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HEADACHE. Andrew Charles, M.D. Professor Director, Headache Research and Treatment Program David Geffen School of Medicine at UCLA. COMMON TYPES OF HEADACHES. PRIMARY HEADACHES MIGRAINE TENSION TYPE CLUSTER HEADACHE AND OTHER TRIGEMINAL AUTONOMIC CEPHALGIAS SECONDARY HEADACHES

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headache
HEADACHE

Andrew Charles, M.D.

Professor

Director, Headache Research and Treatment Program

David Geffen School of Medicine at UCLA

common types of headaches
COMMON TYPES OF HEADACHES
  • PRIMARY HEADACHES
    • MIGRAINE
    • TENSION TYPE
    • CLUSTER HEADACHE AND OTHER TRIGEMINAL AUTONOMIC CEPHALGIAS
  • SECONDARY HEADACHES
    • Headaches due to infection
    • Headaches due to vascular causes
    • Headaches due to tumors
    • Etc., etc.
headache prevalence and impact
HEADACHE: Prevalence and Impact

PREVALENCE

    • 18-25 % women have migraine
    • 6-10 % men have migraine
    • 5% of women have headache more than 15 days per month
  • 112 million bedridden days per year
  • Cost to U.S. Employers -- $13 Billion per year
  • The majority of patients with migraine have not received an appropriate diagnosis, and are not receiving appropriate therapy
slide4

MIGRAINE – A MULTISYMPTOM COMPLEX

PAIN

Sensory, Cognitive, Motor Symptoms

VISUAL SYMPTOMS

PATHOPHYSIOLOGICAL EVENTS

Nausea/Vomiting

VESTIBULAR SYMPTOMS

PAIN

changing concepts of migraine pathogenesis
CHANGING CONCEPTS OF MIGRAINE PATHOGENESIS
  • MIGRAINE IS A DISORDER OF BRAIN EXCITABILITY
  • VASODILATION MAY OCCUR AS PART OF THE DISORDER, BUT IS NOT REQUIRED FOR MIGRAINE PAIN
slide6

Penfield W. A contribution to the mechanism of intracranial pain. Assoc Res NervMent Dis. 1935;15:399-416.

  • Ray BS, Wolff HG. Experimental studies in headache: Pain-sensitive structures of the head and their significance in headache. Arch Surg. 1940;41:813-856.
issues with studies of ray and wolff penfield
Issues with Studies of Ray and Wolff, Penfield
  • Stimulation of vessels was focal external stimulation or mechanical dilation
  • There is no evidence that physiological relaxation of smooth muscle and resultant dilation can cause pain
  • Multiple areas of brain that could evoke pain were not stimulated:
    • Cingulate cortex
    • Brainstem – Stimulation or lesions in brainstem can cause migraine
vasoactive drugs cause migraine after significant delay hours not correlated with vasodilation
Vasoactive Drugs Cause Migraine After Significant Delay (hours), Not Correlated with Vasodilation
  • Nitric oxide donors
  • PDE inhibitors
  • Histamine
  • CGRP

Schoonman, et al. Migraine headache is not associated with cerebral or meningeal vasodilatation--a 3T magnetic resonance angiography study. Brain 131, 2192-2200, 2008.

Kruus, et al. Migraine can be induced by sildenafil without changes in middle cerebral artery diameter. Brain. 26:241-247, 2003.

Rahman et al., Vasoactive intestinal peptide causes marked cerebral vasodilation but does not induce migraine. Cephalalgia. 28, 226-236, 2008.

alternative mechanisms of vascular drugs
Alternative Mechanisms of“ Vascular” Drugs
  • -blockers
    • Inhibit neuronal adrenergic signaling
  • Calcium channel blockers
    • Inhibit neuronal calcium channels
  • Caffeine
    • Neuronal/glial adenosine receptor antagonist
  • Ergotamines
    • Modulate central 5-HT receptors
  • Triptans
    • Activate neuronal 5-HT1 receptors in brainstem and thalamus
slide10

CORTICAL “WAVES” IN MIGRAINE WITH AURA

Olesen, et al. 1981

Hadjikhani et al., 2001

Bereczki et al., 2008

Cao et al., 1999

slide11

…AND MIGRAINE WITHOUT AURA

Woods et al., 1994

After sumatriptan

4 to 6 h after the attack onset

Before sumatriptan

2 to 4 h after the attack onset

Chalaupka, 2008

Denuelle et al., 2008

slide13

MIGRAINE – A MULTISYMPTOM COMPLEX

PAIN

Sensory, Cognitive, Motor Symptoms

VISUAL SYMPTOMS

Cortical

Activation

Brainstem

Activation

Nausea/Vomiting

VESTIBULAR SYMPTOMS

PAIN

when don t you need to get a scan
When Don’t You Need to Get a Scan?
  • Patient with established history of episodic headache
  • Current headache is consistent with previous headaches or is consistent with different manifestation of a primary headache.
  • Normal neurological exam
when you do need to get a scan
When You Do Need to Get a Scan
  • Extremely abrupt onset of headache
  • Persistent unremitting headache
  • New onset of headache in patient over age of 50
  • Fever
  • Papilledema
  • Abnormal neurological examination
general approach to the headache patient
General Approach to The Headache Patient
  • Make a diagnosis (or challenge the diagnosis that a patient has already been given)
  • Identify and change exacerbating environmental factors and medications
  • Establish regimen for acute therapy of headache
  • Determine if preventive therapy is appropriate
ihs criteria for migraine without aura
IHS CRITERIA FOR MIGRAINE WITHOUT AURA
  • At least 5 attacks fulfulling the following:
    • Headaches lasting 4 to 72 hours
    • During headache, at least one of the following:

Nausea and/or vomiting

Photophobia and phonophobia

    • At least 2 of the following criteria

Unilateral location

Pulsating quality

Moderate or severe intensity

Aggravated by physical activity

simplified diagnostic criteria id migraine
Simplified Diagnostic Criteria:ID Migraine
  • Light sensitivity with headache
  • Nausea with headache
  • Decreased ability to function with headache
  • Any 2 out of 3 = Migraine

Migraine should be the default diagnosis for any headache that is brought to the attention of a health care provider

migraine other features
Migraine: Other Features
  • Perimenstrual timing
  • Stereotypical prodromal symptoms
  • Characteristic triggers
  • Abatement with sleep
  • Childhood precursors (motion sickness, somnambulism, episodic vomiting, episodic vertigo)
  • Osmophobia
  • Diarrhea during attack
landmark how likely is it that headache is migraine
Landmark: How Likely Is it That “Headache” Is Migraine?
  • In a prospective, open-label study of 1203 patients with episodic headache
  • 94% (of 377 evaluable patients) had migraine or probable migraine
  • 25% with migraine were not diagnosed by their physician
  • Headaches had a severe impact (HIT–6 score 64)

Probable migraine (n=67)

18%

Migraine (n=288)

76%

Episodic tension-type (n=11)

3%

Unclassifiable (n=11)

3%

Adapted from Tepper SJ et al. Headache. 2004;44:856–864.

landmark patient and physician diagnoses
Patient

If patient self-reports migraine, 99.5% chance migraine or probable migraine

If patient self-reports non-migraine, 86% chance migraine or probable migraine

Physician

If physician diagnoses migraine, 98% chance migraine or probable migraine

If physician diagnoses non-migraine, 82%chance migraine or probable migraine

Landmark: Patient and Physician Diagnoses

In a prospective, open-label study of 1203 patients with episodic headache

  • Self-report or physician diagnosis of migraine was almost always correct
  • Self-report or physician diagnosis of non-migraine was almost always later found out to be migraine

Adapted from Tepper SJ et al. Headache. 2004;44:856–864.

migraines are often misdiagnosed
MIGRAINES ARE OFTEN MISDIAGNOSED
  • SINUS HEADACHES
    • SIMILAR DISTRIBUTION OF PAIN
    • MIGRAINES CAN BE SEASONAL
    • DECONGESTANTS CAN “TAKE THE EDGE OFF” OF MIGRAINE
    • WITHDRAWAL FROM DECONGESTANTS CAN PRECIPITATE MIGRAINES
other common migraine misdiagnoses
OTHER COMMON MIGRAINE MISDIAGNOSES
  • TENSION HEADACHE/CERVICOGENIC HEADACHE
  • NECK PAIN IS A SYMPTOM OF MIGRAINE
    • MIGRAINE COMMONLY ASSOCIATED WITH NECK PAIN
    • NECK PAIN MAY OCCUR BEFORE, DURING, OR AFTER HEADACHE
common headache triggers
COMMON HEADACHE TRIGGERS
  • IRREGULAR MEALS
  • IRREGULAR CAFFEINE, CHOCOLATE, NUTS, BANANAS, ETC.
  • IRREGULAR SLEEP (PARTICULARLY EXCESSIVE SLEEP)
  • STRESS OR “LET-DOWN” FROM STRESS
  • AIR TRAVEL, CHANGE IN BAROMETRIC PRESSURE
  • MENSTRUAL PERIOD
the migraine lifestyle
THE MIGRAINE LIFESTYLE
  • CONSISTENCY
    • TIMING OF MEALS, BALANCE OF DIET –- Don’t skip meals, mix of different food groups
    • SLEEP --- Don’t oversleep or undersleep
    • CAFFEINE – “Minimum daily dose” of caffeine on a daily basis
    • EXERCISE – The more aerobic exercise the better
medications that may make migraines worse
MEDICATIONS THAT MAY MAKE MIGRAINES WORSE
  • ORAL CONTRACEPTIVES
  • HORMONE REPLACEMENT
  • SSRI ANTIDEPRESSANTS
  • STEROIDS (TAPERING)
  • DECONGESTANTS
  • SHORT ACTING SEDATIVES (e.g. Ambien (?)
  • BONE DENSITY MEDICATIONS (?)
  • BOTOX
frequent opioid or barbiturate butalbital use is a risk factor for migraine progression
FREQUENT OPIOID OR BARBITURATE (BUTALBITAL) USE IS A RISK FACTOR FOR MIGRAINE PROGRESSION
  • GROWING EVIDENCE THAT OVERUSE OF ANALGESIC MEDICATIONS LEADS TO WORSENING OF MIGRAINE
  • AMPP DATA (Bigal et al., Neurology 2008)
    • Frequent use of opioids or butalbital (more than 8 days/month) is a risk factor for progression to chronic migraine
    • Triptan use is neutral for progression
    • Nonsteroidal use is protective
acute therapies
ACUTE THERAPIES
  • TRIPTANS – Selective 5HT 1b 1d agonists
    • SUMATRIPTAN (IMITREX TABLETS, NASAL SPRAY, INJECTION), SUMATRIPTAN NAPROXEN COMBINATION
    • RIZATRIPTAN (MAXALT “MELTABS”, TABLETS)
    • NARATRIPTAN (AMERGE TABLETS)
    • ZOLMITRIPTAN (ZOMIG)
    • ALMOTRIPTAN (AXERT)
    • FROVATRIPTAN (FROVA)
    • ELETRIPTAN (RELPAX)
  • DHE NASAL SPRAY (MIGRANAL), INJECTION
  • NSAIDS
  • METACLOPRAMIDE
triptan news
TRIPTAN NEWS
  • TRIPTANS ARE NOW AVAILABLE WIDELY WITHOUT A PRESCRIPTION IN EUROPE.
  • SUMATRIPTAN WILL SOON BE AVAILABLE AS A GENERIC IN MULTIPLE PREPARATIONS.
  • SUMATRIPTAN/NAPROXEN COMBINATION TABLET (TREXIMET) IS NOW AVAILABLE.
evidence based non prescription approaches to migraine
EVIDENCE-BASED NON-PRESCRIPTION APPROACHES TO MIGRAINE
  • Magnesium (300-500 mg. per day)
  • Riboflavin (400 mg. per day)
  • CoQ10 (300 -1200 mg. per day)
  • Melatonin (3 mg. qhs)
  • Petasites (Butterbur 75 mg. BID)
therapeutic options for migraine prophylaxis
THERAPEUTIC OPTIONS FOR MIGRAINE PROPHYLAXIS
  • BETA BLOCKERS
  • TRICYCLICS
  • CALCIUM CHANNEL BLOCKERS
  • VALPROIC ACID (Depakote)
  • TOPIRAMATE (Topamax)
  • ?? MEMANTINE
memantine for migraine prevention
MEMANTINE FOR MIGRAINE PREVENTION?
  • Activity dependent blocker of NMDA receptors
  • Identified as a blocker of CSD in rodents
  • Appears to be effective as a migraine preventive therapy for significant percentage of patients with frequent migraine who had failed other preventive therapies
  • It is generally very well tolerated
  • Well designed studies are warranted

Peeters et al., JPET, 2007

Charles, et al., Journal of Headache and Pain, 2007

Bigal et al., Headache, 2008

migraine and pregnancy
MIGRAINE AND PREGNANCY
  • THE SIGNIFICANT MAJORITY OF WOMEN HAVE AN IMPROVEMENT IN MIGRAINE FREQUENCY DURING THE 2nd and 3rd TRIMESTERS OF PREGNANCY
  • THERE IS NO CONSENSUS OR EVIDENCED BASED APPROACH TO TREATMENT OF HEADACHE DURING PREGNANCY
  • REGULAR SMALL AMOUNTS OF CAFFEINE, MAGNESIUM SUPPLEMENTATION ARE REASONABLE NON-PRESCRIPTION ALTERNATIVES
  • THE ONLY ADVERSE EVENT THAT HAS BEEN IDENTIFIED WITH TRIPTANS AND PREGNANCY IS A SLIGHTLY INCREASED RISK OF PREMATURE DELIVERY….i.e. OK TO USE TRIPTANS IN SEVERE CASES
new therapies on the horizon
NEW THERAPIES ON THE HORIZON
  • ACUTE THERAPIES
    • CGRP Antagonist – Initial placebo controlled trials look very promising.
    • Transcranial magnetic stimulation
    • Inhaled ergotamines
  • PREVENTIVE THERAPIES
    • PFO Closure – Multiple closure devices in clinical trials
    • Memantine – Initial uncontrolled results are promising
    • Occiptial nerve stimulation
    • Tonabersat
cgrp calcitonin gene related peptide in migraine
CGRP (Calcitonin Gene Related Peptide)IN MIGRAINE
  • CGRP IS RELEASED INTO JUGULAR VENOUS SYSTEM DURING A MIGRAINE ATTACK
  • CGRP RECEPTOR ANTAGONISTS EFFECTIVELY ABORT A MIGRAINE ATTACK
  • Calcitonin Gene–Related Peptide Receptor Antagonist BIBN 4096 BS for the Acute Treatment of Migraine. NEJM, 350: 1104-1110, 2004.

JesOlesen, M.D., Hans-ChristophDiener, M.D., Ingo W. Husstedt, M.D., Peter J. Goadsby, M.D., David Hall, Ph.D., Ulrich Meier, Ph.D., StephanePollentier, M.D., and Lynna M. Lesko, M.D., for the BIBN 4096 BS Clinical Proof of Concept Study Group

  • Randomized controlled trial of an oral CGRP receptor antagonist, MK-0974, in acute treatment of migraine. Neurology 70: 1304-1312, 2008.

T. W. Ho, MD, L. K. Mannix, MD, X. Fan, PhD, C. Assaid, PhD, C. Furtek, BS, C. J. Jones, MS, C. R. Lines, PhD, A. M. Rapoport, MD On behalf of the MK-0974 Protocol 004 study group*

potential new therapies for migraine
POTENTIAL NEW THERAPIES FOR MIGRAINE

INHIBITORS OF CORTICAL SPREADING DEPRESSION

Memantine, Tonabersat, Transcranial Magnestic Stimulation

INHIBITORS OF CGRP RECEPTOR

Telcagepant

CIRCULATORY TRIGGERS TO BRAIN EXCITABILITY?

PFO Closure

MODULATORS OF CERVICAL INPUT TO HEADACHE

Occipital Nerve Stimulation

Adapted from Jones HR. Netter’s Neurology, St. Louis, MO; Saunders; 2005.

take home messages
TAKE HOME MESSAGES
  • MIGRAINE IS A COMPLEX DISORDER OF BRAIN EXCITABILITY AND NOT SIMPLY A “VASCULAR HEADACHE”
  • MIGRAINE IS EXTRAORDINARILY COMMON AND UNDERDIAGNOSED.
  • THE MAJORITY OF MIGRAINE PATIENTS CAN BE EFFECTIVELY AND SAFELY TREATED WITH AN ORGANIZED PLAN OF LIFESTYLE MANAGEMENT , ACUTE THERAPY, AND PREVENTIVE THERAPY IF NEEDED
  • PROMISING NEW THERAPIES ARE ON THE HORIZON