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The Diagnosis, Treatment, and Management of Acute Migraine \\Pce-web1.pce.local\WEBSITES\PI\pi-images\Articles\CME_Acute_Migraine\440_220.jpg \\Pce-web1.pce.local\WEBSITES\PI\pi-images\Logos-Banners\1.jpg Scott – insert 440 image here so Brad knows what it will look like and for the PDF Learning Objectives After participating in this educational activity, participants should be better able to 1. Educate patients, using a Collaborative Care Model, to make appropriate therapeutic decisions that improve clinical outcomes 2. Identify key issues that impact accurate diagnosis of migraine 3. Recognize signs and symptoms of migraine to prevent its chronification Introduction Migraine is a common and potentially serious chronic disease. The prevalence of migraine in the U.S. adult population is roughly 18% among women and 7% among men.[1,2] This equates to approximately 30 million American adults who suffer from migraine. Greater than 75% of patients report one to 14 headaches per month with nearly 14% having five to 14 headaches per month.[3] Over half of these attacks produce severe impairment, forcing the individual to bed rest. Estimates range as high as 112 million bedridden days per year, translating into reduced productivity with the likelihood of missing work, planned events, and interfering with daily activities. The financial burden on patients and businesses is immense; with a cost to employers calculated at $13 billion annually.[4] The “real” price that our patients pay, however, is a significant reduction in their quality of life, equated to the quality of life reduction observed in a diabetic.[5] As migraine becomes unmanageable, the migraineur may be coerced into altering or changing his or her career with resultant lost income and lower socioeconomic status. For these reasons, it is imperative for primary care health professionals to understand and treat migraine as a potentially burdensome and chronic disease. Yet, ironically, epidemiological studies show that about 50% of patients seeking medical consultation for migraine are not being diagnosed, regardless of the reported impact and severity of the disorder.[6] Q1. Which of the following is the best interviewing technique when evaluating your patient with headaches? A. Ask direct questions utilizing the International Headache Society criteria for migraine B. To save time, allow the patient only one problem at a time C. Ask open-ended questions, and allow the patient to “tell his/her story” D. Obtain the majority of history from family members, as patients cannot recall specifics Taking the Migraine History Obtaining the history and knowing the criteria for migraine should yield the correct diagnosis and lead to the most effective therapy. The only diagnostic tool for migraine is the medical history; thus, being efficient and proficient in obtaining the information, or the history, is critical for the clinician as well as the patient. It has been demonstrated in clinical trials that open-ended questions, which permit patients to “tell their story,” more effectively align the patient and provider and actually save time. This model of history taking is the foundation for collaborative care whereby the clinician and patient work as two experts to develop a patient-centered strategy for managing migraine. Another tool providing a framework for the interview is a proposed clinical model that addresses diagnosis and care of the migraine patient: it is called the 5 “Ps” or principles of patient evaluation. \\Pce-web1.pce.local\WEBSITES\PI\pi-images\Articles\CME_Acute_Migraine\5ps.jpg The first “P” is pattern. Pattern recognition is a critical component of migraine diagnosis. The migraine pattern is described in the phase model of migraine and is characterized by a recurrent yet stable pattern of disabling headaches. \\Pce-web1.pce.local\WEBSITES\PI\pi-images\Articles\CME_Acute_Migraine\phase_model.jpg The “migraine pattern” is distinct from most other primary and secondary headaches. \\Pce-web1.pce.local\WEBSITES\PI\pi-images\Articles\CME_Acute_Migraine\pattern.jpg The second component of pattern is to understand the evolution of the headache pattern over time. This assessment considers if migraine is improving, stable, or worsening. The second “P” stands for phenotype. This addresses the physiological characteristics of the headache. Asking the person, “What is your worst headache like?” will identify whether the person is indeed experiencing migraine. Less intense headaches may also be migraines when one considers the Convergence Hypothesis, which implies the migraine process can be interrupted and only present as prodromal symptoms or aura without headache, mild tension type headache, or it may progress to full International Headache Society (IHS) migraine headache (see IHS definition). \\Pceweb1.pce.local\WEBSITES\PI\pi-images\Articles\CME_Acute_Migraine\criteria.pdf \\Pce-web1.pce.local\WEBSITES\PI\pi-images\Articles\CME_Acute_Migraine\converg_hypoth.swf Many times these lesser headaches are not reported by the patient. The clinician needs to specifically ask for the frequency of any type of headache, including mild headache. The third “P” stands for person and addresses the physiological function of the person between episodes of severe migraine. This uncovers the transformational process, presence of comorbidity, and the existence of low grade headaches that a patient may not bring to your attention without direct query. Does the person generally feel normal between episodes of migraine or are there disruptions of physiological function between headaches that are increasingly evident? The fourth “P” represents pharmacology. This is critical for assessing frequency of medication use, inappropriate use, and/or illicit drug use. The fifth “P” stands for precipitants or the factors that not only put a person at risk but also protect a person from migraine. The utilization to the 5 “Ps” and understanding of the Convergence Hypothesis, along with openended questioning, which allows the “other expert” to give his or her input, will yield the most accurate history. Q2. When assessing the patient who has complaint of headache, which will you find to be the greatest predictor of migraine? A. Severity and location of the headache pain B. The level of disability caused by the headache and accompanying nausea C. Sensitivity to light D. A & B E. All of the above Diagnostic Criteria for Migraine There are international standardized criteria for migraine. Although criteria were developed to ensure a standard for use in research, they can be applied clinically as well; however, more simplified criteria are often helpful. ID Migraine is a brief diagnostic tool that capitalizes on the patient conversation where the patient describes disabling headaches with the symptom of nausea. These two factors combined have been shown to predict migraine diagnosis with 93% accuracy. The reality is that tension-type headache does not produce associated symptoms and rarely reaches a severity that causes a person to seek medical consultation. In the 2004 Landmark Study, 94% of patients seeking consultation for headache had migraine, only 3% had tension-type headache.[7] The criteria for migraine without aura along with the notes from the 2nd Edition of The International Headache Classification (ICHD-2) can be found on the IHS website (link to: http://www.ihs-classification.org/en/02_klassifikation/02_teil1/01.01.00_migraine.html). The more stringent criteria are as follows with the basic criteria bold in red for quick reference: Click here to review. The limitations with using the IHS criteria as the diagnostic standard in clinical practice include the lack of disability measurements, the exclusion of assessment of comorbidity, and the absence of criteria to stage the patient. As a result, there is no recognition of impending chronicity built into the criteria. Designed primarily for research, these criteria encompass headache phenotypes rather than the clinical care of the patient. Still many times the diagnosis gets sidetracked secondary to the following pitfalls. Pitfalls of Diagnosis Migraine is the great masquerader, often confused with sinus pathology, tension headache, and stress. While an accurate diagnosis of migraine is essential in determining an effective treatment strategy, the diagnosis of migraine may be due to a variety of factors. Knowing the autonomic features common with migraine can eliminate much diagnostic confusion. A case study is provided to illustrate common pitfalls and associated problems that alter migraine.[1] Case Study: Mary Objective: Understand Sinus Headache and consider comorbid problems that can alter migraine threshold Mary is a 23-year-old female who has recently relocated for her job. She has had sinus headaches that are worse in the spring and fall, which have responded to over-the-counter sinus/decongestant medication. She feels most of her problems are because of “changes in the weather.” Mary does get headache with prolonged fasting, but usually not severe. She had asthma as a child and has had no symptoms for several years. She feels she is in good health except for her sinus headaches and recurrent sinus infections. She does admit that she is somewhat compulsive and must keep active. Family History: Positive for sinus headaches, depression, mitral valve prolapse on mother’s side; father’s history, unknown. One older sibling with bipolar disorder, sinus headaches, and asthma. Maternal grandmother and aunt both have diabetes. She presents stating that three weeks ago she awoke with a severe headache and sinus pressure causing her to miss work. Since she had no established clinician, she went to the ER with one of the worse sinus headaches she had ever experienced. An MRI was done showing mild bilateral ethmoid and maxillary sinusitis with mucosal thickening with no other abnormalities. Her treatment was a shot of ketorolac, 7-day prescription of amoxicillin, and tramadol/acetaminophen for pain. She awoke the next morning feeling much better, but was fatigued. She completed her antibiotics as instructed and did not need to take the pain medication until last night. Mary had recurrent severe sinus pressure in her forehead associated with bilateral severe headache which she felt was due to the sudden weather change. In the past, this has precipitated her sinus headache and infection. She has recurrent sinus drainage, associated nausea, and moderate to severe frontal and maxillary pain. She meets with you today hoping for a refill of antibiotics for her recurrent sinus headache and infection. She does state that if not treated she will sometimes end up with bronchitis. Physical Examination: Normal except for clear nasal drainage, afebrile, no focal neurological signs. Laboratory tests reveal normal CBC. What is the most likely diagnosis given the information above? A. Recurrent sinus headache with resistant recurrent sinusitis B. Cluster headache C. Allergic rhinitis D. Migraine headache What would most likely relieve her acute symptoms? A. Change antibiotics to cover methicillin resistant staph given age of patient B. Sumatriptan subcutaneous C. Referral to allergist D. Hold further treatment until further evaluation with limited CT of sinuses to better understand extent of infection \\Pce-web1.pce.local\WEBSITES\PI\pi-images\Articles\CME_Acute_Migraine\threshold_1.swf Three years later Mary returns to the office having been lost to follow-up. She states in the last two years she has gone through a pregnancy complicated by gestational diabetes; postdelivery she developed postpartum depression and has had a 50-pound weight gain. Her care, for the most part, has been with her OB/GYN but he suggested she get back with you for care of her increasing headaches. Mary informs you she is missing too much work because of her increasing headaches; she is fatigued, has trouble sleeping, and has difficulty concentrating. She has one to two severe headaches lasting one to two days each week for the last month. She has missed five days of work in the past month and feels her job may be threatened. Her headaches are unchanged except in frequency of the more severe headaches and increased number of milder headaches, which usually awaken her. She does have moments of doing better for a month or two then does worse for month or so. She would like her FMLA (Family and Medical Leave Act) papers filled out and help with her headaches. Her physical examination is normal except now she has a BMI of 32 with a waist circumference of 36, blood pressure is 120/76, pulse 67 regular, RR 12 unlabored. Mary is somewhat anxious and has no complaints of headache on the day of her visit. She is scheduled for lab work and you ask her to come back the next week, keeping a diary of her headaches during the next seven days. Her lab work returns normal TSH, lipid panel with HDL 42, LDL 93, triglyceride 169, CBC normal, renal and hepatic functions normal, and CRP 6 (nl 0-3). At her next visit she tells you that she is treating her headaches with oral triptan, but the headaches she wakes with are severe and she usually misses work on those days. She does have some milder headaches that she is using OTC acetaminophen/caffeine/aspirin several times a week to prevent the more severe headaches. Overall, the past month the oral triptan doesn’t seem to be working as well. She feels the headaches are making her depressed and fears losing her job. The headaches are also interfering with her marriage. What is your diagnosis of Mary’s headache now? What factors are contributing to her headache? What is the treatment strategy? Q3. It may be easy for you to misdiagnose migraine as sinus headache because A. People with migraine have a high correlation of sinusitis B. The pain is often located in the same area C. Migraine is often associated with sinus symptoms D. Mild mucosal thickening on MRI scan E. A, B & C F. B, C & D Mary’s “migraine threshold” has changed since her first visit several years ago. Mary is having more headaches and it takes less to bring on her migraine attacks. Many factors seem to be associated with and can potentially modify the physiological threshold. Insulin resistance is one comorbid factor and seems to alter the migraine threshold. This could be hinted at on initial visit with headaches coming on with prolonged fasting and family history of diabetes. Over the next several years this became more apparent with episode of gestational diabetes and development of frank metabolic syndrome manifested with elevated triglycerides, glucose, central obesity, and mild elevated blood pressure. Another factor in Mary is depression and the cyclical nature of her headaches, history of postpartum depression, and family history of mood disorder would suggest at least nonspecific mood disorder may be playing a significant role in altering the migraine threshold. With the increase in headache frequency and subsequent increase in medications Mary will be at risk of developing medication overuse or in the past called “rebound headache,” which is defined later in article. So by directing treatment to reverse metabolic syndrome with diet and lifestyle changes and addressing the depression and mood swings a more individualized treatment plan can be developed utilizing a personalized tool box as discussed below. The graphics depict the initial headache threshold and then the altered threshold as depression and metabolic disorder further manifested themselves. So it is important to obtain a thorough history and try to catch early comorbid conditions. Mary presented with one of the most common misdiagnosis, which is sinus headaches. \\Pce-web1.pce.local\WEBSITES\PI\pi-images\Articles\CME_Acute_Migraine\threshold_Migraine.swf Sinus headache, as in Mary’s case, may be the patient’s self-diagnosis due to the symptoms of facial pressure and recurrent headaches that seem to originate in or around the sinuses. These individuals often insist that they need an antibiotic because it has worked in the past. If scans are ordered, the MRI is often read as sinusitis on the basis of mucosal thickening or simple inclusion cyst. Because an MRI notoriously over reads sinusitis, a limited CT scan of the sinuses may give a clearer picture.[9] After further evaluation, no evidence of acute sinusitis with air fluid levels is found for the majority of these patients. If there is no air fluid level, and only minimal mucosal thickening and/or a simple mucous retention cyst, it is unlikely the cause of headache and certainly doesn’t explain recurrent episodic/acute headaches. A recurrent, stable pattern of headache occurring over months to years with disability and nausea is generally migraine with associated autonomic symptoms of sinus pressure and or drainage. The more severe sinus symptoms with migraine may be related to comorbid hypersensitive airway disease, allergies, or mild asthma and may respond to therapy, which often can lead to more appropriate and effective migraine treatment. Another pitfall is tension headaches. Even though very common, they rarely lead a patient to seek treatment. Migraine usually is labeled as tension headache merely on the basis of location and associated tightness in neck muscles. This is one of the reasons that the ICHD abandoned the term tension headache in favor of tension-type headache. It has been shown that migraine produces more severe muscle tension than tension-type headache. The prolonged autonomic contraction of the posturing neck muscles can lead to muscle fatigue and soreness. However, this is more likely part of the migraine process and autonomic features of migraine. The muscles indeed are sore and painful to palpate and misdirect treatment to the neck as the major cause of the headaches. Treatment should focus on migraine not on muscle tightness. Certainly evaluation of neck and sinus pathology should be undertaken. The treatment of these should be based on found pathology and stand on their own merit. If the pattern and phenotype of the headaches meet migraine criteria then treatment should be directed to the aggressive management of migraine to lessen the impact. This will assure proper treatment and lessen the morbidity. Other common symptoms of the migraine process are listed here. \\Pce-web1.pce.local\WEBSITES\PI\pi-images\Articles\CME_Acute_Migraine\symptoms.jpg The Hyperexcitable Brain Some understanding on migraine severity may be appreciated by understanding the migrainous hyperexcitable nervous system. Research has found different levels of central nervous system serotonin, prostaglandins, and dopamine as well as multiple other markers in those with migraine compared with those without migraine. The sensitivity of the migrainous nervous system is best demonstrated by the events in the environment that may trigger an attack in a migraineur but are harmless irritations to those without migraine. A migraineur experiencing a strong odor, change in weather, certain foods, or bright lights may be disabled with severe headache, nausea, and vomiting lasting hours to a few days. A nonmigraineur experiences mild irritation that resolves quickly when the offending event is past. Migraine sufferers definitely have a different neurological response appropriately termed in the past as brain storm; they have inherited or have acquired a more vigilant nervous system. Successful management depends on becoming aware of the unique sensitivities and identifying the physical, biological, and environmental factors that impact this nervous system. Without a reliable, effective plan to manage this nervous system, vigilance becomes a way of life, cosensitizing other bodily systems. This hyperexcitable nervous system may manifest symptoms associated with other comorbid conditions, such as anxiety, depression, irritable bowel syndrome, epilepsy, mitral valve prolapse, asthma, hypersensitive airway disease, endometriosis, chronic cystitis, mood disorders, or fibromyalgia.[10,11] Many of these comorbid or co-existing conditions, like migraine, appear to have a familial or inherited basis. This vigilant nervous system has roots in the rudimentary parts of the brain and involves glia cells that set and regulate sensitivity of neurons as well as the brain stem and the limbic system. The limbic system sets our awareness threshold and is our major emotional center. It receives input from all senses and analyzes the data to determine how safe the environment is. So it is of paramount importance to know what type of headache is being treated as well as fully understanding the patient having the headache. Address treating the whole patient and recognize migraine and the company it keeps. This will help with a proper diagnosis and treatment of migraine directed at stabilizing this vigilant nervous system. This is further reinforced by noting that increasing frequency of migraine also has the potential to produce physical changes in the individual’s nervous system. Studies have demonstrated that white bodies on MRIs increase as a function of migraine frequency and that there is iron deposition in the brain, presumed secondary to oxidative damage in individuals with chronic migraine.[12,13] Finally, the concept of central sensitization, suggesting a lower threshold to pain stimuli, occurs in patients with more frequent migraine attacks. These studies suggest that migraine has chronic consequences and underscores the importance of primary care professionals in identification and management of the population at risk of chronic migraine and aggressively treating in the early stages of transformation. \\Pce-web1.pce.local\WEBSITES\PI\pi-images\Articles\CME_Acute_Migraine\risk.jpg Q4. The stages of migraine address A. The burden of the disease B. The frequency of the headaches C. The therapeutic and educational need of the patient D. All of the above E. None of the above Q5. Being familiar with your patients’ stages of migraine will help you to A. Determine treatment strategies B. Interrupt transformation from acute episodic migraine to chronic migraine C. Assess whether opioids should be prescribed for prevention D. A & B E. All of these Staging the Migraineur A migraineur may be classified into one of four stages. Each stage addresses the burden of disease and can be used to define therapeutic and educational need of the patient. Stage 1, is infrequent episodic/acute migraine. Stage 2 is frequent episodic/acute migraine; Stage 3 is transforming migraine, where migraine attacks are so frequent or of such duration that the nervous system does not have time to fully recover between attacks. This is observed clinically by the persistence of symptoms between episodes of severe migraine. These symptoms vary from anticipatory anxiety and depression to other pain disorders and migraine comorbidities. Stage 4 is chronic migraine (15 or more headache days per month) where the person’s life seems to revolve around disabling headaches and medication. The Stage 4 patient often requires an interdisciplinary treatment approach and is easier to prevent than to treat. Referral or consultation may be necessary for this patient. \\Pce-web1.pce.local\WEBSITES\PI\pi-images\Articles\CME_Acute_Migraine\stages.jpg From the graph it is obvious that the treatment to prevent Stage 4 chronic migraine must be instituted at Stage 2 or 3 in the transformation and stresses the need for optimal management of Stage 1 patients. During Stage 3, patients more than likely have signs of a more vigilant nervous system with multiple comorbid conditions reflecting the need for more aggressive management. The patients with chronic migraine have nearly twice the incidence of depression, anxiety, and other chronic pain. They have significantly higher incidence of asthma, bronchitis, cardiac risk factors including hypertension, diabetes, obesity, and hypercholesterolemia.[14] Therefore, the earlier these patients are identified and treated effectively, the more likely to interrupt transformation to chronic migraine and the serious consequences of this chronic disease process. Optimizing Care in Hopes of Preventing Chronification of Migraine By understanding the consequences of transformation to the far end of the spectrum of migraine, we may be able to identify and interrupt the transformation at an earlier stage. Most of these patients give histories of starting out with episodic, less frequent headaches but over months to years developed more frequent headaches with a more erratic pattern. This can in turn lead to more pain medications that begin to contribute to rebound headaches. The term rebound headache has been redefined as medication overuse headache. Basically stated the more frequent use of certain acute or abortive pain medications the more chance of developing worsening headaches over time. Medication Overuse Headache IHS 8.2 A. Headache present on ≥15 days a month fulfilling criteria C and D B. Regular overuse for >3 months of 1 or more drugs that can be taken for acute and/or symptomatic treatment of headache C. Headache has developed or markedly worsened during medication overuse D. Headache resolves or reverts to its previous pattern within 2 months after discontinuation of overused medication Revision of criteria for MOH. Cephalalgia. 2005;25:460-461. It is important to recognize patients who present with increasing escalation of headache associated with increased medication use. There are usually multiple factors that play a major role in beginning the transformation of episodic migraine to chronic migraine. These might be worsening depression, increasing insulin resistance, physical or psychological trauma, and others that lower the migraine threshold, leading to a more easily activated migraine event.[15] As the migraines become increasingly frequent, the headaches become more variable and the nervous system does not have time to recover to baseline. The pattern of the headaches varies with patients describing sinus headaches, tension headaches, and sick headaches. Since the patients have escalation of headaches and acute medications, they often meet the criteria of medication overuse headaches. The psychological and physical debility may lead to increased depression which in turn can further lower the migraine threshold. It becomes a vicious cycle and difficult to pinpoint comorbid depression and anxiety as contributing to or merely an effect of chronic headache. If the frequency increases and the pattern becomes erratic, transformation is well under way. This must be interrupted in the episodic or acute migraine phase by treating aggressively to prevent the long term debility and consequences of chronic migraine. The patient and provider both are challenged. If not addressed for years, the patient may present with multiple complicating diseases such as cerebral vascular disease, coronary heart disease, or renal disease, which limit medication options. If patients are transitioning to more frequent headaches look for increasing insulin resistance or metabolic syndrome or sleep apnea. Evaluate for anemia, thyroiditis, celiac disease, vitamin D deficiency, fibromyalgia, evidence of inflammatory condition, physical or psychological trauma, or other conditions that may be lowering the headache threshold; especially look for mood disorders and/or worsening depression or anxiety.[16] In order to address the multiple factors necessary, a working trust and confidence with the patient is essential. Giving the patient a “toolbox” of various essentials is of utmost importance. Migraine Toolbox \\Pce-web1.pce.local\WEBSITES\PI\pi-images\Articles\CME_Acute_Migraine\toolbox1.jpg With a strong patient-partnership established, start developing a toolbox to empower your patient to manage his or her headaches. One of the most helpful first tools is the introduction of a headache diary. This serves as an effective communication tool to help both of you get a better idea of the impact migraine is having. Have patients note anything they feel might have contributed to attacks or impaired treatment success. Did the patient have to miss work or other important activities? Gradually worsening headaches, missing work, and an ER visit suggest a significant change in the migraine threshold or ineffective therapy or both. The diary helps to evaluate the timing of treatment and proper use of abortive medications. It also may point to habits and lifestyles that may increase the risk of migraine. Q6. A symptom you can recognize that indicates your patients are likely transforming from acute episodic migraine to chronic migraine is/are A. Increase in abortive medication use B. There are fewer days between headaches where they “feel normal” C. Increase disruption of daily activities or duties D. B & C E. All of the above Pharmacological Management Acute Medication In a patient’s toolbox, medication options are either acute/abortive to stop the attack or preventive to reduce the number of attacks. The acute medications are further broken down to migrainespecific and nonspecific medications. Migraine-specific medications are triptans and ergotamines. In 2000, the treatment guidelines were released by the U.S. consortium. The goals were to achieve rapid and consistent pain relief without recurrence, reduce need to rescue, minimize adverse effects, restore function, and optimize patient self-care. Individuals with nondisabling migraine are those who could consistently manage symptoms with NSAIDs, aspirin, or a combination acetaminophen/aspirin/caffeine. This is in keeping with the stratified model of care that suggests the type of medication based on severity of symptoms. For migraine that is disabling, recommendations were to use migraine-specific or more potent migraine medications at the onset. The drugs of choice would be triptans or DHE, which are migraine-specific. The triptans work at 5HT1b/d receptors with block release of inflammatory substances and cause local vasoconstriction of dilated meningeal arteries. Triptans vary in their half life and mode of administration. Each has its own uniqueness regarding drug interactions and metabolism so it is important to become familiar with the triptan you are prescribing. Also it is listed as contraindicated to mix triptans within the same day. It may be very helpful for patients to have in their toolboxes injectable triptan and tablet or other form to better customize their treatment options. DHE is the so-called parent drug to triptans, coming out in 1945; hence called DHE45. DHE is presently in the United States as injectable and nasal form, with an inhaled form in the pipeline. DHE works as triptans at 5HT1b/d but also all 5HT2 receptors. It is associated with nausea when given intravenous and less so with intramuscular use. The main use of DHE can be to break the cycle in more frequent headaches as studies in the past showed no “rebound headache” with its frequent use.[17,18] It is associated with miscarriage and is listed as category X pregnancy drug so caution when using with child bearing potential women. DHE has been shown to be primarily a vein constrictor but shares contraindication with triptans for patients with known heart disease or peripheral vascular disease. Again should become familiar with drug interactions and contraindications with DHE as with all drugs. With caution in those cases where triptans or DHE are not effective or contraindicated, butorphanol or acetaminophen with codeine could be used. Even though butorphanol has U.S. Food and Drug Administration (FDA) approval for acute treatment, care must be taken with butorphanol or codeine containing medications to avoid medication overuse or addiction. The headache phase of migraine is further divided by pain intensity into mild, moderate, and severe. These divisions have a strong relationship to the efficacy of migraine medications, particularly oral triptans. There is essentially a linear decline in pain-free efficacy from 65% two-hour pain-free efficacy when treatment is initiated early during the mild headache to less than 20% for oral triptans initiated during the severe stage of the headache. Even though the early intervention paradigm has been proven to significantly improve efficacy over treatment during moderate/severe headache, it is often not employed by patients. In fact, it is estimated that early intervention is utilized for only about 50% of attacks even when patients are encouraged to treat early. This occurs in part because of the inaccuracy of the term early intervention. Properly understood, early intervention means treat early when the headache is mild. This is an important educational point for patients who may interpret that treating early means taking medicine as soon as all the symptoms of migraine appear, which in reality is when the headache is severe in intensity. Others reasons patients give for not treating early include believing the headache will not become severe and saving the migraine-specific medicine for the “really bad” migraines. Many of these behaviors can be altered through education. Healthcare professionals should not believe, however, that all attacks of migraine can be treated with oral medications during the early mild headache. Some headaches come on suddenly with moderate to severe pain. Other times a patient may awake with severe headache. In these and other special circumstances, having an effective treatment option in the patient’s toolbox is needed. During headache, associated symptoms of tinnitus, rhinitis, sinus pressure, difficulty concentrating, and finding the right word as well as visual difficulties are common. At those times when the headache is allowed to evolve to a moderate-to-severe level, the migraineur is more likely incapacitated. Based on the pain principle of kindling, frequent moderate-to-severe headaches set up the nervous system for more moderate-to-severe headaches. As episodic migraine increases in frequency, the nervous system fails to return to the normal baseline in between headaches and the process of transformation into chronic migraine begins. The complexity and global effect of migraine is what leads to significant disability during attacks and morbidity to the lives of migraine sufferers. For these reasons, it is imperative to treat aggressively to lessen the burden of migraine. The timing of the medications should always be to treat as early as possible, using the early intervention model, treating when headache is mild. Since the arrival of the triptans in the 1990s initially with sumatriptan, they have become the preferred medication for disabling migraine. Clinical trials demonstrate the efficacy of oral triptans at two hours for pain relief to be in the 40% to 70% range; at two hours, pain free response to be 20% to 40% of subjects; and the headache recurrence rate to fall within the 9% to 34% range. All oral triptans at marketed doses were well tolerated and effective. Studies varied on whether headaches were treated in the mild phase or moderate to severe phase and whether success was measured by headache relief or headache free; however, dose and route of administration certainly are factors. Routes of medications are oral, nasal, or subcutaneous. Meta-analyses of all the studies show that injectable sumatriptan still has higher efficacy over oral routes of other triptans but slightly more side effects. Injectable sumatriptan overall is very well tolerated for most individuals and begins working in 10 minutes.[19,20] The major ergotamine in the United States for acute migraine is DHE45, dihydroergotamine. Approved in 1945, it is not associated with medication overuse headache. It is still used quite a bit at headache clinics or hospital settings with patients presenting with chronic migraine or intractable migraine, especially if medication overuse is suspected; however, patients find DHE45 difficult to use and store. Because its gastric absorption is erratic, it needs to be given intramuscular, subcutaneous, intravenous, or by nasal route. Unlike the triptans, it is a category X pregnancy drug. Otherwise, DHE45 shares basically the same indications and contraindications as the triptans and specifically used for migraine headaches. The specifics of triptans and DHE45 vary some based on half life, metabolism, and drug interactions; therefore, prescriber should become familiar with these prior to use. The effectiveness of medications may vary in given individuals, making the diary a vital communication tool for patients and provider to review and individualize therapy. Treatment options vary depending on particular headache symptoms and the situation in which the headache occurs. Triptan therapy, while the headache is mild, is the preferred treatment unless the patient is pregnant or has contraindications to triptans. For those special circumstances—such as awakening with a full-blown migraine, rapid onset headache, or when headache is associated with severe nausea—it is preferred to use a non-oral route. Injectable sumatriptan has shown efficacy where faster therapy is needed. The individual determines which acute medication is better tolerated and most effective. Working with patients and giving other options if treatment is not ideal will lead to the best outcomes. Continue to educate on early intervention for all acute therapy. Watch for and educate on medication overuse headache but encourage early treatment. For acute headaches, stratified care is preferred. Stratified care is matching the treatment to the severity of the symptoms and treating early with more specific medications: if the attacks are disabling, treat early with migraine specific medication. Early intervention has been shown to abort migraine within two hours for the majority of migraineurs. If individuals wait to treat until the headache intensity is moderate to severe, the pain-free success rate drops 30% at four hours and 40% at two hours. Education on timing of treatment is important to assure optimal treatment outcome. To fully understand early treatment strategy an understanding of the phases of the migraine attack is important. An attack of migraine can be divided into three phases: pre-headache, headache and post-headache. The pre-headache phase occurs in a majority of migraine attacks and may consist of a premonitory phase or prodrome and/or aura, which is observed in approximately 25% of attacks. The distinction between premonitory symptoms and aura is that aura represents focal neurological change while premonitory symptoms are more diffused. The pre-headache phase can begin hours or even days before the onset of headache and can add significantly to the duration and disability of a migraine attack.[21] The headache phase generally lasts between four and 72 hours with most attacks in adults lasting over 24 hours.[22] The headache phase of migraine can be divided on the basis of headache intensity into mild, moderate, and severe. Based on the proven benefits of early intervention, the best time to treat is when the headache is mild. This relates to the treatment response to oral triptans (likely other oral drugs as well) because two-hour, pain-free efficacy declines significantly as the headache severity increases. This decline in efficacy is much less for subcutaneous administration of sumatriptan. The post-headache phase or postdrome is the time following resolution of headache and complete resolution of migraine symptomatology. This typically takes several hours to days and can again add considerably to the overall impact and duration of an attack of migraine. When headaches typically are severe and disabling if left untreated or unsuccessfully treated, educate about the importance of treating early when the headache is mild. \\Pce-web1.pce.local\WEBSITES\PI\pi-images\Articles\CME_Acute_Migraine\phase_model.jpg Sometimes treating when a headache is mild is not an option. What if a patient awakes with a fullblown migraine associated with nausea and vomiting? Then, an injectable or nasal spray formulation of a triptan is recommended.[23] In studies with subcutaneous sumatriptan, it was more efficacious in this setting. By educating the patient on the available options for various conditions, the patient will be empowered, confident, and better able to manage his or her migraines. Often, over time, the patient develops very effective treatment plans. This knowledge reduces anxiety that further improves outcome. Preventive Medication The tool box often needs to contain medications to prevent or decrease the frequency of migraine events. If there is a significant increase in the frequency or pattern of headaches, a thorough evaluation for secondary or precipitating causes is necessary and if not quickly reversed preventive medications begun. If acute therapy is needed more than two days per week or ineffective, preventive medication and other measures to reduce the number of headaches are indicated. Preventive medications are used to reduce the number of headaches. This is important when therapy for acute headache is ineffective or frequency of headache is approaching nine or more days per month, warning of the possibility of medication overuse. The major categories of preventive medications most used are tricyclics, beta blockers, calcium channel blockers, antiepileptics/neurostabilizers, onabotulinumtoxinA, as well as some others. The tricyclics most commonly used are amitriptyline and nortriptyline. Amitriptyline is more sedative with more anticholinergic side effects. It may help some more with sleep if that is a problem. Beta blockers can be used if there is no history of asthma, regular allergy shots, or Raynaud’s. Beta blockers are especially useful if there is comorbid palpitations, tachycardia, or hypertension. Beta blockers are usually well tolerated and not associated with weight gain. Calcium channel blockers sometimes used most commonly are amlodipine and verapamil. Neither is approved for migraine. They are more useful in cluster headache or for hemiplegic migraine. Antiepileptics are used and have some mood stabilizing effects as well. Divalproex and topiramate are the only ones approved. Because there have been birth defects associated with these medications, use in women of childbearing age must be weighed carefully in terms of the risk/benefit ratio. On the other hand, they seem to be a good choice where mood disorder is comorbid. Divalproex is relatively contraindicated in polycystic ovarian syndrome, which it allegedly can rarely cause. Divalproex can contribute to weight gain and high ammonia levels whereas topiramate can be associated with weight loss. Topiramate does have numerous common side effects including altered taste, numbness, decreased cognition, decreased sweating, and increased risk of kidney stones with associated metabolic acidosis. For those who tolerate topiramate well many report improved quality of life. It is prudent to check labs to monitor for acidosis as this can also lead to early osteoporosis. Other anticonvulsants, gabapentin, lamotrigine, zonisamide, and even antihypertensive ACE inhibitors have been used off label and in some mechanism of action for headache not fully understood. None of these latter have FDA approval. OnabotulinumtoxinA has recently been approved for use in chronic migraine as prevention. It is well tolerated but one should be trained on drug and protocol appropriately prior to use. It should not be used routinely as prevention in most migraine suffers. One needs to be familiar with the use and contraindications of any preventive medication. Try to keep dose and number of medications to a minimal. The choice of preventive medication should be one that can help manage comorbid conditions when possible. There are other items that need to be in the migraine toolbox. Education addressing importance of good sleep hygiene, dietary habits, and exercise are extremely important for the toolbox. Biofeedback also needs to be added to toolbox. Biofeedback has been shown to be as effective as amitriptyline for prevention of migraine and the combination has been shown to be better than either alone. Education on development of a sound management plan with periodic follow-up, review, and modification is necessary. In summary, by giving the patient various options for acute treatment, educating on importance of early intervention, adding preventive medications when needed, and using biofeedback and education on healthy habits they will have the best chance to take back control over migraine. If transition toward chronic migraine occurs, prompt and aggressive evaluation for secondary contributing causes should be undertaken. Education on healthy lifestyle habits, stress management, and health maintenance are an essential part of managing migraine. When preventive medications are used, chose those that can benefit comorbid conditions in order to reduce overall numbers of medications. Utilize nonmedical modalities such as physical therapy, stress management, and counseling when needed. By incorporating a strategy for care and utilizing the experience of “both experts” this chronic and often debilitating disease process can be rewarding for both the provider and patient. References 1. Lipton RB, Stewart WF, Diamond S, et al. Prevalence and burden of migraine in the United States: data from the American Migraine Study II. Headache. 2001;41(7): 646-657. 2. Victor TW, Hu X, Campbell JC, et al. Migraine prevalence by age and sex in the United States: a lifespan study. Cephalalgia. 2010;30(9):1065-1072. 3. Migraine. National Headache Foundation Website. http://www.headaches.org/education/Headache_Topic_Sheets/Migraine. Updated 2011. Accessed May 3, 2011. 4. Hu HX, Markson LE, Lipton RB, et al. Burden of migraine in the United States: disability and economic costs. Arch Intern Med. 1999;159(8):813-818. 5. Solomon GD. Evolution of the measurement of quality of life in migraine. Neurology. 1997;48(3 Suppl 3):S10-S15. 6. Lipton RB, Diamond S, Reed M, et al. Migraine diagnosis and treatment: results from the American Migraine Study II. Headache. 2001;41(7):638-645. 7. Tepper SJ, Dahlöf CG, Dowson A, et al. Prevalence and diagnosis of migraine in patients consulting their physician with a complaint of headache: data from the Landmark study. Headache. 2004;44(9):856864. 8. Gruber HJ, Bernecker C, Pailer S, et al. Hyperinsulinaemia in migraineurs is associated with nitric oxide stress. Cephalalgia. 2010;30(5):593-608. 9. Shields G, Seikaly H, LeBoeuf M, et al. Correlation between facial pain or headache and computerized tomography in rhinosinusitis in Canadian and U.S. subjects. Laryngoscope. 2003,113(6):943-945. 10. Wheeler SD. Phenotype-driven preventive strategies for migraine and other headaches. Neurologist. 2009;15(2):59-70. 11. Tietjen GE, Brandes JL, Peterlin BL, et al. Allodynia in migraine: association with comorbid pain conditions. Headache. 2009;49(9):1333-1344. 12. Welch KM, Nagesh V, Aurora SK, Gelman N. Periaqueductal gray matter dysfunction in migraine: cause or the burden of illness? Headache. 2001;41(7):629-637. 13. Kruit MC, van Buchem MA, Hofman PA, et al. Migraine as a risk factor for subclinical brain lesions. JAMA. 2004;291(4):427-434. 14. Buse DC, Manack A, Serrano D, et al. Sociodemographic and comorbidity profiles of chronic migraine and episodic migraine sufferers. J Neurol Neurosurg Psychiatry. 2010;81(4):428-432. 15. Hamed SA. The vascular risk associations with migraine: relation to migraine susceptibility and progression. Atherosclerosis. 2009;205(1):15-22. 16. Lipton RB, Cady RK, Farmer K, Bigal ME. Managing Migraine: A Healthcare Professional’s Guide to Collaborative Migraine Care. Hamilton, Ontario: Baxter Publishing Inc; 2008. 17. Winner P, Ricalde O, Le Force B, et al. A double-blind study of subcutaneous dihydroergotamine vs subcutaneous sumatriptan in the treatment of acute migraine. Arch Neurol. 1996;53(2):180-184. 18. Mathew NT. Dosing and administration of ergotamine tartrate and dihydroergotamine. Headache. 1997;37 Suppl 1:S26-S32. 19. Cady RK, Wendt JK, Kirchner JR, et al. Treatment of acute migraine with subcutaneous sumatriptan. JAMA. 1991;265(21):2831-2835. 20. Winner P, Adelman J, Aurora S, et al. Efficacy and tolerability of sumatriptan injection for the treatment of morning migraine: two multicenter, prospective, randomized, double-blind, controlled studies in adults. Clin Ther. 2006;28(10):1582-1591. 21. Giffin NJ, Ruggiero L, Lipton RB, et al. Premonitory symptoms in migraine: an electronic diary study. Neurology. 2003;60(6):935-940. 22. Headache Classification Committee of the International Headache Society. The International Classification of Headache Disorders, 2nd ed. Cephalalgia. 2004;24(Suppl 1):9-160. 23. Wendt J, Cady R, Singer R, et al. A randomized, double-blind, placebo-controlled trial of the efficacy and tolerability of a 4-mg dose of subcutaneous sumatriptan for the treatment of acute migraine attacks in adults. Clin Ther. 2006;28(4):517-526. Post-test 1. Which of the following is the best interviewing technique when evaluating your patient with headaches? A. Ask direct questions utilizing the International Headache Society criteria for migraine B. To save time, allow the patient only one problem at a time C. Ask open-ended questions, and allow the patient to “tell his/her story” D. Obtain the majority of history from family members, as patients cannot recall specifics 2. When assessing the patient who has complaint of headache, which will you find to be the greatest predictor of migraine? A. Severity and location of the headache pain B. The level of disability caused by the headache and accompanying nausea C. Sensitivity to light D. A & B E. All of the above 3. It may be easy for you to misdiagnose migraine as sinus headache because A. People with migraine have a high correlation of sinusitis B. The pain is often located in the same area C. Migraine is often associated with sinus symptoms D. Mild mucosal thickening on MRI scan E. A, B & C F. B, C & D 4. The stages of migraine address(es) A. The burden of the disease B. The frequency of the headaches C. The therapeutic and educational need of the patient D. All of the above E. None of the above 5. Being familiar with your patients’ stages of migraine will help you to A. Determine treatment strategies B. Interrupt transformation from acute episodic migraine to chronic migraine C. Assess whether opioids should be prescribed for prevention D. A & B E. All of these 6. A symptom you can recognize that indicates your patients are likely transforming from acute episodic migraine to chronic migraine is/are A. Increase in abortive medication use B. There are fewer days between headaches where they “feel normal” C. Increase disruption of daily activities or duties D. B & C E. All of the above