WAPA Winter Conference 2013 Headache Review Sylvia Lucas MD, PhD Clinical Professor of Neurology and Neurosurgery Adjunct Rehabilitation Medicine University of Washington Medical Center January 29, 2013

IHS Classification 2nd Editon – ICHD II Secondary HA 5. Posttraumatic 6. Vascular disease 7. Abnormal ICP, Neoplasm, etc 8. Substances 9. CNS infection 10. Metabolic 11. Cervicogenic, Eyes, Sinuses 12. Psychiatric HA 13. Neuralgias 14. Other Primary HA 1. Migraine 2. Tension-type 3. Cluster and its relatives (TACs) 4. Other primary headaches (exertional, coital, hypnic, etc.)

AGE- AND GENDER-SPECIFIC PREVALENCE OF MIGRAINE Lipton RB, Stewart WF. Neurology. 1993. Migraine Prevalence (%) In both males and females, the prevalence distribution of migraine is an inverted U-shape curve. Prevalence rises through early adult life and then falls after middle life. The second important point to emphasize on this slide is that, at all post-pubertal ages, migraine is substantially more common in women than in men. The prevalence of migraine varies as a function of age. Migraine is a disorder that is most prevalent between the ages of 25 and 55. Part of the reason the condition has such a big impact in the workplace is that it affects people during their peak productive years. Lipton RB, Stewart WF. Migraine in the United States: a review of epidemiology and health care use. Neurology.1993;43(suppl 3):S6-S10.

Secondary Headache Warnings “Worst or first” New headache pattern Change in headache pattern Progressive headache syndrome Onset with valsalva or intercourse Papilledema or abnormal neurological exam New headache over the age of 50 History of cancer or HIV

What kind of headache is this? 32 year old woman Headache since age 12 Severe pain Stabbing, jabbing Knife through her eye Nausea and vomiting Scalp hurts Light hurts Sound hurts Movement hurts Stays in bed Lasts 24-36 hours Can’t work Misses 2 days of work per month 5

Differentiating Migraine and Tension-Type Headaches Usually lasts 4-72 hours Moderate to severe Often unilateral (60%), aura in a minority of patients Exacerbated by routine activity Nausea, vomiting, photophobia, and phonophobia are common Tension type Low impact Usually bilateral, mild to moderate headache Photo- or phonophobia sometimes present No nausea or vomiting Certain features can be used to differentiate migraine from tension-type headache. Migraine is characterized by exacerbation by routine activity, moderate to severe intensity, unilateral presentation, and nausea and vomiting. In contrast, tension-type headache is low impact, usually bilateral, and not accompanied by nausea or vomiting. Dowson AJ, Lipscombe S, Sender J, Rees T, Watson D. New guidelines for the management of migraine in primary care. Curr Med Res Opin. 2002;18:414-439. Dowson AJ et al. Curr Med Res Opin. 2002;18:414-439. 6

ONE-YEAR PREVALENCE OF COMMON HEADACHE DISORDERS % Female Male This slide summarizes the one-year prevalence of some common primary headache disorders. By far, the most common headache disorder in the general population is episodic tension-type headache, which affects 40% of the population. These are the bilateral, pressing or squeezing headaches of everyday life that don’t have many accompanying features. Migraine is also a very common primary headache disorder affecting 18% of women and 67% of men. Frequent headaches occur > 15 days per month and affect 5% of women and 2.8% of men. The two most common frequent headaches are chronic tension-type headache and transformed/chronic migraine, which will be discussed within the context of chronic daily headache. Lipton RB, Stewart WF. Migraine in the United States: a review of epidemiology and health care use. Neurology.1993;43(suppl 3):S6-S10. Schwartz B, Stewart WF, Simon D, Lipton RB. Epidemiology of tension-type headache. JAMA. 1998;279:381-383. Scher AI, Stewart WF, Liberman J, Lipton RB. Prevalence of frequent headache in a population sample. Headache.1998;38:497-506. (>15 attacks per month) Lipton RB, Stewart WF. Neurology. 1993. Schwartz BS et al. JAMA. 1998. Scher AI et al. Headache. 1998. 7

What causes headache? Genetics Environment A headache brain is inherited A headache brain is hypersensitive and hyperexcitable If one parent has migraine: 50% chance that a child will have migraine Environment Internal and external triggers 8

Migraine is a Transmission Problem Same headache-different genes FHM-I CACNA1A: P/Q voltage-gated Ca2+ channel on chr 19 (Ophoff et al. Cell 1996; 87:543-552) FHM-II ATP1A2: Na+/K+ ATPase on chr 1q23 (De Fusco et al. Nat Genetics 2003;33:192-196) FHM-III SCN1A: sodium channel gene on chr 2q24 (Dichgans et al., Lancet 2005;366:371-377) Effect of mutation (SCN5A) 2-4x accelerated recovery from fast inactivation

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Phases of a Migraine Headache Pre-HA Headache Post-HA Intensity Moderate to Severe HA Premonitory/ Prodrome Aura Mild Postdrome Time Adapted from Cady RK. Clin Cornerstone. 1999;1(6):21-32. 11

Activation of the TNC May Result in Referred Pain that Could be Perceived Anywhere along the Trigeminocervical Network 12

Syndrome of Migraine: More than Pain Neurologic Gastrointestinal Autonomic Musculoskeletal Mood Pain

Migraine With Aura At least 2 attacks with at least 3 of the following Fully reversible visual, sensory, or speech symptoms At least 1 aura symptom that develops gradually over 5 minutes and/or different aura symptoms occuring in succession over 5 minutes Each aura symptom lasts 5 minutes and no more then 60 minutes Headache fulfills criteria for migraine without aura Headache begins during aura or follows aura within 60 minutes Not attributed to another disorder Aura symptoms, if they are present, develop 15 to 60 minutes before the onset of headache. These symptoms are transient and commonly include visual signs such as slowly progressing geometric patterns. Migraine aura is believed to originate from the cerebral cortex and represent a cortical spreading depression, a short-lasting depolarization wave that moves across the cortex at a rate of 3 to 5 mm/min, producing gross alterations in ion balance. The relationship between the aura and the headache pain of migraine is not well understood. Headache Classification Committee of the International Headache Society. Cephalalgia. 2004;24(suppl 1):24-25.

About 15-18 % of migraine patients have aura Cortical Spreading Depression Fortification spectra

STRATEGIES FOR MIGRAINE TREATMENT Acute treatment To stop pain and prevent progression Silberstein SD. Cephalalgia. 1997. Establish diagnosis Set realistic goals Educate patients Individualize care Preventive treatment Decrease in migraine frequency warranted Preemptive treatment Migraine trigger time-limited and predictable Treatment can be acute, preemptive, or preventive. Acute treatment is initiated during an attack to relieve pain and disability and to stop progression of the attack. Preemptive treatment is used when a known headache trigger exists, such as exercise or sexual activity, and for patients experiencing a time-limited exposure to a trigger, such as ascent to a high altitude or menstruation. Preventive treatment is maintained for months or even years to reduce attack frequency, severity, and duration. Patients taking preventive medication can also use acute and preemptive medication. Silberstein SD. Preventive treatment of migraine: an overview. Cephalalgia.1997;17(2):67-72. Silberstein SD, Saper JR, Freitag FG. Migraine diagnosis and treatment. In: Silberstein SD, Lipton RB, Dalessio DE, eds. Wolff’s Headache and Other Head Pain. 7th ed. Oxford, England: Oxford University Press. 2001:121-237.

Acute Migraine Medications Nonspecific Simple Analgesics NSAIDS Combination analgesics Opioids Corticosteroids Adjunctive therapies Antiemetics/dopamine antagonists Specific Ergotamine/Dihydroergotamine Triptans

Migraine-Specific Treatment Choices Sumatriptan (Imitrex) Tablet (25, 50,100mg) Injection (6mg, 4 mg stat dose) Single Dose Vial 6mg/0.5cc Nasal Spray (5, 20mg) Needleless injection (Sumavel Dose Pro 6mg) sumatriptan 85 mg and naproxen sodium 500 mg (Treximet) Zolmitriptan (Zomig) Tablet (2.5, 5mg) ZMT (2.5, 5mg) Nasal Spray 5.0 mg Naratriptan (Amerge) Tablet (1, 2.5mg) Rizatriptan (Maxalt) Tablet (5, 10mg) ODT (5, 10mg) Almotriptan (Axert) Tablet (6.25,12.5mg) Frovatriptan (Frova) (Relpax) Tablet 2.5mg Eletriptan Tablet (20,40mg) DHE-45 (dihydroergotamine mesylate) 4mg/cc injectable Migranal Nasal Spray 4mg/cc

Triptan Pharmacology Tmax (h) Biologic Meta- t1/2 Before During Activity bolism Drug (h) Attack Attack (%) Sumatriptan 2 2 2.5 15 Mao-A, renal Zolmitriptan 3 2 2.5 40 Cyp1A2, Mao-A Naratriptan 6 2-3 3-4 70 Renal, Cyp1A2 Rizatriptan 2 1-1.5 1-1.5 42 Mao-A, renal Eletriptan 4 1 2.8 50 Cyp3A4 Frovatriptan 25 3 3 30 Renal, Cyp1A2 Almotriptan 3.5 1.5-3 1.5-3 70 Cyp2d6, 3A4, Mao-A ,renal

Migraine Management in the Office Anticipate the needs of your patients to avoid costly and unpleasant urgent office or emergency department visits Provide a written or easily referenced plan for urgent care to your patients Re-assess and modify treatment plans as needed

Management Issues at First Visit Initial therapy Match treatment needs to attack profile, associated symptoms and level of disability (stratify the care) Explain recurrence Back-up therapy If initial treatment fails Rescue therapy Education Treat early and optimally, lifestyle changes, avoid triggers

Escalation of Migraine Pain Optimal Delivery Fast Intensity Slow Time

Rescue therapy Patient has already used oral and usual medication Injectable treatment used most often Severe pain and later in the headache Gastroparesis, nausea or vomiting Both patient and physician desire rapid relief Need resources for sicker patients Need the room

Urgent Care Delivery: The Outpatient Clinic Some Things to Consider Transportation Drugs may cause sedation or cognitive slowing Timing Patient observation Staffing Avoid being rushed-establish cut-off times for calls Severity of Symptoms Rehydration or electrolyte imbalance may preclude outpatient delivery

Outpatient Treatment Protocols Ask about medication allergy or drug hypersensitivity Recent medication history (everything) Be aware of maximum daily dosing to avoid toxicity Maximum daily dose of sumatriptan is 200 mg orally; 12 mg SQ; 20 mg nasal spray Maximum daily dose of DHE-45® is 3 mg Use rational polypharmacy Respect half-lives of medication and drug interactions

Outpatient Treatment Protocols A combination approach Treatment with injectable anti-nausea medication Dopamine antagonist if sedation is not an issue Ondansetron if sedation is to be avoided Treatment with a migraine specific therapy Subcutaneous sumatriptan DHE-45® Treatment with injectable NSAID (especially if allodynia is present) Ketorolac IM Jakubowski M, Levy D, Goor-Areh I. et al. Headache 2005;45:850-861.

Neuroleptics (D2 receptor antagonists) Phenothiazines Prochlorperazine, chlorpromazine, promethazine Butyrophenones Droperidol, haloperidol Metoclopromide Anti-adrenergic, anticholinergic, antiseritonergic, antihistaminic effects Sedation, drowsiness, EPS Prevent EPS (dystonia and akasthesia) by premedicating with an anticholinergic

Dopamine Antagonists Medication Delivery and Dose Maximum Daily Dose Chlorpromazine 12.5 mg-25 mg IM/IV 300 mg Droperidol 0.625 mg-2.5 mg IV 10mg Prochlorperazine 5-10 mg IM/IV 40 mg Promethazine 12.5-25 mg IM/IV (AE w/IM) 100 mg Metoclopromide 60 mg

Guidelines for Initiating Migraine Prevention Frequency of headache greater than 4-6 per month, disability more than 2-3 days per month or that significantly interferes with quality of life Use of acute medication more than 2-3 times per week on average or escalating use Acute medications contraindicated, not tolerated, or ineffective Presence of uncommon migraine conditions Hemiplegic or basilar migraine Migraine with prolonged aura or migrainous infarction Patient preference AHS Guidelines for Initiating Migraine Prevention Key Point: Simple ways to recognize when preventive therapy is medically appropriate. Source: AAFP/ACP-ASIM Recommendations.

Migraine Prevention: Medications Antidepressants TCAs, SSRIs, MAOIs Amitriptyline, nortriptyline Cardiovascular medications Propranolol* Timolol* Verapamil Antiepileptic drugs (AEDs) Divalproex* Gabapentin Topiramate* Zonisamide Other NSAIDs 5-HT antagonists Methysergide* Other Riboflavin (B2) Feverfew Magnesium (Mg++) Botulinum toxin Petasites ACE inhibitor Angiotensin II antagonist Coenzyme Q Migraine Preventive: Medications Key Point: Many therapies are currently used for migraine prevention; however, only 5 are approved or seeking approval from the FDA. One of which is no longer available in the US. This slide shows the range of treatments currently used for migraine prevention. Interestingly, very few of the implemented therapies hold FDA approval for migraine prevention. Those agents that are either FDA-approved or are currently being reviewed by the FDA for migraine prevention are indicated with an asterisk. Also listed are emerging treatments for migraine prevention. While some of these are drugs others are nutraceuticals that might be of interest to patients that prefer alternative therapies. Butterbur (Petasites), Feverfew, Glucosamine, and Coenzyme Q10 represent alternative therapies that may have efficacy in the treatment of migraine. TCAs=tricyclic antidepressants; SSRIs=selective serotonin reuptake inhibitors; MAOIs=monoamine oxidase inhibitors; NSAIDs=nonsteroidal anti-inflammatory drugs; ACE=angiotensin-converting enzyme. *Currently holds FDA indication for migraine prevention.

Common Comorbidities Comorbid conditions often found in migraineurs include Depression Anxiety Social phobias Bipolar disorder Irritable bowel syndrome Sleep disorders

Migraine Comorbidity May Assist With Selection of Preventive Agent Anxiety Bipolar Depression Epilepsy Insomnia MVP Raynaud’s Agent SSRI/SNRI, AED AED, SSRI/SNRI TCA AED – b-blocker Calcium blocker Comorbidities might influence selection of preventive agents in patients with migraine. This slide lists comorbid conditions and appropriate classes of agents. For example, patients with migraine attacks and a concomitant anxiety disorder might benefit from a selective serotonin reuptake inhibitor or a serotonin-norepinephrine reuptake inhibitor. Lipton R, Silberstein S. 21st Century Prevention and Management of Migraine Headaches. Clinician. 2001;19:1-26. AED=antiepileptic (anticonvulsant) drug; MVP=mitral valve prolapse; SSRI=selective serotonin reuptake inhibitor; SNRI=serotonin norepinephrine reuptake inhibitor; TCA=tricyclic antidepressant Lipton R, Silberstein S. Clinician. 2001;19:1-26.

Other Types of Primary Headache Cluster headache Occurs in episodes, or “clusters” Brief, severe pain around 1 eye lasting 15 min to 3 hours Up to 8 times per day, often waking patient from sleep Pacing headache Tension-type headache Bilateral pressure, vice-like pain of mild to moderate intensity Rarely accompanied by associated symptoms It is important to correctly differentiate migraine from other types of headache before determining the optimal treatment. Cluster headache is the most painful of the primary headaches. It comes on without warning, is unilateral, and is characterized by a rapid increase in pain intensity. It lasts 45-90 minutes on average, compared with 4-72 hours for migraine, and unlike migraine, is not usually associated with aura, nausea, and vomiting. In contrast to migraine, cluster headache predominates in men (M:F ratio 4:1). Tension headache is rarely accompanied by nausea, vomiting, photophobia, and phonophobia. It is often accompanied by tightness of the neck and shoulder muscles. Silberstein SD et al. Wolff’s Headache and Other Head Pain 2001:6-26

Treatment of Cluster Headache Acute therapy Oxygen 100% for 10-12 minutes at 8L/miin via tight-fitting mask Imitrex Injectable 4-6 mg SQ Short-term prevention Triptan or ergot at bedtime Prevention for episodic or chronic Two preventives with rapid induction AED e.g. valproic acid or topiramate Calcium channel blocker e.g. verapamil ( can go up to 480 mg) Corticosteroids

4.4 Primary headache associated with sexual activity 4.4.1 Preorgasmic headache A. Dull ache in the head and neck associated with awareness of neck and/or jaw muscle contraction and fulfilling criteria B. B. Occurs during sexual activity and increases with sexual excitement. C. Not attributed to another disorder 4.4.2 Orgasmic headache A. Sudden severe (explosive) headache fulfilling criteria B. B. Occurs at orgasm. ICHD-II Cephalalgia 2004; 24 (Supplement 1).

Case History 38 year old woman with 25 year h/o episodic headache Gradual increase in frequency and for the last 6-7 years taking Excedrin Migraine initially 2 tab q 6 h, then q 5h, now q 4 h (10 tabs/day) During pregnancy switched to Excedrin Tension, now mixes them. May take Excedrin PM to sleep Rescues with Fiorinal 2 or 3 tab (40/mo). Occasional ER visit Wakes up with suboccipital headache (3/10) which is constant, becoming unilateral with no predominant side, severe pain (10/10) and nausea about twice/mo for 2 d Interferes with taking care of her 6 year old and work Prior neurologist tried sumatriptan, topirimate and amitriptyline

Take 2 tablets every 4 hours until you are addicted.

Syndrome of Medication Overuse Headache (MOH) Occurs in patients with pre-existing migraine/pain Waking with early morning headache Pattern of headaches and overuse of analgesics in predictable and escalating frequency Prevention: limit frequency and dose of meds Treatment: refractory to otherwise appropriate therapy withdrawal therapy restriction of monthly doses for acute treatment Medication overuse and subsequent medication-overuse headache (MOH), also known as rebound headache, is a growing problem. MOH occurs among patients with pre-existing migraine headaches or pain. MOH consists of a pattern of headaches and overuse of analgesics. Withdrawal therapy is the only treatment for MOH and restriction of monthly doses is required for successful prevention. Diener HC, Limmroth V. Medication-overuse headache: a worldwide problem. Lancet Neurol. 2004;3:475-483. Maizels M. The patient with daily headaches. Am Fam Physician. 2004;70:2299-2306.

Medications With Risk of MOH or Rebound HA High Moderate to Low Acetaminophen, aspirin, caffeine Butalbital-containing combinations Short-acting opioids Short-acting NSAIDs Decongestants Dihydroergotamine mesylate Long-acting NSAIDs Simple analgesics Long-acting opioids Triptans Medications with a high risk of medication-overuse headache (MOH) or rebound headache include acetaminophen, aspirin, caffeine, butalbital-containing combinations, and short-acting opioids. Triptan overuse headache is not encountered with great frequency in clinical practice. At this time, however, it appears that all triptans should be considered moderate to low inducers of MOH or rebound headache. It remains to be seen whether triptans with longer half-lives distinguish themselves from those with shorter half-lives with regard to MOH. Smith TR, Stoneman J. Medication overuse headache from antimigraine therapy: clinical features, pathogenesis and management. Drugs. 2004;64:2503-2514. Adapted from Smith TR et al. Drugs. 2004;64:2503-2514.

Principles of Medication Overuse Headache (MOH) Therapy Taper medications most likely to cause MOH/rebound Substitute acute medications that are less likely to cause MOH/rebound Bridging program during withdrawal parenteral dihydroergotamine mesylate low-dose tizanidine with long-acting NSAIDs daily doses of a triptan for up to 10 days short course of steroids, long-acting NSAIDs Preventive Medication Cautions: opiate and barbiturate abstinence syndromes increasing headache during withdrawal period Medications most likely to cause medication-overuse headache (MOH) should be tapered, and acute medications that do not cause this condition should be used as substitutes. Synergistic combination therapy should also be considered. The treating physician should be watchful for opiate and barbiturate abstinence syndromes and increasing headache, which can occur during the withdrawal period. Maizels M. The patient with daily headaches. Am Fam Physician. 2004;70:2299-2306. Maizels M. Am Fam Physician. 2004;70:2299-2306.

Menstrual Migraine Frequency 35 Migraine in women (n=55) 30 No. of attacks 25 20 15 10 Women who experience migraines are more likely to have migraine headaches at the time of menses than at other times during the menstrual cycle. Most women experience these headaches just before or with menstruation. Silberstein SD, Lipton RB, Goadsby PJ. Headache in Clinical Practice. 2nd ed. London, England: Martin Dunitz Ltd.; 2002. 5 34 29 24 19 14 9 4 2 7 12 17 22 27 32 Day of cycle Day 1 = first day of bleeding Used with permission from Headache in Clinical Practice. Copyright © 1998, 2002 Martin Dunitz Ltd. 76

Menstrually Related Migraine (MRM) Occurs Days -2 to +3 Approximately 60% of women who experience migraine relate the frequency of their attacks to the menstrual cycle Pure menstrual migraine occurs from days -2 to +3 of menstruation in at least 2 out of 3 menstrual cycles Menstrually related migraine always occurs on days -2 to +3 in at least 2 out of 3 menstrual cycles, as well as other times of the cycle The occurrence of migraine headaches is strongly influenced by the hormonal fluctuations of the female reproductive cycle. Menstrual migraine occurs immediately before, during, or at the end of the menstrual flow. Pure menstrual migraine occurs during days -2 to +3. Menstrually related migraine occurs on days -2 to +3, as well as other times of the cycle. Allais G, Benedetto C. Update on menstrual migraine: from clinical aspects to therapeutical strategies. Neurol Sci. 2004;25(suppl 3):S229-S231. Allais G, Benedetto C. Neurol Sci. 2004;25 (suppl 3):S229-S231.

Hormone Levels During Menstrual Cycle HORMONAL FLUCTUATIONS DURING THE MENSTRUAL CYCLE Follicular phase Luteal phase Endocrine cycle Ovulation P E2 LH FSH Adapted from Silberstein SD, Lipton RB, Goadsby PJ. Headache in Clinical Practice. 2nd Ed. New York, NY: Martin Dunitz; 2002:102

Case Study: Menstrual Migraine Over Time 23 year old nulliparous female History of true menstrual migraine without aura since menarche Headaches changes 6 months ago with administration of oral contraceptives Now migraines present with aura and weakness never experienced before Concerns with oral contraceptives or alternate etiology

Migraine as a Risk Factor for Stroke (Migraine Coexistent with Stroke) Stroke risk in young (less than 45 years of age) female population is generally very low estimated to be between 5 and 10 per 100,000 woman-years However, there is increased stroke risk (odds ratio) in women migraineurs under age 45: Odds Ratio (OR) Migraine 3 Migraine with aura 6 Migraine plus OC’s 5 - 17 Migraine plus OC’s plus smoking 34 • Relative risk seems high, but absolute risk in migraineurs is low: 17 to 19 in 100,000 There is no evidence that migraine is a risk factor for stroke in women over age 45 MacGregor EA, de Lignieres B. Cephalalgia 2000; 20:157-163. IHS Task Force on Combined OC and HRT. Bousser MG et al. Cephalalgia 2000; 20:155-156.

New persistent headache New onset of migraine with aura Migraine-related Symptoms That May Require Further Evaluation and/or Cessation of Oral Contraceptives New persistent headache New onset of migraine with aura Increased headache frequency or intensity Unusual or prolonged aura symptoms IHS Task Force on Combined OC and HRT. Bousser MG et al. Cephalalgia 2000; 20:155-156.

Summary of Medication Efficacy for Urgent Care

Percent Patients with Pain Relief 82 78 77 70 67 65 60 58 45 43 % 37 32 Weighted averages of percentages of pain relief for all medications for which there were at least 2 randomized trials with drug used as a single agents. Adapted from Fig. 1 in: Kelley NE and Tepper DE. Rescue Therapy for Acute Migraine, Part 3: Opioids, NSAIDs, Steroids, and Post-Discharge Medications. Headache 2012;52:467-482

Percent Patients with Pain Freedom 53 53 40 35 41 36 30 % 21 22 14 Weighted averages of percentages of pain free for all medications for which there were at least 2 randomized trials with drug used as a single agents. Adapted from Fig. 2 in: Kelley NE and Tepper DE. Rescue Therapy for Acute Migraine, Part 3: Opioids, NSAIDs, Steroids, and Post-Discharge Medications. Headache 2012;52:467-482

Summary Prochlorperazine and metoclopromide are the most frequently studied medications used in the ED with efficacy superior to placebo Triptans and DHE are equivalent to the dopamine antagonists for migraine pain relief Opioids are superior to placebo in efficacy Steroid use can decrease headache recurrence after discharge.

Conclusions Based on weighted averages of percentage pain relief for medications studied in at least 2 randomized single agent trials: Recommend combination of: Droperidol or proclorperazine IV (77-82% pain relief) Sumatriptan 6 mg SQ or DHE IV (67-78% pain relief) Ketorolac 30 mg IV or dexamethasone 6 mg IV (69-78% pain relief) Based on weighted averages of percentage pain free for medications studied in at least two randomized trials with drugs used as single agents: Proclorperazine IV or chlorpromazine IV (53% pain free) Meperidine IM, sumatriptan SQ or magnesium IV (30-36% pain free) IV is the preferred route of administration and recurrence many be decreased by the addition of dexamethasone

Thank you!