ArticlePDF Available

Abstract and Figures

Preventive treatment is an approach that is often forgotten in the treatment of migraine: in 2007, Lipton et al. reported that 39% of patients with this condition met the criteria to be considered for or offered preventive medication, yet only 12% currently receive such treatment.¹ Therefore, the updated US evidence-based guidelines for the use of drugs and complementary treatments for migraine prevention, which were recently published in Neurology,2, ³ are a praiseworthy addition to the literature.
Content may be subject to copyright.
A preview of the PDF is not available
... Terapi preventif bertujuan untuk mengurangi frekuensi, durasi, dan keparahan dari sernagan (14). Namun, komponen tatalaksana ini sering dilupakan dan bahkan hanya 12% penderita migrain di Amerika yang mendapat terapi preventif (15). ...
... • Kondisi migrain tertentu: hemiplegia, migrain dengan aura batang otak, infark migrainosus, dan gejala aura yang berat. Agen terapi preventif yang terbukti memiliki efikasi yang baik untuk migrain meliputi beta-blocker (propranolol, metoprolol, timolol), anti-epileptik (sodium divalproex, sodium valproate, topiramate), dan triptan (frovatriptan) (14). Obat dipilih berdasarkan kondisi dan kontraindikasi pasien. ...
... Obat dipilih berdasarkan kondisi dan kontraindikasi pasien. Penghentian profilaksis dilakukan apabila ada efek samping yang signifikan, tidak ada dampak sedikitpun setelah 2 bulan terapi, dan terapi dinyatakan berhasil dan migrain terkontrol (14). Hasil penelitian menunjukkan bahwa terapi preventif dapat mengurangi gejala, meningkatkan quality of life, dan mengurangi biaya yang diperlukan untuk berobat (14). ...
Article
Full-text available
A classic migraine is a recurrent attack of visual, sensory, or other central nervous system symptoms that are unilateral and last several minutes, followed or not followed by a migraine attack. Migraine commonly occurs in 19% of women and 11% of men worldwide, with 20% of sufferers experiencing classic migraine. The etiopathophysiology of classical migraine is not known with certainty, but vascular, neurological, and genetic dysfunction are suspected to be the cause. Classical migraine pathophysiology is associated with the theory of cortical spreading depression, which can explain the process of aura. There are four phases in classical migraine, namely prodromal, aura, headache, and prodromal phases, each of which has its own symptoms. This is the basis for the diagnosis of migraine, which is established based on the history and physical examination. Migraine therapy includes preventive therapy (lifestyle changes and prophylactic administration) as well as abortive therapy (administration of specific and non-specific drugs).
... Patients were instructed to improve the consistency of their sleep hygiene and adhere to a strict migraine diet, which avoids foods that can trigger migraines. 12,13 Nortriptyline and verapamil were first-line medications. Dosage was titrated until patients achieved symptomatic improvement or reduced if the medication was poorly tolerated. ...
... Commonly, dose escalation is necessary for achieving symptomatic control in the treatment of patients with classic migraine headache or VM, highlighting the difficulty in treating these patients. 13,[17][18][19] In our cohort, 6 (54%) patients required dose escalation to achieve symptomatic control. Larger, prospective studies would help further characterize this group of patients with isolated AF with no VM. ...
Article
Full-text available
In this case series, we set out to describe the clinical entity of isolated, prolonged aural fullness (AF) and its relationship with migraine. Patients with isolated, persistent AF for 6 months or more were included with all possible etiologies ruled out. Migraine dietary and lifestyle changes and medical migraine prophylactic therapy were prescribed to all. Eleven patients were included (mean age, 52 years). Six (54%) patients fulfilled International Headache Society criteria for migraine with or without aura. Changes in perceived sensation of AF using the visual analog scale and quality of life questionnaires resulted in a statically significant improvement ( P < .001, 95% confidence interval [CI], 4.7 to 6.72, and P < .001, 95% CI, -5.3 to -2.7, respectively). As such, an improvement of isolated, prolonged AF with migraine lifestyle changes and prophylactic treatment may suggest an etiological association between migraine and prolonged aural fullness.
... 29,32 In our study, all patients required dose escalation to achieve symptomatic control, which along with combination therapy is usually necessary for achieving symptomatic control in classic migraine or vestibular migraine patients. [34][35][36][37] This was the case in 20% of our patients, who needed poly-therapy due to the nature or severity of their disease. ...
Article
Full-text available
Objective: To evaluate the change in quality of life (QOL) of patients with Meniere's disease (MD) after treatment with migraine prophylaxis therapy. Methods: Patients with definite MD were given the Meniere's Disease Outcomes Questionnaire-Retrospective (MDOQ-R) after migraine prophylactic therapy to assess QOL. Changes in physical, emotional, and social parameters affected by MD were calculated, along with a global pre- and posttreatment QOL scores. Results: The MDOQ-R was given to 27 consecutive patients with definite MD. Patients who had at least an 18-month follow-up were included, resulting in 25 questionnaires. The mean change in QOL score was 25 ± 16 (range, -3 to 55), P = .02. Quality of life was improved in 23 (92%) of the respondents in every metric measured, unchanged in 1 (4%), and poorer in 1 (4%) of patients after migraine prophylaxis treatment. Conclusions: Majority of MD patients who had all failed diuretic therapy responded positively to medications used for migraine prophylaxis, as indicated by a significant improvement in QOL. This study may further suggest a correlation between the pathophysiologic basis of disease in MD and vestibular migraine. Patients with MD may be successfully managed with medications intended to treat migraine.
... The first choice for preventive therapy of migraine includes β-adrenoceptor blockers, flunarizine, topiramate, and valproic acid. Rodent evidence has verified the efficacy of AMI as a preventive for migraine, and evidence-based guidelines classified it into secondline therapy options [76,77]. In a cost-effectiveness analysis of interventions for migraine, AMI was found to be more cost-effective than propranolol or topiramate, because it was more effective than proanolol and far cheaper than topiramate [78]. ...
Article
Rodent evidence has confirmed the analgesic effect of tricyclic antidepressants in the treatment of chronic pain, which amitriptyline is rigorously verified. The analgesic effect of amitriptyline, whose mechanisms are complex and unclear, is different from its antidepressant effect. This article reviewed the mechanisms behind amitriptyline’s analgesic properties to further understanding of this drug. Additionally, this article reviewed the clinical evidence of the effectiveness of amitriptyline therapy in treatment of chronic pain to offer guidance for future clinical practice.
... The first choice for preventive therapy of migraine includes β-adrenoceptor blockers, flunarizine, topiramate, and valproic acid. Rodent evidence has verified the efficacy of AMI as a preventive for migraine, and evidence-based guidelines classified it into secondline therapy options [76,77]. In a cost-effectiveness analysis of interventions for migraine, AMI was found to be more cost-effective than propranolol or topiramate, because it was more effective than proanolol and far cheaper than topiramate [78]. ...
Article
Full-text available
Rodent evidence has confirmed the analgesic effect of tricyclic antidepressants in the treatment of chronic pain, which amitriptyline is rigorously verified. The analgesic effect of amitriptyline, whose mechanisms are complex and unclear, is different from its antidepressant effect. This article reviewed the mechanisms behind amitriptyline’s analgesic properties to further understanding of this drug. Additionally, this article reviewed the clinical evidence of the effectiveness of amitriptyline therapy in treatment of chronic pain to offer guidance for future clinical practice.
... Thus, in acute RCTs with oral triptans the placebo response for headache relief at 2 h varied from 17 to 50% [1]. In prophy- lactic RCTs the placebo-response is usually in the 20 to 40% range but 50% and even 70% [2]have been reported. So if two "active" drugs both show similar response rates of 45% and 49% in a prophylactic RCT in migraine one cannot speak of equivalence even with narrow confidence intervals because no "pharmacological " effect has been demon- strated in the patient sample. ...
Article
Full-text available
If feasible placebo should be included in randomized, controlled trials (RCTs) comparing two presumable active drugs. Inclusion of placebo in comparative RCTs was recommended generally by FDA in 1982, by the International Headache Society for migraine in 1991, and by the European Medicines Agency (EMEA) for migraine in 2007.
... All patients were evaluated by a senior psychiatrist to confirm a diagnosis of major depression as well as the presence of OCD. After discharge, pharmacological prevention was started, choosing a compound from those included in the current guidelines for migraine prophylaxis, but avoiding antidepressant compounds [12]. Patients had a baseline-1 month period after discharge, during which they filled an daily headache diary with recording of presence and severity of headache and symptomatic medication consumption . ...
Article
Full-text available
Patients with chronic migraine (CM) and medication overuse (MO) have high frequency of psychiatric comorbidity. Aims of this open label, prospective, independent study were: to evaluate the efficacy of duloxetine in a sample of patients with MO due to CM and with concomitant depression; to investigate, if the presence of OCD influences the outcome in this subgroup of patients. A total of 50 consecutive patients (40 F,10 M, aged 20-65 years, mean 39.4 years) from those attending our Headache Center to undergo an inpatient withdrawal programme followed by anti-migraine prophylaxis was enrolled. After a 1-month baseline period, all patients were prescribed duloxetine 30 mg in the morning for the first week, and 60 mg for the following 12 weeks. They filled a daily headache diary during the whole study period. They also completed Hamilton depression rating scale (HDRS) and migraine disability assessment scale (MIDAS) at baseline and at the 12-week follow-up. The primary outcome measure was the percentage of responders, i.e. of patients with a reduction ≥50 % in headache frequency as well as in symptomatic drug consumption. Comparison between patients with and without OCD was performed. Our results showed a rather high responder rate in the total sample (64 %), while none of the patients with OCD fell among responders. MIDAS and HDRS scores had a more evident decrease in patients without OSD. These findings suggest that duloxetine may be effective in patients with MO due to CM and with comorbid depression. They also confirm the importance of a systematic assessment of the psychopathological profile in these patients, and indicate that clinicians should be aware of the relevant prognostic role of OCD in favoring a poor outcome and persistent disability in headache patients with MO.
Article
Objective: To describe persistent post-stapedotomy vertigo (PSV) and its treatment using migraine prophylaxis. Patients: A retrospective review of all patients with persistent PSV spanning 10 years at a tertiary academic hospital was performed. Patients who experienced persistent vertigo for a minimum of 3 months after surgery were included. Those with possible perilymph fistula, long prosthesis, and benign paroxysmal positional vertigo were excluded. Interventions: All patients received instructions on migraine dietary and lifestyle changes and Vitamin B2 and magnesium. In addition, prophylactic treatment with nortriptyline, verapamil, or a combination thereof was started. Main outcome measure: Changes in vertigo frequency was the main outcome variable. The secondary outcome variables included the time period and medications necessary to achieve symptomatic resolution. Results: Four women and one man with an average age of 53 years were identified that met criteria for persistent PSV indicating an incidence of 0.9% at our institution. The onset of vertigo symptoms was on average 20 days postoperatively. All five patients had daily vertigo episodes and experienced complete resolution with no vertigo episodes after treatment. Symptomatic resolution was achieved over an average of 9 weeks after initiating treatments. Conclusions: Persistent PSV beyond 3 months is a rare occurrence and its treatment can be challenging when there is no evidence of an underlying pathology. This subset of patients may be suffering from migraine, which was triggered postoperatively. Treatment with migraine prophylaxis in this cohort of patients may result in resolution of vertigo.
Article
Full-text available
Cavum septum pellucidum (CSP) and cavum Vergae (CV) are unusual variants and usually asymptomatic, but their expansion or inside lesions can produce symptoms by mass effect. A 46-year-old female Taiwanese worker presented with chronic daily headaches for eight years. Magnetic resonance imaging revealed coexistent CSP and CV. She declined surgical drainage recommended by a neurosurgeon and thus visited our clinic for a second opinion. Physical examination did not show any abnormality. With the help of the patient's one-month headache diary, she was diagnosed with chronic migraine according to the International Classification of Headache Disorders, 2(nd) edition, with further modification in 2006. In addition, hypertension was also identified. Over the following week, taking a daily selective β1-antagonist relieved the headache and hypertension. The medication was continued and the following year was uneventful. Therefore, the chronic daily headache was ascribed to chronic migraine, rather than symptomatic CSP and CV.
Article
Full-text available
Updated guidelines for the preventive treatment of episodic migraine have been issued by the American Headache Society (AHS) and the American Academy of Neurology (AAN). We summarize key 2012 guideline recommendations and changes from previous guidelines. We review the characteristics, methods, consistency, and quality of the AHS/AAN guidelines in comparison with recently issued guidelines from other specialty societies. To accomplish this, we reviewed the AHS/AAN guidelines and identified comparable recent guidelines through a systematic MEDLINE search. We extracted key data, and summarized and compared the key recommendations and assessed quality using the Appraisal of Guidelines Research and Evaluation-II (AGREE-II) tool. We identified 2 additional recent guidelines for migraine prevention from the Canadian Headache Society and the European Federation of Neurological Societies. All of the guidelines used structured methods to locate evidence and linked recommendations with assessment of the evidence, but they varied in the methods used to derive recommendations from that evidence. Overall, the 3 guidelines were consistent in their recommendations of treatments for first-line use. All rated topiramate, divalproex/sodium valproate, propranolol, and metoprolol as having the highest level of evidence. In contrast, recommendations diverged substantially for gabapentin and feverfew. The overall quality of the guidelines ranged from 2 to 6 out of 7 on the AGREE-II tool. The AHS/AAN and Canadian guidelines are recommended for use on the basis of the AGREE-II quality assessment. Recommendations for the future development of clinical practice guidelines in migraine are provided. In particular, efforts should be made to ensure that guidelines are regularly updated and that guideline developers strive to locate and incorporate unpublished clinical trial evidence.
Article
Full-text available
In 1991 the Clinical Trials Subcommittee of the International Headache Society (IHS) published its first edition of the Guidelines on controlled trials of drugs in migraine (1). The Guidelines’ overarching goal was to improve ‘the quality of controlled clinical trials in migraine’, which could be achieved by using scientifically robust methods of clinical research. The report highlighted the complex nature of migraine clinical trial methodologies and offered a road map to clinical investigators who were interested in the field. The Migraine Guidelines were adopted widely (2–7), although – for a variety of reasons, including regulatory restrictions – not universally (8–11), and this was the impetus for the development of similar guidelines for tension-type headache (12,13) and for cluster headache (14). The second edition of the guidelines was published in 2000 (15) and, based on the second edition, the European Medicines Agency published in 2007 ‘Guidelines on Clinical Investigation of Medicinal Products for the Treatment of Migraine’ (16). Have investigators then followed the recommendations in these guidelines for randomized controlled trials (RCTs)? Unlike the case of RCTs for migraine prevention where the recommended primary efficacy measure of migraine attack frequency was used in 72% of 52 RCTs (17), adherence to the recommendations in the guidelines for acute migraine treatment has not been overwhelming. Indeed, the recommended measure of freedom from pain after 2 h was the primary efficacy measure in 31% of 145 acute RCTs between 2002 and 2008 (17). Instead, headache relief after 2 h (a decrease from moderate or severe to none or mild) was used in 39% of such trials. Notwithstanding, the proportion of RCTs using pain freedom as the primary efficacy measure has continued to increase over time (17), and is even used in recent large clinical trials (18–21). Following the publication of the IHS Clinical Trials Guidelines, several clinical drug development programmes emerged, notably for acute migraine (e.g. 5- HT1B/D agonists, triptans) and for prevention (e.g. topiramate). The majority of these RCTs were performed mainly for registration purposes (16). This exponential increase in migraine clinical research, the accumulating experience of clinical researchers and the pharmaceutical industry alike, and the trend towards large multi-centre and multi-national studies, call for a timely revisit and a refresh of the original guidelines and their second edition. The third edition of Migraine Clinical Trials Guidelines is a consensus summary that was developed by experts in the field, and its purpose is to recommend a contemporary, standardized, and evidence-based approach to the conduct and reporting of migraine RCTs. Broader discussions of clinical trials methodologies can be found elsewhere (22–30). Also, ethical considerations in migraine clinical research have been published separately (31). Finally, it should be noted that the revised Guidelines represent Research Practice Parameters and are the highest level in the hierarchy of Evidence-Based Recommendations in the absence of published Standards of Research Practice. Therefore, the IHS endorses the adherence to the Guidelines unless there is scientific justification for deviations from the recommendations. The Third Edition of The Migraine Clinical Trials Guidelines is organized similarly to the previous two editions. Notably, RCTs for acute attacks of migraine are addressed in the first section of these guidelines and are followed by discussions and recommendations relating to RCTs for migraine prevention, including short-term prophylaxis or ‘mini-prophylaxis’ for predictable migraine attacks, such as those associated with menses (32). Sub-sections include: patient selection, trial design, evaluation of results and statistics. A toolbox for each type of trial (acute and prevention) is provided at the end. R 1. IHS. Guidelines for controlled trials of drugs in migraine. First edition. International Headache Society Committee on Clinical Trials in Migraine. Cephalalgia 1991; 11: 1–12. 2. Schoenen J and Sawyer J. Zolmitriptan (Zomig, 311C90), a novel dual central and peripheral 5HT1B/1D agonist: an overview of efficacy. Cephalalgia 1997; 17(Suppl 18): 28–40. 3. Rolan PE and Martin GR. Zolmitriptan: a new acute treatment for migraine. Expert Opin Investig Drugs 1998; 7: 633–652. 4. Dahlof C and Lines C. Rizatriptan: a new 5-HT1B/1D receptor agonist for the treatment of migraine. Expert Opin Investig Drugs 1999; 8: 671–685. 5. Dooley M and Faulds D. Rizatriptan: a review of its efficacy in the management of migraine. Drugs 1999; 58: 699–723. 6. Spencer CM, Gunasekara NS and Hills C. Zolmitriptan: a review of its use in migraine. Drugs 1999; 58: 347–374. 7. Saxena P and Tfelt-Hansen P. Triptans, 5HT1B/1D agonists in the acute treatment of migraine. In: Olesen J, Goadsby PJ, Ramadan NM, Tfelt-Hansen P, Welch KMA (eds) The headaches. Vol. 3, Philadelphia: Lippincott Williams & Wilkins, 2006, pp.469–503. 8. Pilgrim AJ. Methodology of clinical trials of sumatriptan in migraine and cluster headache. Eur Neurol 1991; 31: 295–299. 9. Dechant KL and Clissold SP. Sumatriptan. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic efficacy in the acute treatment of migraine and cluster headache. Drugs 1992; 43: 776–798. 10. Plosker GL and McTavish D. Sumatriptan. A reappraisal of its pharmacology and therapeutic efficacy in the acute treatment of migraine and cluster headache. Drugs 1994; 47: 622–651. 11. Perry CM and Markham A. Sumatriptan. An updated review of its use in migraine. Drugs 1998; 55: 889–922. 12. IHS. Guidelines for trials of drug treatments in tensiontype headache. First edition: International Headache Society Committee on Clinical Trials. Cephalalgia 1995; 15: 165–179. 13. Bendtsen L, Bigal ME, Cerbo R, et al. Guidelines for controlled trials of drugs in tension-type headache: second edition. Cephalalgia 2010; 30: 1–16. 14. Lipton RB, Micieli G, Russell D, et al. Guidelines for controlled trials of drugs in cluster headache. Cephalalgia 1995; 15: 452–462. 15. Tfelt-Hansen P, Block G, Dahlof C, et al. Guidelines for controlled trials of drugs in migraine: second edition. Cephalalgia 2000; 20: 765–786. 16. EMEA CFMPFHU. Guideline on clinical investigation of medicinal products for the treatment of migraine. Vol 2011. London, 2007. 17. Hougaard A and Tfelt-Hansen P. Are the current IHS guidelines for migraine drug trials being followed? J Headache Pain 2010; 11: 457–468. 18. Ho TW, Mannix LK, Fan X, et al. Randomized controlled trial of an oral CGRP receptor antagonist, MK- 0974, in acute treatment of migraine. Neurology 2008; 70: 1304–1312. 19. Ho TW, Ferrari MD, Dodick DW, et al. Efficacy and tolerability of MK-0974 (telcagepant), a new oral antagonist of calcitonin gene-related peptide receptor, compared with zolmitriptan for acute migraine: a randomised, placebo-controlled, parallel-treatment trial. Lancet 2008; 372: 2115–2123. 20. Connor KM, Shapiro RE, Diener HC, et al. Randomized, controlled trial of telcagepant for the acute treatment of migraine. Neurology 2009; 73: 970–977. 21. Tfelt-Hansen P. Pain freedom at 2 hours in migraine after telcagepant 300 mg. CNS Drugs 2011; 25: 269–270. 22. Good C. The principles and practice of clinical trials. Edinburgh: Churchill Livingstone, 1976. 23. Pocock S. Clinical trials. A practical approach. Chichester: John Wiley & Sons, 1984. 24. Meinert C. Clinical trials: design, conduct, and analysis. Oxford: Oxford University Press, 1986. 25. Spilker B. Guide to clinical trials. New York: Raven Press, 1991. 26. Olesen J, Krabbe AA and Tfelt-Hansen P. Methodological aspects of prophylactic drug trials in migraine. Cephalalgia 1981; 1: 127–141. 27. Gerber WD, Soyka D, Niederberger U and Haag G. [Problems in and approaches to the design and evaluation of therapeutic studies in patients with headache.]. Schmerz 1987; 1: 81–91. 28. Tfelt-Hansen P and Olesen J. Methodological aspects of drug trials in migraine. Neuroepidemiology 1985; 4: 204–226. 29. Olesen J and Tfelt-Hansen P. Methodology of migraine trials. In: Orgogozo J-M, Capildeo R (eds) Methods in clinical trials in neurology. Vascular and degenerative brain disease. London: Macmillan, 1988, pp.85–109. 30. Lipton RB. Methodologic issues in acute migraine clinical trials. Neurology 2000; 55: S3–S7. 31. IHS. Ethical issues in headache research and management: report and recommendations of the ethics subcommittee of the International Headache Society. Cephalalgia 1998; 18: 505–529. 32. MacGregor EA. "Menstrual" migraine: towards a definition. Cephalalgia 1996; 16: 11–21.
Article
Full-text available
To evaluate the efficacy and relative adverse effects of tricyclic antidepressants in the treatment of migraine, tension-type, and mixed headaches. Meta-analysis. Medline, Embase, the Cochrane Trials Registry, and PsycLIT. Studies reviewed Randomised trials of adults receiving tricyclics as only treatment for a minimum of four weeks. Frequency of headaches (number of headache attacks for migraine and number of days with headache for tension-type headaches), intensity of headache, and headache index. 37 studies met the inclusion criteria. Tricyclics significantly reduced the number of days with tension-type headache and number of headache attacks from migraine than placebo (average standardised mean difference -1.29, 95% confidence interval -2.18 to -0.39 and -0.70, -0.93 to -0.48) but not compared with selective serotonin reuptake inhibitors (-0.80, -2.63 to 0.02 and -0.20, -0.60 to 0.19). The effect of tricyclics increased with longer duration of treatment (β=-0.11, 95% confidence interval -0.63 to -0.15; P<0.0005). Tricyclics were also more likely to reduce the intensity of headaches by at least 50% than either placebo (tension-type: relative risk 1.41, 95% confidence interval 1.02 to 1.89; migraine: 1.80, 1.24 to 2.62) or selective serotonin reuptake inhibitors (1.73, 1.34 to 2.22 and 1.72, 1.15 to 2.55). Tricyclics were more likely to cause adverse effects than placebo (1.53, 95% confidence interval 1.11 to 2.12) and selective serotonin reuptake inhibitors (2.22, 1.52 to 3.32), including dry mouth (P<0.0005 for both), drowsiness (P<0.0005 for both), and weight gain (P<0.001 for both), but did not increase dropout rates (placebo: 1.22, 0.83 to 1.80, selective serotonin reuptake inhibitors: 1.16, 0.81 to 2.97). Tricyclic antidepressants are effective in preventing migraine and tension-type headaches and are more effective than selective serotonin reuptake inhibitors, although with greater adverse effects. The effectiveness of tricyclics seems to increase over time.
Article
Full-text available
This systematic review of population-based studies of the incidence and early (21 days to 1 month) case fatality of stroke is based on studies published from 1970 to 2008. Stroke incidence (incident strokes only) and case fatality from 21 days to 1 month post-stroke were analysed by four decades of study, two country income groups (high-income countries and low to middle income countries, in accordance with the World Bank's country classification) and, when possible, by stroke pathological type: ischaemic stroke, primary intracerebral haemorrhage, and subarachnoid haemorrhage. This Review shows a divergent, statistically significant trend in stroke incidence rates over the past four decades, with a 42% decrease in stroke incidence in high-income countries and a greater than 100% increase in stroke incidence in low to middle income countries. In 2000-08, the overall stroke incidence rates in low to middle income countries have, for the first time, exceeded the level of stroke incidence seen in high-income countries, by 20%. The time to decide whether or not stroke is an issue that should be on the governmental agenda in low to middle income countries has now passed. Now is the time for action.
Article
To provide updated evidence-based recommendations for the preventive treatment of migraine headache. The clinical question addressed was: Are nonsteroidal anti-inflammatory drugs (NSAIDs) or other complementary treatments effective for migraine prevention? The authors analyzed published studies from June 1999 to May 2009 using a structured review process to classify the evidence relative to the efficacy of various medications for migraine prevention. The author panel reviewed 284 abstracts, which ultimately yielded 49 Class I or Class II articles on migraine prevention; of these 49, 15 were classified as involving nontraditional therapies, NSAIDs, and other complementary therapies that are reviewed herein. Petasites (butterbur) is effective for migraine prevention and should be offered to patients with migraine to reduce the frequency and severity of migraine attacks (Level A). Fenoprofen, ibuprofen, ketoprofen, naproxen, naproxen sodium, MIG-99 (feverfew), magnesium, riboflavin, and subcutaneous histamine are probably effective for migraine prevention (Level B). Treatments considered possibly effective are cyproheptadine, Co-Q10, estrogen, mefenamic acid, and flurbiprofen (Level C). Data are conflicting or inadequate to support or refute use of aspirin, indomethacin, omega-3, or hyperbaric oxygen for migraine prevention. Montelukast is established as probably ineffective for migraine prevention (Level B).
Article
To provide updated evidence-based recommendations for the preventive treatment of migraine headache. The clinical question addressed was: What pharmacologic therapies are proven effective for migraine prevention? The authors analyzed published studies from June 1999 to May 2009 using a structured review process to classify the evidence relative to the efficacy of various medications available in the United States for migraine prevention. The author panel reviewed 284 abstracts, which ultimately yielded 29 Class I or Class II articles that are reviewed herein. Divalproex sodium, sodium valproate, topiramate, metoprolol, propranolol, and timolol are effective for migraine prevention and should be offered to patients with migraine to reduce migraine attack frequency and severity (Level A). Frovatriptan is effective for prevention of menstrual migraine (Level A). Lamotrigine is ineffective for migraine prevention (Level A).
Article
Treatment of aneurysmal subarachnoid hemorrhage (SAH) has changed substantially over the last 25 years but there is a lack of reliable population-based data on whether case-fatality or functional outcomes have improved. We determined changes in the standardized incidence and outcome of SAH in the same population between 1981 and 1986 (Oxford Community Stroke Project) and 2002 and 2008 (Oxford Vascular Study). In a meta-analysis with other population-based studies, we used linear regression to determine time trends in outcome. There were no reductions in incidence of SAH (RR = 0.79, 95% confidence interval [CI] 0.48-1.29, p = 0.34) and in 30-day case-fatality (RR = 0.67, 95% CI 0.39-1.13, p = 0.14) in the Oxford Vascular Study vs Oxford Community Stroke Project, but there was a decrease in overall mortality (RR = 0.47, 0.23-0.97, p = 0.04). Following adjustment for age and baseline SAH severity, patients surviving to hospital had reduced risk of death or dependency (modified Rankin score > 3) at 12 months in the Oxford Vascular Study (RR = 0.51, 0.29-0.88, p = 0.01). Among 32 studies covering 39 study periods from 1980 to 2005, 7 studied time trends within single populations. Unadjusted case-fatality fell by 0.9% per annum (0.3-1.5, p = 0.007) in a meta-analysis of data from all studies, and by 0.9% per annum (0.2-1.6%, p = 0.01) within the 7 population studies. Mortality due to subarachnoid hemorrhage fell by about 50% in our study population over the last 2 decades, due mainly to improved outcomes in cases surviving to reach hospital. This improvement is consistent with a significant decrease in case-fatality over the last 25 years in our pooled analysis of other similar population-based studies.
Article
Migraine is one of the most frequent disabling neurological conditions with a major impact on the patients' quality of life. To give evidence-based or expert recommendations for the different drug treatment procedures in the particular migraine syndromes based on a literature search and the consensus of an expert panel. All available medical reference systems were screened for the range of clinical studies on migraine with and without aura and on migraine-like syndromes. The findings in these studies were evaluated according to the recommendations of the European Federation of Neurological Societies (EFNS) resulting in level A, B, or C recommendations and good practice points. For the acute treatment of migraine attacks, oral non-steroidal antiinflammatory drug (NSAID) and triptans are recommended. The administration should follow the concept of stratified treatment. Before intake of NSAID and triptans, oral metoclopramide or domperidone is recommended. In very severe attacks, intravenous acetylsalicylic acid or subcutaneous sumatriptan are drugs of first choice. Status migrainosus can be treated by cortoicosteroids, although this is not universally held to be helpful, or dihydroergotamine. For the prophylaxis of migraine, betablockers (propranolol and metoprolol) flunarizine, valproic acid, and topiramate are drugs of first choice. Drugs of second choice for migraine prophylaxis include amitriptyline, naproxen, petasites, and bisoprolol.
Article
Propranolol is one of the most commonly prescribed drugs for migraine prophylaxis. We aimed to determine whether there is evidence that propranolol is more effective than placebo and as effective as other drugs for the interval (prophylactic) treatment of patients with migraine. Potentially eligible studies were identified by searching MEDLINE/PubMed (1966 to May 2003) and the Cochrane Central Register of Controlled Trials (Issue 2, 2003), and by screening bibliographies of reviews and identified articles. We included randomised and quasi-randomised clinical trials of at least 4 weeks duration comparing clinical effects of propranolol with placebo or another drug in adult migraine sufferers. Two reviewers extracted information on patients, methods, interventions, outcomes measured, and results using a pre-tested form. Study quality was assessed using two checklists (Jadad scale and Delphi list). Due to the heterogeneity of outcome measures and insufficient reporting of the data, only selective quantitative meta-analyses were performed. As far as possible, effect size estimates were calculated for single trials. In addition, results were summarised descriptively and by a vote count among the reviewers. A total of 58 trials with 5072 participants met the inclusion criteria. The 58 selected trials included 26 comparisons with placebo and 47 comparisons with other drugs. The methodological quality of the majority of trials was unsatisfactory. The principal shortcomings were high dropout rates and insufficient reporting and handling of this problem in the analysis. Overall, the 26 placebo-controlled trials showed clear short-term effects of propranolol over placebo. Due to the lack of studies with long-term follow up, it is unclear whether these effects are stable after stopping propranolol. The 47 comparisons with calcium antagonists, other beta-blockers, and a variety of other drugs did not yield any clear-cut differences. Sample size was, however, insufficient in most trials to establish equivalence. Although many trials have relevant methodological shortcomings, there is clear evidence that propranolol is more effective than placebo in the short-term interval treatment of migraine. Evidence on long-term effects is lacking. Propranolol seems to be as effective and safe as a variety of other drugs used for migraine prophylaxis.
Article
Topiramate and sodium valporate are anticonvulsants, demonstrated to be effective as monotherapy for migraine prevention in placebo-controlled trials. To compare the relative efficacy of topiramate and sodium valporate in the prevention of migraine. A 24-week, randomized, double-blind, crossover, clinical trial was conducted from October 2003 to September 2004. A total of 64 patients with migraine headache, aged 14 to 57 years, were randomly allocated to the 2 treatment groups. The first group received topiramate (25 mg daily increment over 1 week to 50 mg) for a total of 2 months. The second group received sodium valporate (200 mg daily increment over 1 week to 400 mg) for 2 months. Response to treatment was assessed at 0, 1, 8, 16, and 24 weeks after start of therapy. Topiramate appeared to be equivalent in efficacy and safety to sodium valporate. A significant decrease in duration, monthly frequency, and intensity of headache occurred in both groups. Of the 32 patients treated with sodium valporate, the mean standard deviation (SD) of monthly migraine frequency decreased from 5.4 (2.5) to 4.0 (2.8) episode per month, headache intensity from 7.7 (1.2) to 5.8 (1.7) by visual analog scale (VAS), and headache duration from 21.3 (14.6) to 12.3 (10.7) hours (P < .001). Correspondingly, in the 32 patients treated with topiramate, the mean SD of monthly headache frequency decreased from 5.4 (2.0) to 3.2 (1.9) per month, headache intensity from 6.9 (1.2) to 3.7 (1.3), and headache duration from 17.3 (8.4) to 3.9 (2.7) hours (P < .001). This study demonstrates that treatment with topiramate and sodium valporate both significantly reduce migraine headache. This effect of topiramate and sodium valporate has previously been shown to reduce migraine headache, and we postulate that treatment with topiramate and sodium valporate may have a similar benefit.