Headache and migraine med residents-2014

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Headache and migraine med residents-2014

  1. 1. Sarkis M. Nazarian, M.D. Professor of Neurology and Ophthalmology, UAMS Internal Medicine Neurology Lectures Little Rock, Arkansas, July 9, 2014.
  2. 2. 1. Identify and define major primary benign headache syndromes. 2. Differentiate primary benign headaches from secondary, potentially life-threatening headaches. 3. Utilize appropriate medical management and refer patient for non- medical treatments.
  3. 3. This patient was referred for spells of “feeling tired” for up to 24 hours, followed by severe right parietal throbbing headache, associated with “tingling” sensation inside her head, lasting days to weeks. Severe spells once a week. The headaches are preceded by “colors” and “halos” in both visual hemifields, are associated with nausea (occasional emesis), photophobia, phonophobia, and osmophobia. She takes Fioricet, Ketorolac, and Stadol spray 2-3 times a day for 3-4 days a week. She also has frequent “staring spells”, lasting 10 to 60 seconds, from which she can self-arouse; these can occur many times a day, and are preceded by fatigue and right throbbing headache. She has no had no convulsions, tongue biting, or incontinence. She was started on levetiracetam (Keppra) 500 mg bid at her local hospital, where workup with EEG and brain MRI was normal.
  4. 4. At times, her headaches are also preceded by numbness and weakness, which starts in the left face, and spreads to her upper and lower extremities. These symptoms resolve over several weeks. Verapamil 180 mg ER bid has improved frequency of severe headaches. Depakote and Topamax used to help, but have lost efficacy. Inderal was not helpful. Imitrex did not help. PMH is significant for depression (on bupropion 100 mg tid), hypothyroidism (on replacement) and chronic insomnia. Her mother, grandmother, and one daughter have or had similar severe headaches with lateralized weakness. She is a high school graduate, smokes ½ ppd for close to 30 years. No coffee, alcohol, or drugs. General and neurologic exams are unremarkable.
  5. 5. 1) Chronic daily headaches 2) Medication overuse headaches 3) Atypical partial complex epilepsy 4) Conversion disorder 5) Migraine with aura 6) Rasmussen syndrome 7) Hemiplegic migraine 8) Petit mal epilepsy 9) Trigeminal autonomic cephalalgia
  6. 6. 1 year prevalence of 90% Lifetime prevalence of 99% 28 million in US have migraines each year HA is the CC of 20% of patients seen in neurology 9% of adults in US see PCP for HA each year 40 million in US suffer from chronic HAs
  7. 7. …a familial disorder, characterized by recurrent attacks of headache, widely variable in intensity, frequency, and duration. Attacks are commonly unilateral and usually associated with anorexia, nausea, and vomiting. In some cases, they are preceded by, or associated with, neurological or mood disturbances. All of the above characteristics are not necessarily present in each attack or in each patient. World Federation of Neurology Research Group on Migraine and Headache
  8. 8. Irritability Excessive fatigue Depression Mania, euphoria Yawning Salt craving Sugar craving
  9. 9.  Prevalence of migraine with aura reported in 4% of populations in the West, compared to 8% with migraine without aura. Estimated 12M affected in USA.  Peak prevalence is at age 5 in boys and 11-2 in girls, preceding the peak prevalence of migraine without aura.  Four types identified: Visual, in up to 99% Sensory, in 30% - 54%. Language, in 9% - 31% Motor: This is now considered to be part of Familial Hemiplegic Migraine (FHM) exclusively.
  10. 10.  Classic visual aura is migratory and expanding, with positive symptoms (fortification spectrum) preceding negative ones (scotoma). In sensory aura, paresthesias precede numbness. In language aura, patients describe both positive (paraphasias) and negative (anomia) symptoms.  Auras occur sequentially, usually starting with visual, then progressing to sensory, etc. It is almost unheard of for patients to have simultaneous different aura types.  Women are more likely to have hemianopia rather than fortification spectra than men (Alvarez, AJO 1960).
  11. 11.  Lashley in 1941 gave the most detailed analysis of his own scotomas, and mapped them to progress at a rate of 3-4 mm/min across the visual cortex, postulated it was due to a spreading cortical abnormality.  Aura usually starts near fixation and spreads peripherally, gaining velocity as it expands.  Always hemianopic; usually not confined to a quadrant. Very rarely complete hemianopia.  Zig-zag lines at periphery; may be in color or mono- chromatic. Center has scotoma, which gradually recovers vision as outer edge of aura continues to expand.  Leao first described in 1944 the phenomenon of spreading depression (SD) at 3-4 mm/min in lab animals whose cortex was subjected to mechanical or chemical trauma.
  12. 12.  Arm affected 96% of the time, face 67%, leg 24%, and torso 18%.  Usual progression is from fingers up to arm, then jumping to face before the shoulder, eventually affecting the lips, mouth, and tongue.  Language aura is more common in hemiplegic migraine (47% compared to 20% in classic). About 80% have paraphasias or expressive loss, compared to 40% with loss of comprehension.
  13. 13.  Scintillations or other visual, later other symptoms.  Build-up of scintillations  “March” of paresthesias  Two or more similar spells  Headache (present in 50%)  15-25 minute spells (95% of TIAs last <15 mins)  “Flurry” of spells around age 50  Benign course  Normal cerebral angiography  Exclusion of cerebral thrombosis, embolism, dissection, epilepsy, thrombocythemia, polycythemia, TTP.
  14. 14. Cady et al. Poster presented at: 10th IHC; June 29-July 2, 2001; New York, NY. 66% 40% 20% 63% 63% 63% 53% 57% 67% 0% 33% 67% 100% Vomiting Phonophobia Pulsating Nausea Unilateral Worsened by Activity Photophobia Moderate-Severe Pain Drainage Stuffiness 99% Weather Associated n=30 (subjects may report more than one symptom) Headache Symptoms at Screen Common symptoms associated with sinus 73%
  15. 15.  Allodynia is the phenomenon of normally non- painful cutaneous stimuli being perceived as painful.  Present in 60-75% of migraine  Usually in ipsilateral trigeminal distribution (scalp, head, neck), but often spreads to the ipsilateral upper extremity.  Typically develops within an hour of headache onset, and can persist for hours after headache resolution.
  16. 16. Data from the Centers for Disease Control and Prevention, US Census Bureau, and the Arthritis Foundation. Disease Prevalence in the US Population 1% 5% 6% 7% 12% Rheumatoid arthritis Asthma Diabetes Osteoarthritis Migraine
  17. 17. Vascular (Graham & Wolff, 1938-1963) Neural (Moskowitz, 1984) Unified, or neurovascular 5-HT or serotonin (Anthony & Lance, 1969) Channelopathy
  18. 18.  Migraine is a disturbance of subcortical sensory modulation systems.  “Normal light is unpleasant, normal sounds uncomfortable and, probably, normal pulsing of vessels felt as pain” (Goadsby, 2003).  Throbbing pain is mediated by sensitization of peripheral trigeminovascular neurons, cutaneous allodynia by central sensitization (Burstein, 2003).  Triptans are successful in preventing induction of sensitization in central, but not peripheral, trigeminovascular neurons.
  19. 19. 5-HT receptors have been classified into seven different families. The 5-HT3 receptor is a ligand-gated ion channel; all other 5-HT receptors belong to a superfamily of G-protein-coupled receptors with seven transmembrane domains. 5-HT1B/1D, 5-HT1F, 5-HT2B, 5-HT7 subtypes have been implicated in migraine.
  20. 20.  Autosomal dominant disorder, mutation in a P/Q calcium channel (CACNL1A4) gene on Chromosome 19p. Same gene defect causes episodic ataxia type 2.  Close to 19p locus for CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy), which often includes migraine.  MELAS (mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes) also in the differential diagnosis of FHM, presents with episodic sudden headache and convulsions.
  21. 21. Menses, ovulation, pregnancy Birth control/hormone replacement (estrogen) Illness Intense or strenuous activity/exercise Sleep deprivation/excess, jet lag Fasting, missing meals
  22. 22. Bright or flickering lights Excessive or repetitive noises Odors/fragrances/tobacco smoke Weather/seasonal changes High altitudes Medications
  23. 23. Chocolate Sour cream Ripened cheeses (Cheddar, Brie, etc) Cured meats (sausage, hot dogs, etc) Chicken livers, pate Herring, pickled or dried
  24. 24. Pickled, fermented, or marinated foods MSG Freshly baked yeast products, bread Nuts or nut butters Beans: broad, lima, fava, snow peas Onions
  25. 25. Figs, raisins, papayas, avocados, red plums Citrus foods Bananas Caffeinated beverages (withdrawal) Alcoholic beverages Aspartame/phenylalanine cont. foods
  26. 26. Aspartame/phenylalanine MSG Sulfites Nitrites Tartrazine (FD&C yellow dye) Benzoic acid
  27. 27. Birth control/hormone replacement drugs (estrogen) Vasodilators - e.g. trinitroglycerine, persantine PDE-5 inhibitors – e.g. sildenafil Catecholamine depleters - e.g. reserpine
  28. 28. Stroke (esp. with smoking and OCPs) Patent Foramen Ovale Obesity & metabolic syndrome Essential tremor Sleep disorders, Obstructive Sleep Apnea Collagen-vascular disorders Antiphospholipid syndrome Ehlers-Danlos Syndrome Anxiety, depression, bipolar disorder Preeclampsia, orthostatic hypotension
  29. 29. Migraineurs are 2-2.5 times as likely to have stroke as non- migraineurs. PFO (patent foramen ovale) has been found in 48% of patients with migraine aura, 23% in non-aura migraineurs, and 25% in controls (Anzola et al, Neurology 1999). Divers with PFO are more likely to develop headaches after a dive, suggesting gas bubbles can ppt. migraine (Wilmhurst et al, Lancet 2000). Is it microemboli in the brain vasculature or vasoactive substances in blood unfiltered by the lungs that causes the migraine? Does closure of the PFO reduce the incidence of migraine aura and headache? Do anticoagulants decrease the incidence of aura and migraine?
  30. 30. Used since the 1940s; inexpensive Available as po (w/ caffeine), pr forms Powerful vasoconstrictors (veno>arterial) Retro-pleural, -peritoneal, endocardial fibrosis Painful dysesthesias (St. Anthony’s fire) Raynaud’s phenomenon Psychoactive properties: Salem witch trials
  31. 31. Sumatriptan 6 mg sq DHE 1 mg IM DHE nasal spray 2 mg Sumatriptan nasal spray 20 mg Ergotamine suppository 2 mg Triptan tablets (various), sprays Midrin (isometheptene, dichloralphenazone, APAP); Sansert (methysergide), had been taken off the market, recently re-introduced. AVOID butalbital (Fiorinal) and opioids.
  32. 32.  Less arterial constriction compared to ergots.  Very effective: 70-75% pain-free at 1 hour.  Available as IV, IM, sq injection or nasal spray.  Peak levels in 2-11 mins (IV), 15-45 mins (sq), 30 mins (IM), 30-60 mins (nasal).  Lower headache recurrence compared to Imitrex.  Lower cost than triptans.  Side effects: N/V, diarrhea, leg cramps, abdominal discomfort; effect on dopamine receptors.
  33. 33. Metoclopramide (MC) 10 mg IV over 30’; DHE test dose 0.5 mg over 2-3’ Nausea No DHE x 8°, then repeat DHE 0.3-0.4 mg q 8° prn w/ MC, for up to 3 days Headache persists, no nausea DHE 0.5 mg w/o MC in 1° Headache resolved, no nausea DHE 0.5 mg q 8° for 2 days, with MC prn Nausea DHE 0.75 mg q q 8° for 2-5 days, with MC No Nausea DHE 1 mg q q 8° for 2-5 days, with MC
  34. 34.  Poorly absorbed orally, 14% bioavailable;  Tmax: 2-2.5 hours.  Plasma half-life 2 hours only.  Receptor binding is reversible.  Metabolized by MAO; possible “serotonin syndrome”.  In meta-analysis, response 56% for 50 mg, 58% for 100 mg; recurrence in 30-35%.  Side effects: “Chest-related symptoms”, tingling, paresthesias, warm feeling, dizziness, flushing.
  35. 35. Sumatriptan (Imitrex, Glaxo Wellcome) Naratriptan (Amerge, Glaxo Wellcome) Zolmitriptan (Zomig, Glaxo Wellcome) Rizatriptan (Maxalt, Merck) Eletriptan (Relpax, Pfizer) Almotriptan (Axert, Pharmacia) Frovatriptan (Frova, Elan)
  36. 36. Better oral pharmacokinetics: Higher bioavailability (45-75%) More rapid therapetic plasma levels: 30-60 minutes. Longer half-lives (esp. frova & nara) Greater potency at 5-HT1B/1D receptor Increased lipophilicity and brain entry
  37. 37.  May rarely occur when triptans are used with serotonergic drugs (SSRIs, MAOIs, TCAs, Li+, LSD, tramadol, L-DOPA, St. John’s wort, L-tryptophan, Buspar, cocaine, Demerol, Talwin, trazodone, fenfluramine, MDMA “ecstasy”)  Neuromuscular (myoclonus, hyperreflexia, shivering, rigidity, tremor, incoordination), autonomic (tachycardia, diaphoresis, fever, GI hyperactivity, pupils), neuropsychiatric (anxiety, delirium, lethargy, seizures, coma)
  38. 38. New combination medication Treximet Fixed combination sumatriptan (85 mg) and naproxen sodium (500 mg) Relief was superior to either individual medication used as monotherapy in trials Decreased use of using rescue medication compared to monotherapy Need to remind patients not to take Naprosyn or other NSAIDS with this medication
  39. 39. Triptans plus Prokinetics During a migraine there is impaired gastric motility and delayed gastric emptying. This can lead to nausea and impaired absorption of medications. Prokinetics such as Reglan not only increase gastric emptying, but also reduce nausea. Prokinetics may speed up absorption of triptans and therefore alleviate headache faster and prevent central sensitization.
  40. 40. Tricyclic antidepressants Beta-blockers: Proporanolol, atenolol, etc. Flunarizine (not locally available) Divalproex, topiramate, other AEDs Tizanidine NSAID’s (Naproxen, indomethacin) Riboflavin 400 mg/d Magnesium 400 mg/d, fish oil (??)
  41. 41.  Keep daily headache log or diary  Avoid daily pain medications; DO take the daily meds for headache prevention.  Avoid undue stress reduction – read “Don’t Sweat the Small Stuff – and It’s All Small Stuff”, by Richard Carlson.  Exercise several times a week  Keep regular sleep and meal schedules  Avoid caffeine, alcohol, and tobacco  Avoid foods such as chocolate, cheese, and nuts if they cause headaches  Avoid NutraSweet, MSG (Accent), nitrites (hot dogs), sulfites (wine), food dyes (FD&C Yellow 5).
  42. 42. Headache occurring >15 days/month is usually due to affective and somatoform disorders. These headaches are refractory to most migraine and tension headache therapies. Topiramate and Botox A injections have been shown to be of benefit in prophylaxis and approved for this indication. Fibromyalgia, Myofascial Pain, Chronic Fatigue Syndrome, etc., also have headache as major components of their symptomatology.
  43. 43. Tricyclic Antidepressants Other migraine prophylaxis agents Combinations of the above
  44. 44. Wrenching and displacement of pain structures during head trauma Example is postconcussion Chronic HA Neck pain Nervousness Emotional lability Crying spells Inability to concentrate
  45. 45.  “Drug rebound headache”, “transformed migraine”  Diffuse, bilateral headache; daily, constant, present on awakening  Aggravated by mild mental or physical exertion  Associated with neurovegetative symptoms of depression: asthenia, anxiety, insomnia, poor memory  Associated with overuse of NSAIDs, triptans, ergots, benzos, barbiturates, opioids  Tolerance to acute migraine agents  No response to preventive migraine meds
  46. 46. Caffeine: Limit coffee to one cup/day NSAIDs: 10-15 treatment days/month; 5 treatment days/month is protective. Combinations: 10 treatment days/month Ergots, triptans: 10 treatment days/month; use ergots with caution. Opioids: 8 treatment days/month Butalbital: 5 treatment days/month Bigal M et al. Headache 2008;48:1157
  47. 47.  Cluster headache: 7:1 men:women; associated with smoking. Non-pulsating, “boring” pain. Often wakes patient from sleep. Unable to sit still, agitated, restless. Activation in ipsilateral hypothalamus, rather than contralateral midbrain. High suicide risk.  Acute treatment: Ergots, DHE, triptans, intranasal lidocaine; may respond to high-flow (7-15 L/min) oxygen for 10-20 minutes.  Prophylactic treatments: Verapamil, divalproex, lithium carbonate, corticosteroids, indomethacin.
  48. 48.  Cluster headache: 7:1 men:women; associated with smoking. Non-pulsating, “boring” pain. Often wakes patient from sleep. Unable to sit still, agitated, restless. Activation in ipsilateral hypothalamus, rather than contralateral midbrain. High suicide risk.  Acute treatment: Ergots, DHE, triptans, intranasal lidocaine; may respond to high-flow (7-15 L/min) oxygen for 10-20 minutes.  Prophylactic treatments: Verapamil, divalproex, lithium carbonate, corticosteroids, indomethacin.
  49. 49. Chronic Paroxysmal Hemicrania: More frequent (>5/d) and of shorter duration (2-30 mins.) than cluster. 3:1 women. Responds to indomethacin. SUNCT: Short-lasting, unilateral, neuralgiform headaches with conjunctival injection and tearing. At least 20 attacks a day, each lasting 10-60 seconds; refractory to treatment. Lamotrigine may be useful in prevention. Hemicrania Continua: Continuous cluster-like headache, more common in women; responds to indomethacin. Hypnic headache: Short (~30 minutes) attacks of bilateral pain that awaken patient, usually same time every night. Common in older patients.
  50. 50. Biofeedback: Thermal technique (warming or cooling hands), found to reduce headache frequency by 35%. Relaxation Therapy: Four types - with tension, using imagery, by breathing exercises, by hypnosis. Overall 35% reduction in headache frequency. Relaxation & thermal feedback together - 56% reduction. Acupuncture. Botulinum A toxin: Has been found effective in chronic migraine.
  51. 51. Exertional headache Cough headache Coital headache Cold stimulus headache: “ice cream” Idiopathic stabbing headache: “ice-pick” External compression headache: “swim goggle”
  52. 52. Infection, fever Hypoxia, anemia, dehydration Hypoglycemia Hangover Caffeine and CNS stimulant withdrawal Opioid withdrawal Decompression
  53. 53. “Thunderclap headache”: Severe, maximal at onset Neck and intrascapular pain, photophobia 20% have minimal or mild headache, gradually worsening Headache worsened by movement 75% have meningismus
  54. 54.  Pain in face, head, or neck, followed by retinal or brain stroke within hours to days. Pain is most commonly in anterior neck, frontal or parietal area, present in 80-85%. Headache may be insidious, or “thunderclap”. It resolves within a week in 90%, but it can last for several years.  Horner’s syndrome develops in about half the patients. Baumgartner et al found it in 28% of patients with stroke, but in 53% of those without.  Cranial nerve palsies (IX-XII) develop in about 12%. Pulsatile tinnitus is present in 10%.  TIAs or strokes of retina and brain develop in 50- 95% of patients; TIA often precedes stroke.
  55. 55. Presents with thunderclap headache First described in a 1988 by Call, Fleming, et al. Mostly in women, 20-50 year-old range; resolves in 3 months, and 89% of patients have excellent prognosis. Angiography reveals segmental intracranial stenoses. Mostly benign, but focal deficits in 43%, strokes in 39%, SAH in 34%, bleeds in 20%, seizures in 17% in a recent review of 193 patients. [Singhal AB et al, Arch Neurol 2011;68:2005] Ppt. by vasoactive drugs (cocaine, amphetamines, etc.); also common in peripartum period.
  56. 56. 1. Decreased alertness or cognition 2. Onset of pain with exertion, coitus, coughing or sneezing 3. Worsening under observation 4. Nuchal rigidity 5. Focal neurological signs 6. First headache in patient over 50 7. Worst headache ever experienced 8. Headache not fitting a defined pattern
  57. 57.  “Pseudotumor cerebri”  Young, obese women predominate  Headache, papilledema, visual loss; few cases without papilledema  CSF pressure >15 cm H2O  Normal cerebrospinal fluid formula  May be due to intracranial sinus thrombosis, especially in post-partum women  Rarely, due to hypervitaminosis A  Visual outcome worse if patient anemic
  58. 58.  ESR>55 mm/hr, age>55 years; elevated C-RP  Temporal headache, jaw claudication  Assoc w/ polymyalgia rheumatica  Anorexia, anemia, weight loss  Blindness due to optic nerve infarct from posterior ciliary artery involvement  Biopsy: Multinucleated giant cells, internal elastic membrane loss  High-dose corticosteroids to keep ESR nl
  59. 59.  Brief, lancinating pain in trigeminal nerve distribution (usually V2 or V3)  Trigger zones, often inside mouth  Avoidance behavior  Onset in middle age, except younger in MS  Treatment: Carbamazepine, other AEDs, baclofen, tizanidine  Surgery: Radiofrequency lesion of Gasserian ganglion, Jannetta procedure
  60. 60.  Lancinating pain on background of dull, steady occipital pain  Paresthesias and hyperalgesia of occiput  Radiating pain with pressure over occipital nerve  Usu. in setting of cervical spine disease  Treatment: Local anesthetic & steroid block, TCAs, AEDs
  61. 61.  26-gauge, 1/2” needle introduced medial to the external occipital protuberance.  Needle advanced to periosteum, then withdrawn 1-2 mm.  Mixture of bupivacaine (Marcaine) 0.5%, 1-2 ml, and triamcinolone (Kenalog) 40 mg/ml, 0.5 ml, injected slowly in 0.5 cc aliquots, with aspiration prior to each injection.
  62. 62. Two randomized, placebo-controlled studies of onabotulinumtoxinA injections (12 weeks apart) for the prevention of chronic migraine headaches, with follow- up for 24 weeks (679 and 705 subjects), revealed no change in frequency, but fewer headache days and migraine days com pared to placebo, and HIT-6 scores were lower in treated patients. Most common adverse effects with Botox injections were neck pain, muscle weakness, eyelid ptosis, myalgia, and muscle stiffness, as well as, paradoxically, worsening migraine.
  63. 63.  Lipton RB et al: Migraine prevalence, disease burden, and the need for preventive therapy. Neurology 2007;68:343-349.  Montagna P: The Primary headaches: genetics, epigenetics, and a behavioural genetic model. J Headache Pain 2008;9:57-69.  Goadsby PJ: Emerging therapies for migraine. Nature Clin Pract Neurol. 2007;3(11):610- 619.  Goadsby PJ: Neurostimulation for primary headache syndromes. Expert Rev Neurother 2007;7(12):1785-1789.  Ho TW et al. Randomized controlled trial of an oral CGRP receptor antagonist, MK- 0974, in acute treatment of migraine. Neurology 2008;70:1304-1312.  Bigal ME, Lipton RB: The differential diagnosis of chronic daily headaches: an algorithm-based approach. J Headache Pain 2008;8:263-272.  Goadsby PJ: Advances in the understanding of headache. Brit Med Bull 2005;73 and 74:83-92.  Ferrari MD: Migraine. Lancet 1998; 351:1043-51.  Russell MB: Epidemiology and genetics of cluster headaches. Lancet Neurol 2004;3:279- 283.  Headache Classification Committee of the International Headache Society. The International Classification of Headache Disorders, second edition. Cephalalgia 2004;24(Suppl 1):1-160.  www.aan.com/professionals/practice/guideline/index.cfm  www.americanheadachesociety.org  www.migraines.org

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