Headache School 2013 Norton Headache and Concussion Center
Headache School2013
Norton Headache and Concussion Center
Why Headache School?
• Headache is one of the most common reasons for patients to seek medical attention
• Of patients seeking medical attention for headache, the majority will be diagnosed with migraine
• Migraine affects approximately 12% of the population
Why Headache School?
• Formal educational programs have been shown to produce better outcomes for patients with headache
• Opportunity for patients to interact with physicians and other patients in an informal setting
What Can You Do?
• Come to classes• Bring a friend, spouse, etc.• Come with questions• Share your story
– Interact with those around you– Migraine is a lot more common than you think– You are NOT the only one
Upcoming Classes
• Medication Maze– April 11
• How Diet Affects Headaches– May 16
• Women and Headaches– June 13
What Is Migraine?
A Common Problem
• 45 million Americans with headache disorders• 30 million Americans with migraine, the most
common disabling form of headache• 12% of the US population has migraine• 18% of women, 6% of men are affected by
migraine
One Year Prevalence of Migraine
Lipton R B et al. Neurology 2007;68:343-349
Migraine is more common than diabetes and asthma combined!
1%
7%
6%
7%
13%
0% 5% 10% 15% 20%
Migraine
Osteoarthritis
Diabetes
Asthma
RheumatoidArthritis
Commonly Mis- / Un-Diagnosed
Diagnosed Migraine
Undiagnosed Migraine
39%
61% 52%
48%
19891999
Lipton et al., 2001
American Migraine Study II
A Costly Problem
• Chronic headache disorders are among the top 20 causes of disability in the US according to the World Health Organization (WHO)
• 4% of Americans experience 4 hours of headaches per day, at least 15 days per month
• Headache disorders are responsible for more than $31B in economic costs in the US annually
Diagnosis of Migraine Without Aura
• No single feature required or sufficient for diagnosis• Characteristics (2/4)
– Unilateral (40% bilateral or generalized)– Throbbing (50% non-pulsating)– Moderate-severe intensity (~20% mild)– Pain worsened by exertion (>95%)
• Associated symptoms (1/2)– Nausea (86% – 95%) or vomiting (47% – 62%)– Photophobia (82% – 95%), phonophobia (61% – 98%)
Russell MB et al. Cephalalgia. 1996.Pryse-Phillips WEM et al. Can Med Assoc J. 1997.
Additional Features of Migraine
• Predictable timing around menstruation and ovulation
• Stereotyped prodromal symptoms• Characteristic triggers• Improves with sleep (more effective in young pts)• Positive family history• Childhood precursors (cyclic vomiting, abdominal
“migraine”, episodic vertigo, probably motion sickness)
• Osmophobia (smell sensitivity)
“I have sinus headaches”
Eross E, Dodick D, Eross M. The sinus, allergy and migraine study (SAMS)
86% Migraine
3% Sinus related headache
Patients self diagnosing “sinus headaches”
What Causes Migraine?
• The Vascular Theory
• Blood vessels constricting (aura)Followed by
• Blood vessels dilating
The Vascular Theory
• Does not explain prodrome• Not supported by blood flow studies• There are effective nonvascular drugs, such as
NSAIDs• Most patients do not have aura
• THIS IS NOT CORRECT
The Neurovascular Theory
• Referred pain from dura mater and blood vessels
• Peripheral Neural Processing• Central Neural Processing
Pain Perceiving Structures Inside the Skull
The most important structures that register pain in the head are the large cranial vessels, proximal cerebral vessels and dural arteries and the large veins and venous sinuses
A More Sensitive Brain
Pain control mechanisms are partially defective in migraine patients
Wang, Schoenen. Cephalalgia. 1998.
People with migraine process visual and auditory stimulation differently that people without migraine. In this example with repeated stimulation non-migraine patients have decreased response with repeated stimulation whereas migraine patients have an increased response.
Migraine Triggers
• Most frequently reported triggers– Stress– Menstruation– Changes in sleep– Skipping meals– Changes in weather– Diet (alcohol most frequent)
• Time from trigger to onset of headache can be up to 72 hours - hard to track
Migraine Triggers
If summation of triggers are greater than threshold – a headache happens
Migraine Aura
Migraine Aura
• A reversible focal neurological deficit– Most commonly visual
• Cortical spreading depression– Think a wave of activity moving across the brain
followed by decreased activity– The part of the brain inactivated causes the
neurological deficit• Occipital lobes = vision
Spreading Depression of Leão
EEG activity is suppressed and moves in a wave, correlates with symptoms
Aura is from brain cells (neurons)
The Pain
Neuropeptides
• Cranial levels of both substance P and calcitonin gene-related peptide (CGRP) are increased by stimulation of the trigeminal ganglion in humans
• In migraine CGRP is elevated in external jugular vein blood, whereas substance P is not
• CGRP infusions can trigger headache and migraine
A Growing Snowball• Trigeminal nerve and its blood supply (neurovascular)
– Release of neuropeptides• CGRP• Substance P• 5-HT (serotonin) --> “triptans”• Nitric oxide
– Vasodilatation (CGRP) leads to further activation, and the process spreads
– Brainstem, thalamus, cortex become activated leading to “central sensitization”
• Amplified pain signaling in the central nervous system– Allodynia: pain due to a non-noxious stimulant
Cutaneous Allodynia
Migraineurs develop increased sensitivity to stimuli as a result of increased nerve excitability
80% of migraine patients had cutaneous allodynia during attacks
Non painful stimuli perceived as painful
After allodynia occurs, triptans lose effectiveness
Burstein R, et al. Brain. 2000.
1-Peripheral Trigeminal Sensitization
1-Peripheral Trigeminal Sensitization
2-Central Trigeminal Sensitization
2-Central Trigeminal Sensitization
3-Forehead Allodynia3-Forehead Allodynia
4-Extracephalic Allodynia
4-Extracephalic Allodynia
Importance of treating earlyNo Allodynia Allodynia
Pain free @2hrs 28 (93%) 5 (15%)
Not pain free @2hrs 2 (7%) 29 (85%)
30 34
R Burstein, 2003
Allodynia is a risk factor for developing chronic migraine
Earliest Possible Treatment to Stop Migraine Progression and Chronification
Inherited threshold for
trigeminal activation
Triggers or stressors
Episodic migraine
Ineffectivepain
control
Ineffectivepain
control
Medicationoveruse
Medicationoveruse
Increasedheadache frequency
Increasedheadache frequency
Chronic migraineChronic
migraine
Graphic adapted from: Calhoun AH. In: Headache Newsletter: American Headache Society Committee for Headache Education; Veteran’s Day, 2010.
Medication Overuse Headache
• Headache present on ≥15 days/month• Regular overuse for ≥3 months of one or more drugs
that can be taken for acute and/or symptomatic treatment of headache
• Headache has developed or markedly worsened during medication overuse
• Headache resolves or reverts to its previous pattern within 2 months after discontinuation of overused medication
Chronification of MigraineMedication Overuse Headache
The Cleveland Clinic Manual of Headache Therapy p. 156
Bigal ME, et al. Headache. 2008;48:1157-1168.
Bigal ME, et al. Pain. 2009;142:179-182.
Medication Overuse Headache
• Simple analgesics:• Acetaminophen (Tylenol)• Ibuprofen (Advil, Motrin)• Aspirin (Bayer)• Naproxen (Aleve)
• Combination products:• Fioricet• Excedrin
• Opiates:– Lortab (hydrocodone)– Percocet (oxycodone)– Many others
• Triptans:– Imitrex, Maxalt, Relpax,
Zomig, Frova, Amerge, Axert, Treximet
• DHE
Why opiates are bad
Other Associated Symptoms
Nausea• Gastroparesis occurs frequently,
both during and outside of acute migraine attacks1-3
– May correlate with intensity ofheadache, nausea, and photophobia4
• Absorption of orally administered drugs used to treat migraine may be delayed by gastroparesis, postponing the drug’s onset of action1,5-7
1. Krymchantowski AV, et al. Cephalalgia. 2006;26(7):871-874; 2. Aurora SK, et al. Headache. 2006;46(1):57-63; 3. Aurora S, et al. Headache. 2007;47(10):1443-1446; 4. Boyle R, et al. Br J Clin Pharmacol. 1990;30(3):405-409; 5. Thomsen LL, et al. Cephalalgia. 1996;16(4):270-275; 6. Volans GN. Br J Clin Pharmacol. 1975;2(1):57-63; 7. Tokola RA and Neuvonen PJ. Br J Clin Pharmacol. 1984;18(6):867-871; 8. Tfelt-Hansen P. Headache. 2007;47(6):929-930; 9. Dahlöf C. Curr Opin Neurol. 2002;15:317-322; 10. Lychkova AE. Bull Exp Biol Med. 2004;138(2):127-130.
Other Associated Symptoms
• Blurry vision (29%)• Neck pain (31%)• Nasal congestion (28%)• Sweating (30%)• Dizziness (16%)
Why is it important to understand the science of migraine?
• Treatment– Prevention of triggers– Preventative medications– Rescue medications
Triggers
• We now understand that patients with migraine have an “excitable” brain– Need to be careful with:
• Sleep• Diet• Medication overuse• Stress management
Preventative Medications
• Antiseizure drugs– Topamax– Depakote
• Antidepressants– Amitriptyline (Elavil)– Effexor
• Blood pressure medications– Propranolol (Inderal)– Verapamil
Rescue Medications
• Triptans• NSAIDs• DHE
Triptans
Selective agonists (activators) of serotonin blocking the release of other inflammatory chemicals during a migraine attack
Triptans work here
Triptans
• Prevent release of neuropeptides• Once enough activation has occurred the
process of central sensitization begins– Manifested by allodynia– Remember 15% vs. 93% chance of success
NSAIDs
• Ketorolac infusion has been shown to reverse central sensitization
• IV ketorolac is not practical in the outpatient setting
• Further discussed next month
DHE
• Can also reverse central sensitization• More side effects• A little less convenient to give in the home
setting
• Will be discussed further next month
Summary
• Hyperexcitable brain: more susceptible to triggers
• Aura: spreading excitation and depression• Throbbing head pain: trigeminal inflammation• Allodynia: common, important and due to
central sensitization
Future Classes
• Medication Maze– April 11
• How Diet Affects Headaches– May 16
• Women and Headaches– June 13
Questions?
Thanks
NortonHealthcare.com/HeadacheandConcussion