Using Multi-Informant Qualitative Data to Inform Adaptations to Mindfulness-Based Interventions for Adolescents with Chronic Migraine.

Migraine

Psychiatric comorbidity in patients with headache contributes to poorer prognosis, chronification of disease, poor response to treatment, increased cost of treatment, and decreased quality of life. The purpose of the present study was to evaluate the depressive symptoms in adolescents with chronic and episodic migraines and healthy adolescents. The study was performed between November 2010 and November 2011. All patients completed a detailed headache questionnaire comprising of demographical and clinical data and were instructed to fill out a headache diary over a 2-month period. The subjects ranged in age from 13 to 19years. To evaluate depression symptoms, all of the subjects were asked to fill out the Beck Depression Inventory (BDI). A total of 137 participants were evaluated; 44 had episodic migraine (EM), 46 had chronic migraine (CM) and 47 were control subjects. Patients with a history of chronic migraine had significantly higher scores on the BDI than the other participants. Patients with chronic migraine had BDI scores that were 8.8 points higher than controls [95% CI (β)=5.0, 12.6] and 5.8 points higher than patients with EM [95% CI (β)=2.2, 9.4]. The main finding of this study was that chronic migraine is strongly associated with depression symptoms, regardless of demographic data. Comorbid depression may increase the total burden of migraine and diagnosis and treatment of depression in adolescents with migraine is likely to result in a better prognosis.

( Headache 2011;51:1058‐1077) Objective.— To evaluate and compare healthcare resource use and related costs in chronic migraine and episodic migraine in the USA and Canada. Background.— Migraine is a common neurological disorder that produces substantial disability for sufferers around the world. Several studies have quantified overall costs associated with migraine in general, with recent estimates ranging from $581 to $7089 per year. Although prior studies have characterized the clinical and humanistic burden of chronic migraine relative to episodic migraine, to the best of our knowledge only 1 previous study has compared chronic migraine and episodic migraine healthcare costs. The purpose of this study was to quantify and compare the direct medical costs of chronic migraine and episodic migraine using medical resource use data collected as part of the International Burden of Migraine Study. Methods.— Cross‐sectional data were collected from respondents in 10 countries via a Web‐based survey. Respondents were classified as chronic migraine (≥15 headache days/month) or episodic migraine (<15 headache days/month). Data collection included socio‐demographic and clinical characteristics and medical resource use for headache (clinician and emergency department visits and hospitalizations over the preceding 3 months and medications over the preceding 4 weeks). Unit cost data were collected outside of the Web‐based survey using publicly available sources and then applied to resource use profiles. Cost estimates are presented in 2010 US and Canadian dollars. Results.— In this manuscript, the analysis included data from respondents with migraine in the USA (N = 1204) and Canada (N = 681). The most common medical services utilized by all respondents included headache‐specific medication, healthcare provider visits, emergency department visits, and diagnostic testing. In the USA, approximately one‐quarter (26.2%) of chronic migraine participants vs 13.9% of episodic migraine participants reported visiting a primary care physician in the preceding 3 months ( P < .001). In Canada, one‐half (48.2%) of chronic migraine participants had a primary care physician visit, compared with 12.3% of episodic migraine subjects ( P < .0001). Total mean headache‐related costs for participants with chronic migraine in the USA were $1036 (±$1334) over 3 months compared to $383 (±807, P < .001) for persons with episodic migraine. In Canada, total mean headache‐related costs among chronic migraine subjects were $471 (±1022) compared to $172 (±920, P < .001) for episodic migraine subjects. Conclusions.— Chronic migraine was associated with higher medical resource use and total costs compared to episodic migraine. Therapies that reduce headache frequency could become important approaches for containing or reducing headache‐related medical costs.

Clinical Guidelines19 November 2002Pharmacologic Management of Acute Attacks of Migraine and Prevention of Migraine HeadacheFREEVincenza Snow, MD, Kevin Weiss, MD, Eric M. Wall, MD, MPH, and Christel Mottur-Pilson, PhD, for the American Academy of Family Physicians and the American College of Physicians–American Society of Internal Medicine*Vincenza Snow, MDFrom American Academy of Family Physicians, Leawood, Kansas; Hines Veterans Affairs Medical Center and Northwestern University Feinberg School of Medicine, Chicago, Illinois; and American College of Physicians–American Society of Internal Medicine, Philadelphia, Pennsylvania., Kevin Weiss, MDFrom American Academy of Family Physicians, Leawood, Kansas; Hines Veterans Affairs Medical Center and Northwestern University Feinberg School of Medicine, Chicago, Illinois; and American College of Physicians–American Society of Internal Medicine, Philadelphia, Pennsylvania., Eric M. Wall, MD, MPHFrom American Academy of Family Physicians, Leawood, Kansas; Hines Veterans Affairs Medical Center and Northwestern University Feinberg School of Medicine, Chicago, Illinois; and American College of Physicians–American Society of Internal Medicine, Philadelphia, Pennsylvania., and Christel Mottur-Pilson, PhDFrom American Academy of Family Physicians, Leawood, Kansas; Hines Veterans Affairs Medical Center and Northwestern University Feinberg School of Medicine, Chicago, Illinois; and American College of Physicians–American Society of Internal Medicine, Philadelphia, Pennsylvania., for the American Academy of Family Physicians and the American College of Physicians–American Society of Internal Medicine*Author, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-137-10-200211190-00014 SectionsAboutVisual AbstractPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Migraine headache is a common disorder seen in primary care. It affects 18% of women and 6.5% of men in the United States, almost half of whom are undiagnosed or undertreated (1, 2). These guidelines, developed by the American Academy of Family Physicians and the American College of Physicians–American Society of Internal Medicine, with assistance from the American Headache Society, are based on two previously published papers (3, 4). The papers, titled "Evidence-Based Guidelines for Migraine Headache in the Primary Care Setting: Pharmacological Management of Acute Attacks," by Matchar and colleagues (3), and "Evidence-Based Guidelines for Migraine Headache in the Primary Care Setting: Pharmacological Management for Prevention of Migraine," by Ramadan and coworkers (4), can be found at www.aan.com/professionals/practice/guidelines.cfm. 1 The target audience for this guideline is primary care physicians. The guideline applies to patients with acute migraine attacks, with or without aura, and patients with migraine who are candidates for preventive drug therapy. Although these guidelines are all based on the articles by Matchar and Ramadan and colleagues, the recommendations may differ because different thresholds of evidence were needed for making a positive recommendation. Table 1 compares the AAFP/ACP–ASIM guideline and the U.S. Headache Consortium Guideline.Table 1. Summary of U.S. Headache Consortium Recommendations Compared with AAFP/ACP–ASIM RecommendationsThroughout the text, asterisks indicate drugs that are currently not available in the United States.DiagnosisHeadache has many potential causes. Most headaches are caused by the primary headache disorders, which include migraine, cluster, and tension-type headaches. Secondary headaches, which are those with underlying pathologic causes, are far less common. Migraine is a chronic condition with recurrent acute attacks whose characteristics vary among patients and often among attacks within a single patient. Migraine is a syndrome with a wide variety of neurologic and non-neurologic manifestations. The International Headache Society (6) has developed diagnostic criteria for migraine with and without aura (Appendix Table 1). This classification system serves to diagnose headache syndromes, not patients. Thus, one patient could have more than one type of headache disorder. For example, it is not uncommon for migraine patients to also have episodic tension-type headaches.Management of Acute AttacksEffective long-term management of patients with migraine is challenging because of the complexity of the condition. Experts suggest several goals for successful treatment of acute attacks of migraine. These include treating attacks rapidly and consistently to avoid headache recurrence, to restore the patient's ability to function, and to minimize the use of backup and rescue medications.Clinicians need to educate people with migraine about their condition and its treatment and encourage them to participate in their own management. The physician must help the patient establish realistic expectations by discussing therapeutic options and their benefits and harms. Patient input can provide the best guide to treatment selection and helps the physician to better understand and accommodate patient treatment goals. Developing an effective acute migraine management strategy can be complex, and an engaged patient is more likely to negotiate this process successfully. Encouraging patients to identify and avoid triggers (Table 2) and to be actively involved in their own management by tracking their own progress may be especially useful.Table 2. Some Commonly Reported Triggers of Migraine HeadacheOnce a diagnosis of migraine is established, patients and their health care providers should decide together how to treat acute attacks and whether the patient is a candidate for preventive medications. A wide range of acute treatments with varying efficacies is currently in use (Appendix Table 2). A comprehensive review of the scientific literature, especially the data from randomized, controlled trials, provides a list of treatments that have demonstrated efficacy in the management of acute migraine headache. It also provides a clear understanding of the adverse events associated with various agents.The Headache Consortium's review of the evidence on antiemetics, barbiturate hypnotics, ergot alkaloids and derivatives, nonsteroidal anti-inflammatory drugs (NSAIDs), combination analgesics and nonopiate analgesics, opiate analgesics, triptans, and other agents found good evidence of the efficacy of only a few agents in the treatment of acute migraine (3).Available AgentsNSAIDsTheir demonstrated efficacy and favorable tolerability make NSAIDs a first-line treatment choice for all migraine attacks, including severe attacks that have responded to NSAIDs in the past. Among the NSAIDs, the most consistent evidence exists for aspirin (8-10), ibuprofen (11, 12), naproxen sodium (13, 14), tolfenamic acid* (8, 15), and the combination agent acetaminophen plus aspirin plus caffeine for the acute treatment of migraine (16). The evidence shows that acetaminophen alone is ineffective (17).Serotonin1B/1D Agonists (Triptans)There is good evidence for the effectiveness of the oral triptans naratriptan (18, 19), rizatriptan (20-23), sumatriptan (24-31), and zolmitriptan (32-34). In addition, there is good evidence for the effectiveness of subcutaneous (35-38) and intranasal (39-41) sumatriptan, making it an option for patients with nausea and vomiting. Adverse effects of the triptans include chest symptoms, but postmarketing data indicate that true ischemic events are rare. Triptans are contraindicated in patients with risk for heart disease, basilar or hemiplegic migraine, or uncontrolled hypertension. Subcutaneous sumatriptan is associated with a very rapid onset of action, and oral naratriptan is associated with a slower onset of action.ErgotaminesThere is good evidence for the efficacy and safety of intranasal dihydroergotamine (DHE) as monotherapy for acute migraine attacks (42-46). Placebo-controlled studies of intravenous DHE did not clearly establish its efficacy in the acute treatment of migraine (47, 48). The evidence was inconsistent to support efficacy of ergotamine or ergotamine–caffeine, and the studies documented frequent adverse events.OpioidsIt is well recognized that opiates are good analgesics, but there is good evidence only for the efficacy of butorphanol nasal spray (49, 50). Although opioids are commonly used, surprisingly few studies of opioid use in headache pain document whether overuse and the development of dependence are as frequent as clinically perceived. Until further data are available, these drugs may be better reserved for use when other medications cannot be used, when sedation effects are not a concern, or the risk for abuse has been addressed.Other AgentsFair evidence suggests that the antiemetic metoclopramide, given intravenously, may be an appropriate choice as monotherapy for acute attacks (51-53), particularly in patients with nausea and vomiting when the sedating side effect may also be useful. Isometheptene and isometheptene combinations obtained only borderline significance in relieving headache pain (17, 54, 55). Other agents used in practice, such as intravenous corticosteroids and intranasal lidocaine, are not effective.Choice of TreatmentSince patient responses to these therapies are not always predictable, individualized management is important. The choice of treatment should be based on, among other characteristics, the frequency and severity of attacks; the presence and degree of temporary disability; and the profile of associated symptoms, such as nausea and vomiting. The patient's history of, response to, and tolerance for specific medications must also be considered. Coexisting conditions (such as heart disease, pregnancy, and uncontrolled hypertension) may limit treatment choices.No studies document the effectiveness of specific treatment schedules, but experts suggest that acute therapy should be limited to no more than two times per week to guard against medication-overuse headache (or drug-induced headache). Medication-overuse headache is thought to result from frequent use of acute medication and has a pattern of increasing headache frequency, often resulting in daily headaches. In patients with suspected medication overuse or patients at risk for medication overuse, preventive migraine therapy should be considered.Although some use the term rebound headache interchangeably with the term medication-overuse headache, rebound headache is a distinct entity. Rebound headache is associated with withdrawal of analgesics or abortive migraine medication. There is no uniform agreement about which agents can cause rebound headache, although ergotamine (not DHE); opiates; triptans; and simple and mixed analgesics containing butalbital, caffeine, or isometheptene are generally thought to do so. There is less uniform opinion about other antimigraine agents.Another clinical consideration is the use of a self-administered rescue medication for patients with severe migraine attack that is not responding to (or failing) other treatments. A rescue medication is an agent such as an opioid or a butalbital-containing compound that the patient can use at home when other treatments have failed. Although rescue medications often do not completely eliminate pain and allow patients to return to normal activities, they permit the patient to achieve relief without the discomfort and expense of a visit to the physician's office or emergency department. A cooperative arrangement between provider and patient may extend to the use of rescue medication in appropriate situations.Summary of Treatment of Acute MigraineA body of evidence now points to effective first- and second-line agents for acute treatment of migraine. Beyond the choice of agent lies the choice of management strategy. Recently, interest and research in step care versus stratified care have increased. Step care refers to the initial use of safe, effective, and inexpensive medications as first-line agents in acute attacks of any severity. If the initial agent fails, a second-line, more expensive, migraine-specific medication is then used. The stratified care model initially stratifies migraine attacks by severity, advocating migraine-specific agents for moderate to severe attacks, regardless of previous response to or an unknown response to other agents. Which approach is more effective is still an open question (56).Management of Migraine with Preventive TherapyOnce patients and their health care providers decide how to treat acute attacks, use of preventive medications should be considered. Generally accepted indications for migraine prevention include 1) two or more attacks per month that produce disability lasting 3 or more days per month; 2) contraindication to, or failure of, acute treatments; 3) the use of abortive medication more than twice per week; and 4) the presence of uncommon migraine conditions, including hemiplegic migraine, migraine with prolonged aura, or migrainous infarction. Other factors to consider are adverse events with acute therapies, patient preference, and the cost of both acute and preventive therapies. (The U.S. Headache Consortium also produced a document on behavioral and other nonpharmacologic therapies for headache prevention, which can be found at www.aan.com/professionals/practice/guidelines.cfm.)A wide range of preventive treatments with varying efficacies is currently in use (Appendix Table 3). A comprehensive review of the scientific literature, especially the data from randomized, controlled trials, provides a list of treatments that have demonstrated efficacy in the prevention of migraine headache. It also provides a clear understanding of the adverse events associated with various agents. The Headache Consortium's review of the evidence on α2-agonists, anticonvulsants, antidepressants, β-blockers, calcium-channel blockers, NSAIDs, serotonergic agents (ergot derivatives, methysergide, and others), hormone therapy, feverfew, magnesium, and riboflavin found that there was good evidence of the efficacy of only a few agents in migraine prevention. A summary of these results follows.Available Agentsβ-BlockersEvidence consistently showed the efficacy of propranolol, 80 to 240 mg/d (57-63), and timolol, 20 to 30 mg/d (63-65), for the prevention of migraine. One trial comparing propranolol and amitriptyline suggested that propranolol is more efficacious in patients with migraine alone; amitriptyline was superior for patients with mixed migraine and tension-type headache (66). There is limited evidence of a moderate effect for atenolol (67, 68), metoprolol (69-71), and nadolol (72-74). β-Blockers with intrinsic sympathomimetic activity (acebutolol, alprenolol, oxprenolol, pindolol) seem to be ineffective for the prevention of migraine. Adverse effects reported most commonly with β-blockers were fatigue, depression, nausea, dizziness, and insomnia. These symptoms appear to be fairly well tolerated and seldom caused premature withdrawal from trials.AntidepressantsAmitriptyline has been more frequently studied than the other antidepressants and is the only one with consistent support for efficacy in migraine prevention (75-77). The dosages that were most efficacious in the clinical trials ranged from 30 to 150 mg/d. Drowsiness, weight gain, and anticholinergic symptoms were frequently reported with the tricyclic antidepressants studied, including amitriptyline. There is no evidence for the use of nortriptyline, protriptyline, doxepin, clomipramine, or imipramine. There is limited evidence of a modest effect for fluoxetine at dosages ranging from 20 mg every other day to 40 mg per day (78, 79). There is no evidence from controlled trials for the use of fluvoxamine, paroxetine, sertraline, phenelzine, bupropion, mirtazapine, trazodone, or venlafaxine.AnticonvulsantsFor the anticonvulsants, there is good evidence for the efficacy of divalproex sodium (80-82) and sodium valproate (83, 84). Adverse events with these therapies are not uncommon and include weight gain, hair loss, tremor, and teratogenic potential, such as neural tube defects. These agents may be especially useful in patients with prolonged or atypical migraine aura. Carbamazepine and vigabatrin* have been shown to be ineffective, and there is limited evidence for moderate efficacy of gabapentin (85).NSAIDsA meta-analysis (4) of five of seven placebo-controlled trials of naproxen or naproxen sodium showed a modest effect on headache prevention (62, 86-92). Similar trends were observed in single placebo-controlled trials of flurbiprofen, indobufen*, ketoprofen, lornoxicam*, and mefenamic acid and in two trials of tolfenamic acid*. Placebo-controlled trials of aspirin, aspirin plus dipyridamole, fenoprofen, and indomethacin were inconclusive. There is no evidence for the use of ibuprofen or nabumetone in the prevention of migraine.Side effect rates for naproxen were not significantly higher than those seen with placebo. The most commonly reported adverse events with all NSAIDs were gastrointestinal symptoms, including nausea, vomiting, gastritis, and blood in the stool. In the trials reviewed, such symptoms were reported by 3% to 45% of participants (86).Serotonergic AgentsOf these agents, time-released DHE* had the strongest support, with consistently positive findings in four placebo-controlled trials (93-96). Evidence is insufficient for the efficacy of ergotamine or ergotamine plus caffeine plus butalbital plus belladonna alkaloids or methylergonovine for migraine prevention. Limited information was reported on adverse events associated with these agents. The most commonly reported events for all the ergot alkaloids were gastrointestinal symptoms.There is strong evidence for the efficacy of methysergide (97-100), a semisynthetic ergot alkaloid. However, there are reports of retroperitoneal and retropleural fibrosis associated with long-term, mostly uninterrupted administration. The manufacturer suggests that methysergide therapy be discontinued for 3 to 4 weeks after each 6-month course of treatment. Other adverse events most commonly reported included gastrointestinal symptoms and leg symptoms (restlessness or pain).Other serotonergic agents that have been evaluated for the prevention of migraine include pizotifen*, lisuride*, oxitriptan*, iprazochrome*, and tropisetron*. Only lisuride (101-104) and pizotifen (87, 99, 105-110) have consistent evidence that supports their efficacy in the prevention of migraine. Published data on adverse events associated with lisuride are limited, and pizotifen is often associated with weight gain and drowsiness.Calcium-Channel BlockersThe evidence for nifedipine, nimodipine, cyclandelate*, and verapamil is poor quality and difficult to interpret, suggesting only a modest effect (see reference 4 for study references). There is no evidence for the use of diltiazem in the prevention of migraine. Symptoms reported with these agents included dizziness, edema, flushing, and constipation.Flunarizine*, 10 mg/d, has proven efficacy in the prevention of migraine and is commonly used in countries where it is available (111-115). Adverse events reported with flunarizine include sedation, weight gain, and abdominal pain. Depression and extrapyramidal symptoms can be observed, particularly in elderly persons.α2-AgonistsThere is good evidence for the lack of efficacy of the α2-agonist clonidine in the prevention of migraine (116-120). Limited evidence shows moderate efficacy of guanfacine (121).Hormone Therapy, Feverfew, Magnesium, and RiboflavinThere is fair evidence for modest efficacy of these agents in certain circumstances, but more trials need to be done. Most of the existing trials had small sample sizes, had self-referred or special patient samples, or had other methodologic flaws (see reference 4 for more details and references).Summary of Preventive TherapyTo alleviate the suffering of many patients with migraine, clinicians need to be aware of the commonly accepted indications for preventive therapy and initiate effective therapy in those patients. Although many agents are available for the preventive treatment of migraine, only a few have proven efficacy. Once an agent has been chosen, clinicians should initiate therapy with a low dose and titrate the dose slowly up until clinical benefits are achieved in the absence of adverse events or until limited by adverse events. Because a clinical benefit may take as long as 2 to 3 months to manifest, each treatment should be given an adequate trial. Once preventive treatment is under way, interfering medications, such as overused acute medications such as ergotamine, should be avoided. After a period of stability, clinicians should consider tapering or discontinuing treatment. Patient and clinician need to engage in an ongoing dialogue in which patient expectations and goals for therapy are taken into account when agents are chosen, titrated, or discontinued.RecommendationsRecommendation 1: For most migraine sufferers, nonsteroidal anti-inflammatory drugs (NSAIDs) are first-line therapy.To date, the most consistent evidence exists for aspirin, ibuprofen, naproxen sodium, tolfenamic acid*, and the combination agent acetaminophen plus aspirin plus caffeine. There is no evidence for the use of acetaminophen alone.Recommendation 2: In patients whose migraine attack has not responded to NSAIDs, use migraine-specific agents (triptans, DHE).There is good evidence for the following triptans: oral naratriptan, rizatriptan, and zolmitriptan; oral and subcutaneous sumatriptan; and DHE nasal spray. Few data in the literature demonstrate which triptans are more effective. Oral opiate combinations and butorphanol may be considered in acute migraine when sedation side effects are not a concern and the risk for abuse has been addressed.Recommendation 3: Select a nonoral route of administration for patients whose migraines present early with nausea or vomiting as a significant component of the symptom complex. Treat nausea and vomiting with an antiemetic.Evidence is limited, but in some patients, concomitant treatment with an antiemetic and an oral migraine medication may be appropriate. Antiemetics should not be restricted to patients who are vomiting or likely to vomit. Nausea itself is one of the most aversive and disabling symptoms of a migraine attack and should be treated appropriately.Recommendation 4: Migraine sufferers should be evaluated for use of preventive therapy.Generally accepted indications for migraine prevention include 1) two or more attacks per month that produce disability lasting 3 or more days per month; 2) contraindication to, or failure of, acute treatments; 3) use of abortive medication more than twice per week; or 4) the presence of uncommon migraine conditions, including hemiplegic migraine, migraine with prolonged aura, or migrainous infarction.Recommendation 5: Recommended first-line agents for the prevention of migraine headache are propranolol (80 to 240 mg/d), timolol (20 to 30 mg/d), amitriptyline (30 to 150 mg/d), divalproex sodium (500 to 1500 mg/d), and sodium valproate (800 to 1500 mg/d).Medications with proven efficacy but limited published data on adverse events or frequent or severe adverse events include flunarizine*, lisuride*, pizotifen*, time-released and migraine sufferers about the of acute attacks and preventive therapy and engage them in the of a management should be on a is strong about the need for people with migraine. The physician must help the patient establish realistic expectations by discussing therapeutic options and their benefits and such as medication-overuse headache. Encouraging patients to be actively involved in their own management by tracking their own progress daily for example, may be especially useful. should attack frequency, severity, and resulting disability; response to type of and adverse effects of medication. Patient input can provide the best guide to treatment Table 1. International Headache Society Table 2. Summary of the Evidence for Acute Table Summary of the Evidence for Preventive M. and of migraine in the United data from the American Migraine Migraine diagnosis and results from the American Migraine Matchar guidelines for migraine headache in the primary care management of acute at www.aan.com/professionals/practice/guidelines.cfm. Ramadan guidelines for migraine headache in the primary care management for prevention of migraine. at www.aan.com/professionals/practice/guidelines.cfm. Matchar guidelines for migraine of and at www.aan.com/professionals/practice/guidelines.cfm. and diagnostic criteria for headache disorders, and pain. Headache of the International Headache and diagnosis of Headache in Clinical Medical acid is as effective as ergotamine migraine of an acetaminophen mg combination versus aspirin mg and in acute migraine and aspirin versus aspirin or for migraine a Treatment of acute migraine ibuprofen and A study of ibuprofen versus in the treatment of acute migraine a migraine naproxen sodium ergotamine plus caffeine. M. sodium in the treatment of migraine. metoclopramide, caffeine and their combinations in the treatment of migraine and safety of aspirin, and caffeine in migraine headache randomized, placebo-controlled Treatment of migraine with and a trial. is effective and well tolerated in the acute treatment of migraine. of a is effective and well tolerated in the acute treatment of migraine. of a The study of in migraine. sumatriptan in the acute treatment of migraine. A study of rizatriptan in the acute treatment of migraine.

Each year approximately 3% of people with episodic migraine experience “chronification” of their headache disorder. “Chronic” migraine implies that the migraineur who previously was suffering relatively infrequent headache attacks now is plagued with headache at least 15 days out of the month, with at least 8 (but not necessarily all) of their headaches being migrainous in character. Chronic migraine is far from rare; as many as 6 to 8 million Americans may be afflicted by this malignant variant of migraine that is particularly inclined to diminish one's quality of life and is relatively difficult to subdue with the medical therapies currently available. While –at last– research involving headache is shifting to address the needs of the chronic migraine population, it remains and, whatever new treatments emerge, is likely to remain a disorder best treated by preventing its development in the first place. Once chronic migraine has developed, its successful treatment – with remission back to the episodic form – will require active participation on the part of the patient. While our knowledge of the biologic factors that promote and sustain migraine “chronification” is far from complete, we have come to identify a number of factors that are associated with the disorder . . . and a few that clearly appear to herald its development. Not surprisingly, a steady increase in headache attack frequency is a potent risk factor for the development of chronic migraine. In parallel with this, overuse of medications intended to treat headache acutely may accelerate the “chronification” process and reinforce chronic migraine once it has developed. Even relatively low levels of use of certain classes of drugs may be linked to eventual “chronification”; opiates/opioids (“narcotics”) and barbituate-containing compounds have been reported to be the most potent offenders in this regard. A number of studies have reported obesity and chronic migraine to correlate strongly, and an association between chronic migraine and disorders of mood (notably, anxiety and depression) has been well established. Chronically disrupted sleep may predispose to – or, at least, reinforce – chronic migraine. Finally, a history of severe emotional or physical trauma may predispose to chronic migraine, and the traumatic event itself may be widely separated in time from the onset of migraine “chronification” process. So what can you, the migraineur, do to assist in preventing chronic migraine or, if you are already at that point, achieve remission back to episodic headache? Even if you have episodic migraine of stable frequency, minimize – or avoid altogether – use of opiates/opioids (eg, Vicodin, Lortab, Lorcet, Vicoprofen, Percodan, Percocet) or butalbital-containing compounds (eg, Esgic, Fioricet, Fiorinal). If you find your previously low level of headache frequency to be steadily increasing over a period of weeks or months, seek medical attention now! The chronification process is far easier to halt and reverse if treatment intervention is undertaken early; do not wait until your headaches reach a level of daily occurrence before you seek help. If your migraine is “chronifying” or already has become chronic: treat acute headache intensifications early and aggressively . . . but avoid overuse of any single medication or class of medications; seek your healthcare provider's assistance in creating a balanced plan for acute headache treatment. begin- and stick with- a regular aerobic exercise program (one recent study found regular aerobic exercise to correlate strongly with remission from chronic migraine); again, seek your provider's assistance in devising an exercise plan appropriate to your capabilities and general health. if you are overweight, work with your provider to develop a diet/(aerobic) exercise weight loss program. seek treatment for any coexisting disorder of mood or sleep. Take an active role in the management of your migraine disorder, and as your headaches decrease, you will enjoy an accompanying improvement in both your quality of life and your general health.

Objective To analyze the effects of intervention on the migraine patients with comorbidity of depression and anxiety among offshore marine personnel. Methods One hundred and forty-two migraine patients that met the migraine, depression and anxiety diagnostic standards were chosen from the offshore marine personnel, and were randomly divided into 2 groups, each consisting of 71 patients. At the onset of the disease, the patients of both groups were given painkillers, and during remission they were administered with preventive drugs (SNRI) for the recurrence of the disease. One of the groups was provided with additional treatment of 5-hydroxytryptamine and noradrenergic inhibitor. Migraine attack frequency, Visual Analogue Score (VAS), SF-36 Health Survey Scale, Hamilton Depression Scale (HAMD) and Hamilton Anxiety Scale (HAMA) evaluation results were recorded both before treatment and at week 6 and 12 after treatment. The whole observation period lasted for 12 weeks. Results At week 6, migraine attack frequency and visual analogue scores for the venlafaxine treatment group were obviously reduced, as compared with those of the non-venlafaxine treatment group (P<0.05), while the mode of depression was obviously improved (HAMD value, P<0.05). However, no changes could be seen in the mode of anxiety (HAMA value, P<0.05). For the venlafaxine treatment group, the scores of physiological function (PF), body pain (BP), general health (GH) status, vitality (VT) of SF-36 were higher than those of the non-venlafaxine treatment group (P<0.01 and P<0.05). At week 12, attack frequency and visual analogue scores were significantly reduced, as compared with the non-venlafaxine treatment group (P<0.01), while the depression and anxiety scores obviously improved (HAMD value, P<0.01; HAMA value, P<0.05). For the venlafaxine treatment group, the scores of RP, BP, GH, VT, social function (SF), RE, mental health (MH) of SF-36 were higher than those of the non-venlafaxine treatment group (P<0.01). Conclusions Treatment of migraine patients with comorbidity of depression and anxiety by using anti-depression and anti-anxiety drugs could obviously reduce migraine attack frequency, seriousness of pain and in the mean time improve the status of mental disorder and the life quality of the patients as well. Key words: Migraine; Mental disorder; Depression; Anxiety

48.: The effect of brief biofeedback intervention on headache disability and analgesic use in episodic or chronic migraine and chronic tension type headache

Secular Mindfulness-Based Interventions: Efficacy and Neurobiology.

The relationship between migraine and alcohol consumption is unclear. We assessed the association between chronic migraine and alcohol use disorder(AUD), relative to chronic disease controls, and in conjunction with common comorbidities. We conducted a retrospective, observational study. The primary outcome was the odds ratio for AUD in patients with chronic migraine or with chronic migraine and additional comorbidities relative to controls. A total of 3701 patients with chronic migraine, 4450 patients with low back pain, and 1780 patients with type 2 diabetes mellitus met inclusion criteria. Patients with chronic migraine had a lower risk of AUD relative to both controls of low back pain (OR 0.37; 95% CI: 0.29-0.47, p < 0.001) and type 2 diabetes mellitus (OR 0.39; 95% CI: 0.29-0.52, p < 0.001). Depression was associated with the largest OR for AUD in chronic migraine (OR 8.62; 95% CI: 4.99-14.88, p < 0.001), followed by post-traumatic stress disorder (OR 6.63; 95% CI: 4.13-10.64, p < 0.001) and anxiety (OR 3.58; 95% CI: 2.23-5.75, p < 0.001). Patients with chronic migraine had a lower odds ratio of AUD relative to controls. But in patients with chronic migraine, those with comorbid depression, anxiety, or PTSD are at higher risk of AUD. When patients establish care, comorbid factors should be assessed and for those at higher risk, AUD should be screened for at every visit.

Background The study on the importance of being mentally, socially, and physically healthy as a medical student is a deficient area in the scientific research in developing countries. Migraine has a negative effect on the general health as well as educational performance. Medical students, especially females, may be at a higher risk to manifest migraine associated with anxiety and/or depression. Aims The aims of this study were to determine the prevalence of migraine headache, to investigate its effect, and to assess some comorbid psychiatric disorders (anxiety and depression) among female medical students at Al-Azhar University in Cairo. Participants and methods A cross-sectional study was carried out on 599 female medical students from grade 1 to grade 6 at Faculty of Medicine for Girls, Al-Azhar University, Cairo, over a period of 1 month during the academic year 2014–2015. The studied female medical students were 18–26 years old. Through a self-administrated questionnaire, sociodemographic data were reported. In students without migraine with aura symptoms, the effects of migraine on daily activities, sleeping pattern, seeking of medical care, educational attendance, and influence on career decision were investigated. For each student, the reported migraine neurological symptoms were verified through meeting the International Headache Society (IHS) criteria for diagnosis, whereas comorbid psychiatric evaluation was assessed through the valid and reliable version of Neuropsychiatric Assessment by Hospital Anxiety and Depression Scale. Results The reported migraine prevalence among the studied female medical students was 35.8%. The mean age of students having migraine was significantly higher than those without migraine (21.09±1.98 vs. 20.61±1.91 years) (P 0.05). Conclusion and future vision The prevalence of migraine is considered high among the studied female medical students. It is found to be an important health problem because of its negative effect on diminishing students’ performance, disrupting their sleep, and implied stress. Anxiety and/or depression among medicals students with migraine as well as those without are urgent burdens that should be investigated more and targeted by health care providers. Curriculum should include stress-coping tools, counseling, and psychosocial support to reduce distress and severe effect of migraine on students’ well-being.

ObjectiveThis post hoc analysis evaluated the efficacy of galcanezumab for the prevention of migraine in patients with and without comorbid anxiety and/or depression.BackgroundPatients with migraine have a higher risk of anxiety and/or depression. Given the high prevalence of psychiatric symptoms and their potential negative prognostic impact, determining the efficacy of migraine treatments in patients with these comorbidities is important.MethodsThe results of 2 phase 3 episodic migraine studies of patients with 4‐14 migraine headache days (MHD) per month were pooled. A third chronic migraine study, which was evaluated separately, enrolled patients with ≥15 headache days per month, of which ≥8 had migraine‐like features. Patients in all 3 studies were randomized 2:1:1 to placebo, galcanezumab 120 mg, or galcanezumab 240 mg. The efficacy of galcanezumab on migraine was measured in subgroups of patients with anxiety and/or depression (current or past) and patients without. A repeated measures model was used to compare treatment groups within each subgroup and to test for consistency of treatment effect across the anxiety/depression subgroups (subgroup‐by‐treatment interaction) during the double‐blind treatment phases.ResultsAmong 1773 intent‐to‐treat patients with episodic migraine, both doses of galcanezumab demonstrated statistically significant improvements relative to placebo in overall number of MHD for the subgroups of patients with anxiety and/or depression (mean change difference from placebo [95% CI]: −2.07 [−2.81, −1.33] for galcanezumab 120 mg [P < .001], −1.91 [−2.78, −1.04] for 240 mg [P < .001]) and without anxiety and/or depression (mean change difference from placebo [95% CI]: −1.92 [−2.36, −1.47] for 120 mg [P < .001], −1.77 [−2.20, −1.33] for 240 mg [P < .001]), as was observed for the secondary outcomes of MHD with acute medication use and functional impairment. Among 1113 intent‐to‐treat patients with chronic migraine, those with anxiety and/or depression had significant reductions in overall MHD frequency with the 240‐mg dose (mean change difference from placebo [95% CI]: −1.92 [−3.52, −0.33]; P = .018), whereas significant reductions were observed at both the 120‐mg (mean change difference from placebo [95% CI]: −2.29 [−3.26, −1.31]; P < .001) and 240‐mg (−1.85 [−2.83, −0.87]; P < .001) doses in patients without anxiety and/or depressions. Significant reductions (P < .01) in MHD with acute medication use were observed at both doses within both anxiety/depression subgroups and for overall functional impairment for patients without anxiety and/or depression, though neither dose significantly reduced overall functional impairment beyond placebo in the subgroup with anxiety and/or depression. In the episodic and chronic migraine studies, the subgroup‐by‐treatment interaction was not statistically significant for MHD, MHD with acute medication use, or functional impairment (chronic study only), suggesting a lack of evidence of differential effect between subgroups. Furthermore, differences between subgroups in the mean change differences from placebo, as well as overlapping 95% confidence intervals for the subgroups, indicated lack of a clinical or statistical difference between subgroups for these outcome variables. There was a significantly higher percentage of patients with episodic migraine attaining ≥50%, ≥75%, and 100% reductions, and a higher percentage of patients with chronic migraine attaining ≥50% and ≥75% reductions from baseline with galcanezumab compared with placebo, regardless of medical history of anxiety and/or depression.ConclusionsA medical history of anxiety and/or depression does not seem to interfere with response to galcanezumab among patients with episodic migraine, and both doses of galcanezumab appear efficacious for these individuals regardless of this psychiatric history. Among patients with chronic migraine and comorbid anxiety and/or depression, the 240‐mg dose, but not the 120‐mg dose, significantly decreased overall MHD, but neither dose resulted in significantly greater functional improvement. Patients with migraine and comorbid anxiety and/or depression often require additional interventions, and this may be more important in chronic migraine.

Purpose: To evaluate how migraine impacts the risk for postpartum depression (PPD) in women of reproductive age as well as the effect of comorbidities on this risk. Methods: This is a retrospective observational study in a tertiary neurology center involving 6248 women with migraine and 4154 women without migraine between the ages of 18 and 45 seen from January 1, 2017, to January 30, 2024. The primary outcome was the odds ratio (OR) for PPD in migraine relative to women without migraine. Secondary outcomes included the OR for PPD in women with chronic migraine who also had comorbidities. Results: After adjusting for demographic factors and comorbid conditions, only chronic migraine, with and without aura, was associated with higher OR for PPD; chronic migraine without aura had the highest risk for PPD (OR: 2.13; 95% CI: 1.29 to 3.53, p = 0.003). In patients with chronic migraine, preeclampsia was associated with the largest OR for PPD, followed by depression, gestational diabetes, and premenstrual dysphoric disorder. Anxiety, advanced maternal age, endometriosis, and post-traumatic stress disorder were not associated with a statistically significant increase in OR for PPD. Conclusions: Chronic migraine, with and without aura, is associated with a higher OR for PPD relative to non-migraine controls. Patients with chronic migraine, preeclampsia, depression, gestational diabetes, and premenstrual dysphoric disorder were also associated with increased risk of PPD. These data support screening patients with both chronic migraine and these comorbidities for PPD with validated screening tools to connect them with optimal resources best.

Whether ultrasound-guided stellate ganglion block (SGB) is a valuable therapeutic option for the treatment of patients with chronic migraine (CM) is worth exploring. If SGB is proven to be effective for CM, the identification of potential predictors for the effectiveness of SGB warrants further investigation. This study aimed to investigate the effectiveness and safety of SGB in patients with CM and to explore the predictive factors for its treatment effectiveness. This is a retrospective observational study. We retrospectively analyzed the effects of SGB for the treatment of patients with CM under ultrasound guidance, between January 2018 and June 2022. The follow-up time was approximately 1 month, 2 months, and 3 months after the last SGBs. The response criterion was defined as a reduction in pain intensity of > 50% measured using the most severe numerical rating scale (NRS) score compared to pretreatment baseline, without an increase in the dose or the type of analgesic or anxiolytic/antidepressant medication, otherwise unresponsive to SGB. Univariable and multivariable analyses were performed to identify the predictive factors for SGB response. Ninety-seven patients were included in this study. SGB was effective in most of the CM patients, with an effective rate of 90.7%, 82.5%, and 71.1% after 1, 2, and 3 months of the last SGBs, respectively. At 3-month follow-up, 95.7% responsive patients benefited from repeated SGBs. In patients receiving repeated SGB treatments, the number of SGBs in responsive patients was significantly greater than those in patients with no response at 3-month follow-up (3.41 ± 1.31 vs. 2.68 ± 0.67, p=0.02). Comorbid anxiety or depression was a negative predictor of SGB effectiveness at 3-month follow-up (B=-0.25, 95% CI -0.45 to -0.05, p=0.01). The overall adverse events rate associated with ultrasound-guided SGB was 9.3%. There were no serious complications; all adverse events were transient, with hoarseness being the most common adverse event. Ultrasound-guided SGB was an effective and safe treatment for CM patients. The majority of responsive patients with CM benefited from repeated SGBs. CM patients who needed repeated SGBs may obtain good and sustained analgesic effect after receiving a greater number of SGBs. Patients without comorbidities such as anxiety or depression were more likely to benefit from SGB treatments.

ObjectiveTo evaluate the efficacy of fremanezumab in patients with chronic migraine (CM) and moderate to severe depression.BackgroundFremanezumab, a fully humanized monoclonal antibody that selectively targets calcitonin gene–related peptide, has been approved for the preventive treatment of migraine in adults. CM and depression are highly comorbid.MethodsThe 12‐week, Phase 3 HALO trial randomized patients with CM to fremanezumab quarterly (675 mg/placebo/placebo), fremanezumab monthly (675/225/225 mg), or placebo. Post hoc analyses evaluated the effects of fremanezumab in patients with moderate to severe depression (baseline 9‐item Patient Health Questionnaire sum score ≥10) on monthly number of headache days of at least moderate severity; monthly migraine days; Patient Global Impression of Change (PGIC); 6‐item Headache Impact Test (HIT‐6) scores; and depression.ResultsFor the 219/1121 (19.5%) patients with moderate to severe depression at baseline, fremanezumab was associated with a significant reduction in monthly number of headache days of at least moderate severity for active treatment versus placebo (least‐squares mean change ± standard error for quarterly dosing: −5.3 ± 0.77; for monthly dosing: −5.5 ± 0.72; and for placebo: −2.2 ± 0.81; both p < 0.001). More patients achieved a ≥50% reduction in headache days of at least moderate severity with fremanezumab (quarterly: 31/78 [39.7%]; monthly: 39/96 [40.6%]) than placebo (9/67 [13.4%]; both p < 0.001). Compared with placebo, fremanezumab improved PGIC and HIT‐6 scores.ConclusionsFremanezumab demonstrated efficacy in the preventive treatment of CM and reduced headache impact in patients with comorbid depression.

The difficulty in distinguishing episodic tension-type headache from migraine headache is widely acknowledged. The misdiagnosis of migraine as tension-type headache has potentially significant consequences because it may preclude patients with disabling headaches from receiving appropriate treatment. This article explores the symptomatologic, epidemiologic, and pathophysiologic relationships among migraine and tension-type headaches with the aim of elucidating ways to improve their diagnosis and treatment. Clinical, epidemiologic, and pharmacologic data converge to suggest that rigid adherence to the IHS criteria in diagnosing migraine and tension-type headache may result in misdiagnosis of some headaches. Many migraine attacks are accompanied by tension headache-like symptoms, such as neck pain. Conversely, IHS-defined tension-type headaches are often accompanied by migraine-like symptoms, such as photophobia or phonophobia and aggravation by activity. The health-care provider caring for patients with headache should be cognizant of these overlaps and their implications for the management of patients with headache.