What is migraine march 2013
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What is migraine march 2013






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What is migraine march 2013 What is migraine march 2013 Presentation Transcript

  • Headache School 2013Norton 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 MigraineLipton R B et al. Neurology 2007;68:343-349
  • Migraine is more common than diabetes and asthma combined! Migraine 13%Osteoarthritis 7% Diabetes 6% Asthma 7% Rheumatoid 1% Arthritis 0% 5% 10% 15% 20%
  • Commonly Mis- / Un-Diagnosed Diagnosed Migraine 48% 39% Undiagnosed 61% Migraine 52% 1999 1989 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” Patients self diagnosing “sinus headaches” 86% Migraine 3% Sinus related headacheEross E, Dodick D, Eross M. The sinus, allergy and migraine study (SAMS)
  • 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 SkullThe 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 BrainPain control mechanisms are partially defective in migraine patients
  • 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.Wang, Schoenen. Cephalalgia. 1998.
  • 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 TriggersIf 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 LeãoEEG 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
  • 1-Peripheral Trigeminal Sensitization 3-Forehead Allodynia 2-Central Trigeminal Sensitization 4-Extracephalic AllodyniaBurstein R, et al. Brain. 2000.
  • Importance of treating early No Allodynia Allodynia Pain free @2hrs 28 (93%) 5 (15%) Not pain free @2hrs 2 (7%) 29 (85%) 30 34R Burstein, 2003
  • Allodynia is a risk factor fordeveloping chronic migraine
  • Earliest Possible Treatment to Stop Migraine Progression and Chronification Inherited Medication threshold for overuse trigeminal activation Chronic Ineffective migraine pain control Triggers or stressors Increased headache Episodic frequency migraineGraphic adapted from: Calhoun AH. In: Headache Newsletter: American Headache SocietyCommittee 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 Migraine Medication Overuse HeadacheThe Cleveland Clinic Manual of Headache Therapy p. 156Bigal ME, et al. Headache. 2008;48:1157-1168.Bigal ME, et al. Pain. 2009;142:179-182.
  • Medication Overuse Headache• Simple analgesics: • Opiates: • Acetaminophen (Tylenol) – Lortab (hydrocodone) • Ibuprofen (Advil, Motrin) – Percocet (oxycodone) • Aspirin (Bayer) • Naproxen (Aleve) – Many others• Combination products: • Triptans: • Fioricet – Imitrex, Maxalt, Relpax, • Excedrin 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 of headache, nausea, and photophobia4 • Absorption of orally administered drugs used to treat migraine may be delayed by gastroparesis, postponing the drug’s onset of action1,5-71. 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. TokolaRA 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
  • TriptansSelective agonists (activators) of serotoninblocking the release of other inflammatorychemicals 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? ThanksNortonHealthcare.com/HeadacheandConcussion