recurring moderate to severe headache is migraine until proven otherwise 15% of patients have a neurological aura IHS criteria do not require GI symptoms Vomiting occurs in < 1/3 of patients 41% of migraine patients report bilateral pain 50% of the time, pain is non-pulsating Russell MB, et al. Cephalalgia . 1996. Pryse-Phillips WEM, et al. Can Med Assoc J . 1997. No single criterion necessary nor sufficient for diagnosis

Premonitory, aura and postdromal symptoms
Prodrome
Occurs in 60% of attacks
Alterations in
mood
alertness
appetite
Originate in hypothalamus and frontal lobes
Silberstein and Lipton (1994); Lance (1993); Blau (1992)
Aura
Occur in MA (20% patients)
Visual symptoms
blurring, rippling
spots or flashes
fortification spectra
scotoma
Sensory symptoms
numbness/tingling
Motor symptoms
hemiparesis
Postdrome
Occurs in 90% patients
Symptoms can persist for several days
lethargy
exhaustion
impaired concentration
irritability
sluggishness
diminished appetite
euphoria

MIGRAINE WITH AURA (FORMERLY “CLASSIC” MIGRAINE) Visual > sensory > motor, language, brainstem Gradual evolution: 5–20 minutes (<60 minutes) May or may not be associated with headache Complex array of symptoms reflecting focal cortical or brainstem dysfunction International Headache Society. Cephalalgia. 1988;8;(suppl 7):1-96.

MIGRAINE AURA “Cheiro-oral”

Fortification Spectrum

DIAGNOSIS AND TESTING Detailed History and Examination
Primary Headache?
Preliminary Diagnosis
NO Secondary Headache Diagnostic Testing Atypical Features YES

Alice in Wonderland

REASONS FOR MISDIAGNOSIS OF MIGRAINE AS TTH OR SINUS Sinus Up to 50% of migraine patients report their headaches are influenced by weather 45% of migraine patients report attack related ‘sinus’ symptoms including lacrimation, rhinorrhea, nasal congestion Tension-Type Headache 75% of migraine patients report posterior neck pain/tightness/stiffness during attacks Stress/anxiety frequent migraine trigger Migraine is bilateral in up to 40% of patients Raskin NH. Headache. 2nd ed. 1988; Barbanti P, et.al. Cephalalgia. 2001; Kaniecki R. Cephalalgia . 2001. Migraine is a referred pain syndrome (V1, C1-C3)

Differential diagnosis of primary headaches Dubose et al (1995); Goadsby (1999); Marks and Rapoport (1997) Family history Yes Sex More females Onset Variable Location Usually unilateral in adults Character/severity Pulsatile Throbbing Frequency/ 2–72 h/attack duration 1 attack/year to >8 per month Associated Visual aura symptoms Phonophobia Photophobia Pallor Nausea/vomiting Clinical feature Migraine No More males During sleep Behind/around one eye Excruciating/ sharp Steady 15–90 min/attack 1–8 attacks/day for 3–16 weeks 1–2 bouts/year Sweating Facial flushing Nasal congestion Ptosis Lacrimation Conjunctival injection Pupillary changes Cluster headache Yes More females Under stress Bilateral in band around head Dull Persistent Tightening/pressing 30 min to 7 days 3–4 attacks/week to 1–2 attacks/year Mild photophobia Mild phonophobia Anorexia Tension headache

WORRISOME HEADACHE RED FLAGS “SNOOP” O lder: new onset and progressive headache, especially in middle-age >50 (giant cell arteritis) S ystemic symptoms (fever, weight loss) or S econdary risk factors (HIV, systemic cancer) N eurologic symptoms or abnormal signs (confusion, impaired alertness, or consciousness) O nset: sudden, abrupt, or split-second P revious headache history: first headache or different (change in attack frequency, severity, or clinical features)

Headache ‘red flags’
First or worst headache
Significant change from previous headache pattern
no longer fulfils IHS criteria
New onset headache in middle age or later
New or progressive headache that lasts for days
Precipitation of headache by coughing/sneezing/ bending down
Systemic symptoms such as myalgia, fever, malaise, weight loss, scalp tenderness, jaw claudication
Focal symptoms, seizures, confusion, impaired conciousness, physical examination abnormalities
Pryse-Phillips et al (1997)

EVALUATION STRATEGIES Red Flags” “ Investigate the Atypical and the

SUDDEN ONSET HEADACHE Primary Secondary SAH Pituitary apoplexy Venous sinus thrombosis Arterial dissection Meningoencephalitis Acute hydrocephalus Acute hypertension Spontaneous intracranial hypotension Idiopathic thunderclap headache (TCH) Exertional headache Cough headache Sexual headache deBruijn, SF, et al. Lancet . 1996; Lancet . 1998.

LUMBAR PUNCTURE Headache associated with fever, confusion, meningism, or seizures Thunderclap headache with negative CT head Subacute progressive headache High or low CSF pressure suspected (even if papilledema is absent) The first unusually severe headache Evans RE, Rozen TD, Adelman JU. In: Wolff’s Headache And Other Head Pain . 2001.

SENSITIVITY OF CT SCAN IN SUBARACHNOID HEMORRHAGE (SAH) van Gijn J, van Dongen KJ. Neuroradiology . 1982. Kassell NF et al. J Neurosurg. 1990. TIME AFTER HEADACHE ONSET PROBABILITY (%) DAY 0 95 DAY 3 80 1 WEEK 50 2 WEEKS 30 3 WEEKS ~0

DIAGNOSIS TESTING CT AND MRI
Consensus expert opinion
MRI is more sensitive
Role of CT or MRI in patients with nonmigraine headache is unclear
In patients with recurrent migraine, neither CT nor MRI is warranted except in cases where:
Recent substantial change in headache pattern
History of seizures
Focal neurologic symptoms or signs
Report of Quality Standards Subcommittee of AAN. Neurology . 1994.

DIAGNOSTIC TESTING ELECTROENCEPHALOGRAPHY
EEG may be useful in those patients with
Alteration or loss of consciousness
Residual focal neurologic defects or encephalopathy
Atypical migrainous aura
EEG is not useful
In the routine evaluation of patients with headache to exclude structural cause
Report of Quality Standards Subcommittee of AAN. Neurology . 1995.

MR AND CONVENTIONAL ANGIOGRAPHY MR Angiography Angiography Acute SAH Arterial dissection CNS vasculitis Aneurysm (>5 mm) Arterial dissection Venous thrombosis (MR venography) AV malformation Leclerc X et al. Neuroradiology . 1999.

INDICATIONS FOR GADOLINIUM ENHANCED MRI
Cerebrovascular
Arterial dissection (MRA)
Cerebral venous sinus thrombosis (MRV)
CNS vasculitis
Tumors
Posterior fossa
Pituitary
Leptomeninges
Herpes encephalitis High and low intracranial pressure syndromes MRA = magnetic resonance angiography. MRV = magnetic resonance venography. Bousser MG et al; Wall M et al; Mokri B; and Newman C, Solomon S. In: Wolff’s Headache And Other Head Pain . 2001 . Tien RD et al. AJR Am J Roentgenol. 1993 .

CEREBRAL VENOUS SINUS THROMBOSIS Bousser MG et al. In: Wolff’s Headache And Other Head Pain . 2001 .

Sleepers Awake!! Treatment

STRATEGIES FOR MIGRAINE TREATMENT Preemptive treatment Migraine trigger time-limited and predictable Preventive Treatment Decrease in migraine frequency warranted Acute treatment To stop pain and prevent progression Silberstein SD. Cephalalgia . 1997.

ACUTE MIGRAINE TREATMENT Discuss problems that arise in the acute management of migraine Evaluate the general principles of treatment Review the clinical evidence for acute treatment alternatives Present an approach for selecting and sequencing acute therapies Objectives

PRINCIPLES OF MIGRAINE MANAGEMENT
Patient education and behavioral management
Nature and mechanism of the disorder
Strategies for identifying and avoiding triggers
Behavioral strategies
Regular sleep, exercise, meals
Stress management, biofeedback
Cognitive behavioral therapy
Establish a therapeutic partnership
Pharmacologic management
Acute treatment
Preventative strategies

NONPHARMACOLOGIC TREATMENTS
Insufficient evidence to recommend: GRADE C
Acupuncture
TENS
Cervical manipulation
Occlusal adjustment
Hyperbaric oxygen
Hypnosis
The benefits of behavioral therapy (eg, biofeedback, relaxation) are in addition to preventive drug therapy (eg, propranolol, amitriptyline): GRADE B Goslin RE et al. Behavioral and Physical Treatments for Migraine Headache . 1999.
Effective: GRADE A
Relaxation training
Thermal biofeedback with relaxation training
EMG biofeedback
Cognitive behavioral therapy

Goals of Treatment
Establish diagnosis
Educate patient
Discuss findings
Establish reasonable expectations
Involve patient in decisions
Encourage Pt to avoid triggers
Choose the best treatment (tailoring)
Create treatment plan

MIGRAINE TRIGGERS Diet Hormonal changes Head trauma Stress and anxiety Sleep deprivation or excess Environmental factors Physical exertion

ACUTE MIGRAINE MEDICATIONS
Nonspecific
NSAIDs
Combination analgesics
Opioids
Neuroleptics/antiemetics
Corticosteroids
Specific
Ergotamine/DHE
Triptans

ACUTE THERAPIES FOR MIGRAINE
Nonspecific Prescription Medications
Butorphanol IN
Ibuprofen/Naproxen sodium
Prochlorperazine IV
GROUP 1a: Substantial empirical evidence and pronounced clinical benefit in migraine Silberstein SD. Neurology . 2000.
Migraine-Specific Medications
Triptans
DHE
SC, IM, IN, IV (plus antiemetic)

ACUTE THERAPIES FOR MIGRAINE GROUP 2: Moderate empirical evidence and clinical benefit
Opioids  Others
Over-the-Counter Analgesics
Aspirin
Acetaminophen, aspirin, plus caffeine
Silberstein SD. Neurology . 2000. GROUP 1b: Substantial empirical evidence of clinical benefit in restricted populations

CONSIDERATIONS IN INITIAL ACUTE THERAPY As disability increases, nonspecific treatments less likely to work In the most severely afflicted 25% of migraine sufferers, an NSAID-metoclopramide combination is successful in only 25% of patients Try to get the treatment “right” the first time
Match treatment intensity to attack severity (stratified care)
Ask about migraine disability and impact
Silberstein SD. Neurology . 2000.

Trigeminovascular model of migraine Efferent Adapted from Goadsby and Olesen (1996) Dura mater Afferent Trigeminal ganglion Peptide releasing neurones Dura mater Efferent Trigeminal nerve Afferent Blood vessels Efferent CGRP/SP release Dilatation Cranium

Mechanisms for treatment CGRP NK SP 5-HT 1F 5-HT 1D 5-HT 1B Blood vessel Trigeminal nerve Adapted from Goadsby (1997) CGRP calcitonin gene related peptide NK neurokinin A SP substance P triptan CONSTRICTION INHIBITION

TRIPTANS
As a class, relative to nonspecific therapies, triptans provide
Rapid onset of action
High efficacy
Favorable side effect profile
Adverse events and contraindications Selective 5-HT 1B/1D/1F agonists Silberstein SD. Neurology . 2000.

TRIPTANS: TREATMENT CHOICES
Are there differences between the triptans?
If one triptan fails, will another triptan work?
Zolmitriptan
Tablet (2.5, 5 mg)
Nasal spray (5 mg)
Rizatriptan
Tablet (5, 10 mg)
Naratriptan
Tablet (1, 2.5 mg)
Almotriptan
Tablet (6.25, 12.5 mg )
Frovatriptan
Tablet (2.5 mg)
Question and Answer
Sumatriptan
Tablet (25, 50, 100 mg)
Injection (6 mg)
Nasal spray (5, 20 mg*)
* Pediatric efficacy shown Ferrari MD et al. Lancet . 2001.
Eletriptan
Tablet (20, 40 mg)

ROUTES OF ADMINISTRATION Suppositories: antiemetics, ergots, opioids Oral therapies: most medications Nasal sprays: sumatriptan, DHE, butorphanol, zolmitriptan Injectable (SL, IM, IV) sumatriptan, DHE, injectable NSAIDs, opioids, neuroleptics

FORMULATION: ONSET Increasing Speed Parenteral Oral Tablet SL IN PR IM/SC IV

Sumatriptan
Sumatriptan (Glaxo Wellcome)
5-HT 1B/1D agonist
Major advance – good efficacy with subcutaneous formulation
Slow onset (2–4 h p.o.); LogD -1.5
Short t 1/2 (2 h)
Ferrari et al (1995)

Headache responses continue to improve over time after eletriptan dosing Time course for headache response 0 20 40 60 80 100 0 1 2 3 4 Time post dose (h) n =563 Pfizer, data on file % Patients with response Placebo 20 mg eletriptan 40 mg eletriptan Study 314 ** P <0.05 vs placebo for all doses 80 mg eletriptan ** ** **

ACUTE TREATMENT PRINCIPLES Early intervention Use correct dose and formulation Use a maximum of 2 – 3 days/week     Use preventive therapy in selected patients  stratified care Silberstein SD. Neurology . 2000; Lipton RB, et al. JAMA . 2000.

STEP VS. STRATIFIED CARE Start Start A B C A B C

BASIS OF STRATIFICATION
Symptom profile
Prominent nausea and vomiting may require parenteral therapy
Headache frequency
Consider risk of medication overuse
Patient history and preferences
Consider adverse events and prior experience
   
Headache onset and severity
Fast onset may benefit from parenteral therapy
Disability predicts treatment needs
Silberstein SD. Neurology . 2000.

MIDAS Score Days in Last 3 months
You’ve missed work or school due to your headaches?
Your productivity at work or school reduced by half or more due to your headaches? (Please do not include days you counted in question 1 where you missed work or school)
You not do household work because of your headaches?
Your productivity in household work reduced by half or more because of your headaches? (Do not include days you counted in question 3 where you did not do household work)
You missed family, social or leisure activities because of your headaches?
A. Had a Headache? If a headache lasted more than one day count each day.
B. On a scale of 1-10 on average how painful were those headaches? (Where 0 is no pain, 10 is as bas as pain could be??

GradeDefinitionScore
I Minimal or infrequent disability 0-5
II Mild or infrequent disability 6-10
III Moderate disability 11-20
IV Severe disability 21+

DISABILITY IN STRATEGIES OF CARE (DISC) STUDY
Step care across attacks
ASA + M
Assess response after 3 attacks
Escalate treatment to zolmitriptan if ASA + M fails 2/3 or 3/3
Stratification based on disability
MIDAS Grade II — ASA + M
MIDAS Grade III, IV — Triptan (zolmitriptan)
Step care within attacks
ASA + M  Assess response at 2 hours
Rescue with zolmitriptan prn
Stratified care produces better headache response less disability time Disability can be used to predict treatment needs Compared 3 strategies of migraine management over 6 attacks Lipton RB et al. JAMA. 2000.

TREAT MIGRAINE WHEN PAIN IS MILD Retrospective analysis of 3 studies confirmed triptan treatment while pain is mild provided higher pain-free response at 2 h than ergotamine plus caffeine or aspirin plus metoclopramide, and reduced need for redosing Prospective rizatriptan study of 1919 patients confirms triptan effectiveness at all levels of pain but enhanced benefit if taken while pain is mild Post-hoc analysis of Spectrum study (26 patients) showed sumatriptan provided more effective relief with less recurrence when taken while pain was still mild Cady RK et al. Headache . 2000; Cady RK et al. Clin Ther . 2000; Hu XH et al. Headache . 2002.

TRIPTANS IN THE SPECTRUM OF MIGRAINE In patients with migraine, sumatriptan effectively treats all 3 types In patients with pure TTH, sumatriptan is not effective In migraine sufferers TTH, has a migraine-like mechanism, whereas pure TTH has a different mechanism Therefore, sumatriptan can effectively treat TTH in migraine sufferers, probably because it is a form of mild migraine Patients with disabling migraine have different headache types, including migraine, migrainous, and tension-type headache (TTH) Lipton et al. Headache. 2000; Cady RK et al. Cephalalgia. 1997.

RECURRENCE & REBOUND Rebound: Recurring headache induced by repetitive and chronic overuse of acute headache medication
Recurrence: Return of episodic headache during the same attack following acute treatment
Prevention: Treat early, add NSAID. Use long duration triptan or DHE
Treatment: Repeat initial acute headache drug; almost always effective
Tfelt-Hansen P et al. Drugs . 2000; Capobianco DJ et al. Headache . 2001.

APPROACH TO DIFFICULT HEADACHE PROBLEMS Problem Strategy Headache recurrence Treat earlier, add NSAID, increase dose, change triptans (consider naratriptan or frovatriptan), or switch to DHE Elderly Use acetaminophen, COX 2 inhibitors, opioids, atypical neuroleptics Pregnancy Use acetaminophen, opioids, corticosteroids, neuroleptics Adverse effects Switch triptans, use a different class
Lack of response
Treat earlier, increase dose, add metoclopramide or NSAID, change formulation or triptan. Add preventive. Silberstein SD et al. Wolff’s Headache and Other Head Pain . 2001.

SUMMARY OF ACUTE MIGRAINE MANAGEMENT Identify coexistent conditions that influence therapy Make a specific, credible diagnosis and communicate it Assess migraine severity and it’s impact on the patient Determine the patient’s preferences and needs (eg, fast relief, adverse effects tolerance) Develop a therapeutic partnership with realistic expectations Create plan based on migraine type and severity, as well as patient’s needs, preferences, and comorbidities Consider need for preventive treatment

Chronic Daily HA

Tension (v. migraine)
 10 attacks lasting 30 min–7 days
 2 of the following 4
Bilateral
Not pulsating
Mild or moderate intensity
Not aggravated by routine physical activity
No nausea or vomiting
One or neither photophobia or phonophobia
Not attributable to another disorder

MIGRAINE ADDITIONAL FEATURES Abatement with sleep Stereotyped premonitory symptoms Characteristic triggers Positive family history Childhood precursors (motion sickness, episodic vomiting, episodic vertigo) Osmophobia Predictable timing around menstruation (or ovulation) Pryse-Phillips WEM, et al. Can Med Assoc J . 1997.

UNDIAGNOSED MIGRAINE SUFFERERS OFTEN RECEIVE OTHER MEDICAL DIAGNOSES Lipton RB et al. Headache . 2001.

AURA: MIMICS AND SECONDARY CAUSES TIA Carotid artery dissection Venous sinus thrombosis Vasculitis Tumor Simple partial seizure AVM Bousser MG et al. In: Wolff’s Headache And Other Head Pain . 2001; Campbell JK, Sakai F. In: The Headaches . 2000; Silberstein SD, Lipton RB, Goadsby PJ. Headache in Clinical Practice . 2002.

LATE-LIFE MIGRAINE ACCOMPANIMENTS VS TIA Mild headache in 50% Progression from one accompaniment to another Repetition (  2 similar attacks) Duration 15 – 25 minutes Characteristic midlife flurry of attacks Build up of scintillations — “march” of paresthesias Fisher CM. Can J Neurol Sci . 1980; Silberstein SD, Saper JR, Freitag FG. In: Wolff’s Headache And Other Head Pain . 2001.

MIGRAINE AND STROKE Clinical manifestations of underlying disease (MELAS, CADASIL) Causal Comorbid Coexistent Bousser MG et al. In: Wolff’s Headache And Other Head Pain . 2001 .

CADASIL

CSF XANTHOCHROMIA AFTER SAH SPECTROPHOTOMETRY Vermeulen M et al. J Neurol Neurosurg Psychiatry . 1989. TIME AFTER HEMORRHAGE PROBABILITY (%) 12 HOURS 100 1 WEEK 100 2 WEEKS 100 3 WEEKS >70 4 WEEKS >40

Preventive Management of Migraine

GUIDELINES: WHEN TO USE PREVENTIVE MANAGEMENT Uncommon migraine conditions Acute medications contraindicated, ineffective, intolerable AEs, or overused Frequent headache (  2 attacks per week) Patient preference Cost considerations Silberstein SD et al. Wolff’s Headache And Other Head Pain . 2001. Migraine significantly interferes with patient’s daily routine, despite acute R x

GOALS OF PREVENTIVE TREATMENT Improve responsiveness to acute R x Improve function and decrease disability Silberstein SD et al. Headache in Clinical Practice . 2nd ed. 2002. Decrease attack frequency (by 50%), intensity, and duration

Migraine Prevention

GENERAL PRINCIPLES OF PREVENTIVE TREATMENT
Evaluate therapy
Use headache calendar (diary)
Attempt to taper and discontinue treatment when headaches well controlled
Adequate trial (2 – 3 months) at an appropriate dosage Avoid interfering, overused, and contraindicated medications Silberstein SD et al. Headache in Clinical Practice . 2nd ed. 2002.
Start low and increase dose slowly
Use long-acting formulation if compliance an issue

PREVENTIVE MEDICATIONS: DRUG CLASSES Ca 2+ -Channel blockers Antidepressants  -Blockers NSAIDs 5-HT antagonists
Other
Vitamins
Minerals
Herbs
Botulinum Toxin A
Silberstein SD. Cephalalgia . 1997. Anticonvulsants

GENERAL PRINCIPLES OF PREVENTIVE TREATMENT Assess Coexisting Conditions Be aware of drug interactions Do not use migraine drug if contraindicated for other condition Do not use drug for other condition that exacerbates migraine Special concern for women of childbearing potential Silberstein SD et al. Headache in Clinical Practice . 2nd ed. 2002. Select drug to treat both disorders

Comorbidities

Depression “SALSA”
S leep Disturbance
A nhedonia
L ow
S elf-esteem
A ppetite Change

COMORBID AND COEXISTENT CONDITIONS Coexistent disorders are commonly present
Therapeutic limitations
Avoid  -blockers with depression, asthma, or hypotension
Silberstein SD et al. Headache in Clinical Practice . 2nd ed. 2002.
Therapeutic opportunities
Treat two disorders with a single drug
Hypertension or angina — use  -blocker
Depression — use TCAs or SSRIs
Epilepsy or mania — use divalproex or topiramate

PREVENTIVE TREATMENT: DRUG CHOICE COMORBID CONDITION DRUG EFFICACY* SIDE EFFECTS* RELATIVE CONTRAINDICATION RELATIVE INDICATION Anticonvulsants Divalproex 4+ 2+ Liver disease, bleeding disorders Mania, epilepsy, impulse control Topiramate 3+ 2+ Kidney stones Epilepsy, mania, neuropathic pain Gabapentin 2+ 2+ Epilepsy, neuropathic pain Antidepressants TCAs 4+ 2+ Mania, urinary retention, heart block Other pain disorders, depression, anxiety disorders, insomnia SSRIs 2+ 1+ Mania Depression, OCD MAOIs 2+ 4+ Unreliable patient Refractory depression Silberstein SD et al. Headache in Clinical Practice . 2nd ed. 2002. Gray RN et al. Drug Treatments for the Prevention of Migraine . 1999. *On a scale of 0 to 4

PREVENTIVE TREATMENT: DRUG CHOICE COMORBID CONDITION DRUG EFFICACY* SIDE EFFECTS* RELATIVE CONTRAINDICATION RELATIVE INDICATION Antiserotonin Methysergide 4+ 4+ Angina, PVD Orthostatic hypotension  -Blockers 4+ 2+ Asthma, depression, CHF, Raynaud’s disease, diabetes HTN, angina Calcium channel blockers Verapamil 2+ 1+ Constipation, hypotension Migraine with aura, HTN, angina, asthma Silberstein SD et al. Headache in Clinical Practice . 2nd ed. 2002. Gray RN et al. Drug Treatments for the Prevention of Migraine . 1999. *On a scale of 0 to 4

PREVENTIVE TREATMENT: DRUG CHOICE COMORBID CONDITION DRUG EFFICACY* SIDE EFFECTS* RELATIVE CONTRAINDICATION RELATIVE INDICATION NSAIDs Naproxen 2+ 2+ Ulcer disease, gastritis Arthritis, other pain disorders Other Riboflavin 2+ 1+ Preference for natural products Feverfew Botulinum Toxin A 2+ 2+ 2+ 1+ Myasthenia gravis Dystonia or Spasticity *On a scale of 0 to 4 Silberstein SD et al. Headache in Clinical Practice . 2nd ed. 2002. Gray RN et al. Drug Treatments for the Prevention of Migraine . 1999.

PREVENTIVE TREATMENT: USE OF ACUTE MEDICATION
Can use acute and preventive treatment together
Limit acute drug use to prevent drug-induced headache
Certain drugs require caution or cannot be used together
Acute medications may have more benefit
Breakthrough attacks need treatment Silberstein SD. Cephalalgia . 1997. Preventive treatment does not eliminate all attacks

CAUTIONS IN ACUTE MEDICATION USE Silberstein SD. Cephalalgia . 1997. PREVENTIVE CAUTION CONTRAINDICATION Methysergide Ergots, Triptans MAOIs Sumatriptan (subcutaneous) and zolmitriptan Meperidine, Midrin, sumatriptan (po, IN) and rizatriptan Propranolol Rizatriptan NSAIDs Other NSAIDs or ASA Divalproex Butalbital

NONPHARMACOLOGIC TREATMENT: POTENTIAL INDICATIONS Poor tolerance, response, or contraindications to drug therapy Pregnancy, planned pregnancy, or nursing History of overuse Significant life stress or deficient stress-coping skills Goslin RE et al. Behavioral and Physical Treatments for Migraine Headache . 1999. Patient preference

SUMMARY OF PREVENTION Use preventive medications when needed Treat long enough Avoid acute medication overuse Take coexisting conditions into account Use drug with the best efficacy for individual patient

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Neurological lectures...Migraine

by Professor Yasser Metwally on Mar 20, 2009

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