Quels sont les médicaments dangereux selon Prescrire et l'ANSM? -

Quels médicaments sont vraiment dangereux ? La réponse varie en fonction des interlocuteurs. Selon Le Guide des 4000 médicaments utiles, inutiles ou dangereux, des professeurs Bernard Debré et Philippe Even, 50% des médicaments sont inutiles, dont 5% potentiellement dangereux. La semaine dernière, la revue médicale indépendante Prescrire a publié sa liste des "médicaments plus dangereux qu'utiles" pour lesquels elle demande un retrait du marché. En janvier 2011, en plein scandale sanitaire du Mediator, l'Agence nationale de sécurité du médicament (ANSM) avait publié sa liste des 77 médicaments placés sous surveillance renforcée. L'Express y avait, à l'époque, consacré un dossier complet.  

Nous avons comparé les deux inventaires. Au total, près de 20 médicaments sont pointés du doigt à la fois par l'ANSM et par Prescrire. Ceux-ci disposent toujours d'une autorisation de mise sur le marché (AMM) mais on peut penser que, faisant en quelque sorte l'unanimité contre eux, ce seront les prochains à être retirés de la vente. Il s'agit, par ordre alphabétique, de:  

- Arcoxia (douleur, rhumatologie) 

- Champix (dépendances) 

- Cymbalta (psychiatre) 

- Ferrisat (cancérologie - hématologie) 

- Hexaquine (douleur - rhumatologie) 

- Januvia (diabétologie - nutrition)  

- Ketum gel (douleur - rhumatologie) 

- Nexen (douleur - rhumatologie) 

- Onglyza (diabétologie - nutrition)  

- Pholcodine (pneumologie - ORL)  

- Praxinor (cardiologie)  

- Primalan (dermatologie - allergologie) 

- Procoralan (cardiologie) 

- Protelos (douleur - rhumatologie) 

- Tysabri (neurologie) 

- Valdoxan (psychiatrie) 

- Vastarel (cardiologie)  

- Zyban (psychiatrie - dépendances)  

Parmi le recensement de l'Agence du médicament, figurent par exemple le Di-Antalvic (douleur - rhumatologie) et le Subutex (psychiatrie - dépendances) sans que leur efficacité ne soit remise en cause par la revue médicale. A l'inverse, le Motilium (gastro-enthérite) et le Thiovalone (pneumologie - ORL), entre autres, sont dans le viseur de Prescrire alors que l'ANSM ne les surveille pas avec une attention particulière.  

via lexpress.fr

Ou on voit qu'il est plsu facile de se passe rde médicament lorsqu'on est pas malade : n'est-ce pas les journaleux et médecins spécialistes de ce genre de sujet !

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Microsoft prédit l'avenir grâce à un logiciel qui analyse le passé

Connais le passé, et tu connaîtras l'avenir. Une équipe de Microsoft et de chercheurs israéliens travaillent sur un logiciel capable de prédire les catastrophes à venir, à partir des évènements présents et passés.

Le journal Technology Review édité par le MIT indique que des chercheurs de Microsoft et de l'Institut israélien de Technologie Technion ont mis au point un logiciel censé prédire les catastrophes futures, grâce à une analyse du présent et des évènements passés.

Le système a été "nourri" par 22 années d'archives du New York Times, de 1986 à 2007, et exploite de nombreuses autres sources tirées du web. En particulier, le système utilise DBpedia, qui structure les informations de Wikipédia sous forme de base de données exploitable, WordNet, qui permet de comprendre le sens des mots anglophones, et OpenCyc, une autre base de données de connaissances diverses. En tout, 90 sources seraient ainsi compilées.

Ainsi, le logiciel d'analyse aurait permis (rétroactivement dans des simulations) de prévenir le risque d'une épidémie de choléra en Angola, suite aux sécheresses connues par le pays en 2006, parce que le système aurait détecté une corrélation entre l'apparition du choléra dans certaines régions et les phénomènes de sécheresse. De même en 2007, le risque d'une épidémie de choléra aurait été signalé après d'importantes tempêtes en Afrique, et la maladie a effectivement été détectée une semaine plus tard.

"Dans des tests impliquant des prévisions de maladies, violences et un nombre significatifs de morts, les avertissements du système étaient corrects entre 70 et 90 % du temps", indique le MIT.

En soit, ces travaux n'ont rien de surprenant ni d'inédit. Google lui-même pratique des prédictions sanitaires, comme lorsqu'il tente d'analyser la progression de la grippe à partir des recherches de symptômes menées par les internautes. Mais le système de Microsoft tente d'automatiser l'analyse, et d'affiner les prédictions en croisant les données de situations comparables. Par exemple, le système va rapprocher les risques de deux villes ayant sensiblement les mêmes données géographiques (température, humidité, taux de couverture du territoire en eau, ...) et économiques (revenu moyen par habitant, infrastructures sanitaires...). 

Dans un premier temps, Microsoft souhaite mettre le logiciel à disposition des associations humanitaires, pour qu'elles puissent mieux se préparer à intervenir là où risquent de se déclencher les catastrophes. La firme ne parle pas encore de le mettre en vente. Mais riches seront ceux qui pourront prédire l'avenir, en particulier les cycles macro et micro-économiques...

via numerama.com

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Les Français très inégaux devant le cancer - Le Progrès

<blockquote class='posterous_long_quote'><h2 class="accroche">Ce lundi, journée mondiale de lutte contre la maladie qui est à l’origine d’environ 147 000 décès par an. Le prochain plan cancer sera axé sur une prévention ciblée pour lutter contre les inégalités sociales, géographiques et génétiques qui ne cessent de s’aggraver en France face à la maladie.</h2> <div class="mod detailGallery "> <div class="photo"> <div class="photoContent"> <div class="photoContainer" style=""> <img title="/ Infographie Patrick Villard" src="http://www.leprogres.fr/fr/images/ED225F0B-8D1B-4632-92B6-38B89A5B587E/LPR_03/infographie-patrick-villard.jpg" height="487" alt="/ Infographie Patrick Villard" width="680" /> <div title="Agrandir l'image" class="imgZoom"></div></div> <div class="legende"> <table border="0" width="100%"> <tr> <td width="70%" style=""> <span class="legendeTxt">/ Infographie Patrick Villard</span></td></tr></table></div></div></div></div></blockquote>

via leprogres.fr

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Montre-moi ton Facebook et je te dirai ta maladie mentale ?

Et si votre activité sur Facebook était le reflet de votre état de santé psychique ? C'est l'hypothèse émise par des chercheurs américains, qui ont découvert une corrélation entre l'activité de leurs cobayes sur le réseau social, et  les symptômes de troubles psychiatriques qu'ils présentaient.

via numerama.com

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Il faut cesser de s'en prendre à l'industrie pharmaceutique

Serrer la main d'un industriel de la pharmacie revient aujourd'hui à se commettre avec Satan. Que doivent penser les employés de ces firmes qui travaillent honnêtement ? Exposés à la vindicte publique, ils ne peuvent réagir, alors qu'ils sont plus de 100.000 en France à oeuvrer au développement et à la production de médicaments qui sauvent des milliers de vies et soulagent tant d'hommes, de femmes et d'enfants. Oui, l'industrie médicale, dans le cadre de contrats de partenariat et de protocoles réguliers, a fourni à de nombreux acteurs sanitaires, chercheurs et services hospitaliers en tête, des aides financières que les recettes publiques ne pouvaient supporter. L'affaire du Mediator, puis celle des pilules de dernières générations anéantissent ces collaborations au prétexte de dérives médiatisées à outrance occultant les vrais enjeux. C'est un changement profond de nos mentalités qu'il faut opérer afin de promouvoir ce renversement conceptuel qu'appelle l'indispensable collaboration directe entre les patients et une industrie honorable et utile.

Deux raisons plaident pour cette collaboration. Premièrement, l'amélioration de la qualité des produits et des prestations offerts passe toujours par un accès direct à ceux qui les utilisent, les malades. En matière de santé, les intermédiaires que nous sommes, médecins prescripteurs, sont les seuls évaluateurs des résultats. Erreur partielle de cible, car, si nous savons analyser l'action et les éventuelles complications d'un produit, nous ne pouvons en déterminer l'effet profond, sauf à devenir malade nous-mêmes. Deuxièmement, la montée en puissance du malade, acteur de sa souffrance et non plus patient ignare, sans voix ni jugement. Son immixtion dans la sphère de la décision thérapeutique devient incontournable dans les maladies chroniques, où il acquiert une connaissance fine de ce qui lui arrive, des risques encourus et des modifications à adopter pour y parer. Il sait parfois mieux que le médecin comment gérer personnellement son traitement ! Refuser cette collaboration entre industrie et patients serait une erreur magistrale en ce qu'elle perpétue un ordre sanitaire fondé sur l'ignorance de celui qui subit les traitements au bénéfice exclusif du professionnel « sachant » qui les prescrit.

Se dessine donc un nouveau rôle pour les industriels de la santé : celui de conseil en éducation et observance thérapeutique auprès des malades, nouveaux lanceurs d'alertes visant à informer directement les fabricants. La puissance des systèmes informatiques devrait grandement aider à cette collection inestimable de données transmises en temps réel. J'entends d'ici les cris d'orfraie des amateurs de la pureté divine et les tenants de la séparation des intérêts. Revendiquons au contraire haut et fort ces liens entre les deux parties : intérêt du malade à guérir, intérêt de l'industriel à produire un médicament à l'effet primaire puissant et aux effets nocifs minimes. Sortons de ce débat stérile, englués que nous sommes dans une sémantique moralisatrice perverse. De la notion de lien, on est passé sciemment à celle de « conflit d'intérêts », ruinant tout effort de travail partagé. Il existe, bien sûr, des comportements déviants et des pratiques malhonnêtes qui méritent sanction, mais regardons d'abord le bénéfice thérapeutique apporté aux malades, qui, lui, dépasse et de loin les conséquences nocives de ces attitudes scandaleuses.

via pharmanetwork.info

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Autisme : mieux connaître le syndrome d'Asperger

Le syndrome d'Asperger est une forme d'autisme qui concerne des enfants d'intelligence normale. Il fait l'objet de l'attention croissante des chercheurs et des éducateurs.

« Je n'aime pas les étrangers, parce que je n'aime pas les gens que je n'ai jamais vus. J'ai du mal à les comprendre (...). Quand il y a un nouveau membre du personnel à l'école (...) je l'observe jusqu'à ce que je sois sûr qu'il n'est pas dangereux. Puis (...) je lui demande ce qu'il sait des missions spatiales Apollo, je lui fais dessiner le plan de sa maison, et comme ça, je le connais. Alors ça m'est égal d'être dans la même pièce que lui (1). » Christopher, 15 ans, protagoniste d'un roman de Mark Haddon, est atteint du syndrome d'Asperger.

Décrit par Hans Asperger en 1944, ce syndrome est une forme d'autisme, touchant des sujets d'intelligence normale. La description de l'autisme avait été donnée un an plus tôt par Leo Kanner mais le travail d'Asperger, lui, est resté ignoré jusqu'en 1983.

Depuis 1980, le syndrome d'Asperger est, avec l'autisme, classé parmi les « troubles envahissants du développement » (TED) dans les classifications des troubles psychiques, à savoir le DSM-IV américain et le CIM 10 de l'Organisation mondiale de la santé. La recherche s'emploie aujourd'hui à recenser les différences entre les cerveaux d'autistes et les autres, sur les plans anatomique, biochimique, génétique. Grâce à l'imagerie par résonance magnétique fonctionnelle (IRMf), on peut observer le cerveau au travail - et l'on constate que les zones cérébrales activées, lors de tâches de reconnaissance des visages ou des voix par exemple, ne sont pas les mêmes chez les autistes que chez les sujets normaux. Il semble donc probable que des différences dans le traitement de l'information par le cerveau des autistes expliquent les anomalies de leur comportement.

Un comportement différent

Bébé, déjà, l'enfant ne recherche pas le regard de sa mère ; il ne cherche pas à diriger son attention vers un objet qui l'intéresse (ce qu'on appelle l'« attention conjointe »). L'enfant atteint du syndrome d'Asperger apprend à parler. Cependant, comme tous les autistes, il est fermé au langage non verbal : il ne comprend pas l'expression des émotions chez les autres, il rit à contretemps... Dans le domaine verbal, son utilisation du langage est anormale : il emploie de grands mots sortis d'un dictionnaire, il ne sait pas quand ni comment s'introduire dans une conversation - et peut s'attirer ainsi des moqueries.

Plus largement, le comportement social pose problème. L'enfant « Asperger » n'apprend pas d'instinct, ni par imitation, les règles du jeu social ; il n'arrive pas à voir les situations du point de vue de l'autre (2). Il dit « vous avez un gros nez », et ne comprend pas pourquoi l'autre est blessé ; il parle pendant des heures d'un sujet qui le passionne, comme les horaires des trains, sans voir que les autres ne s'y intéressent pas.

Autres traits caractéristiques de ces sujets : un attachement à leurs habitudes, et à des règles qu'ils se donnent ; une hypersensibilité au bruit, au toucher ; et un profil d'intelligence en dents de scie, avec des pics de compétence - l'intelligence visio-spatiale, la mémoire, le calcul mental... - et des déficiences, dans la compréhension du langage, dans les problèmes complexes. Nombreux aussi sont ceux qui pensent en images plutôt qu'en mots.

Ces enfants sont donc différents. Mais si ces différences posent des problèmes à leur entourage, elles ne sont pas toutes négatives, loin de là. Ils sont, par exemple, incapables de mentir et ils se montrent soucieux des règles ; leur mémoire, leur bonne vision des détails, leurs « pics de compétences » parfois spectaculaires, leur pensée en images constituent une « autre intelligence », dont notre société pourrait s'enrichir, selon certains auteurs, si elle savait s'adapter à eux, tout en leur offrant les moyens de s'adapter à elle (3).

Ces moyens existent : aider à identifier l'expression des émotions, apprentissage de « scénarios sociaux » qui expliquent les comportements normaux en classe, en récréation, au restaurant, etc. (4). Dans certaines écoles, l'intervention de spécialistes de l'autisme pour apprendre aux enseignants à recourir plus largement au mode visuel, pour expliquer aux élèves ce que ressent leur camarade... permet une intégration des enfants atteints d'un syndrome d'Asperger. Ces écoles sont encore rares - mais le « plan autisme », annoncé en novembre dernier, prévoit la création, d'ici 2006, de centres de ressources autisme (CRA) dans toutes les régions françaises. Par ailleurs, une association de jeunes autistes a créé son propre site Internet (www.satedi.org).

L'intelligence des enfants « Asperger » leur permet donc d'utiliser de l'aide pour progresser ou s'entraider. On citera par exemple le témoignage de cette autiste américaine Temple Grandin qui, devenue adulte, a raconté son expérience (5). Grâce à un de ses professeurs, dont elle dit : « Il n'a pas essayé de m'attirer vers son monde mais il est entré, au contraire, dans le mien », elle est devenue experte internationale en équipements pour animaux d'élevage. « J'ai appris, dit-elle, - par coeur - comment il fallait se comporter dans des circonstances données. » Par exemple, elle a appris à parler en public en regardant des cassettes vidéo.

Les 13 et 14 mai 2005, un colloque sur le syndrome d'Asperger, sous la direction de Tony Attwood (6) et Peter Vermeulen, offrira une occasion de s'informer sur ce syndrome.

via scienceshumaines.com

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Evidence-based guideline update: Pharmacologic treatment for episodic migraine prevention in adults

1. S.D. Silberstein, MD, FACP,
2. S. Holland, PhD,
3. F. Freitag, DO,
4. D.W. Dodick, MD,
5. C. Argoff, MD and
6. E. Ashman, MD

+ Author Affiliations

1. From Thomas Jefferson University (S.D.S.), Jefferson Headache Center, Philadelphia, PA; the Armstrong Atlantic State University (S.H.), Savannah, GA; Comprehensive Headache Center (F.F.), Baylor University Headache Medicine Center, Dallas, TX; Mayo Clinic (D.D.), Scottsdale, AZ; New York University School of Medicine (C.A.), Albany; and Elmendorf Air Force Base (E.A.), AK.

1. Correspondence & reprint requests to American Academy of Neurology: guidelines@aan.com

+ Author Disclosures: S.D. Silberstein

Scientific Advisory Boards:

1. Allergan; Amgen; Capnia; Coherex; GlaxoSmithKline; Iroko Pharmaceuticals; Lilly; MAP; Medtronic; Merck; Neuralieve; NINDS; NuPathe; Pfizer; St. Jude Medical

Gifts:

1. NONE

Funding for Travel or Speaker Honoraria:

1. NONE

Editorial Boards:

1. Cephalalgia; Current Pain and Headache Reports

Patents:

1. NONE

Publishing Royalties:

1. NONE

Employment, Commercial Entity:

1. NONE

Consultancies:

1. Amgen; Nautilus; Novartis; Opti-Nose; Zogenix Speakers’ Bureaus:; Allergan; Endo Pharmaceuticals; GlaxoSmithKline; Zogenix; Merck

Speakers’ Bureaus:

1. NONE

Other Activities:

1. NONE

Clinical Procedures or Imaging Studies:

1. NONE

Research Support, Commercial Entities:

1. GlaxoSmithKline; Allergan; Merck; Novartis; NIH; Neurolieve; MAP; Endo

Research Support, Government Entities:

1. NIH

Research Support, Academic Entities:

1. NONE

Research Support, Foundations and Societies:

1. AHS; IHS

Stock/Stock Options/Board of Directors Compensation:

1. NONE

License Fee Payments, Technology or Inventions:

1. NONE

Royalty Payments, Technology or Inventions:

1. NONE

Stock/Stock Options, Research Sponsor:

1. NONE

Stock/Stock Options, Medical Equipment & Materials:

1. NONE

Legal Proceedings:

1. NONE

+ Author Disclosures: F. Freitag

Scientific Advisory Boards:

1. Zogenix pharmaceuticals; Allergan pharmaceuticals; Nautilus

Gifts:

1. NONE

Funding for Travel or Speaker Honoraria:

1. GlaxoSmithKline; Zogenix; Merck; Nautilus

Editorial Boards:

1. NONE

Patents:

1. NONE

Publishing Royalties:

1. NONE

Employment, Commercial Entity:

1. Baylor University Medical Center Speakers’ Bureaus:; GlaxoSmithKline; Zogenix; Merck

Consultancies:

1. NONE

Speakers’ Bureaus:

1. NONE

Other Activities:

1. Vice President, Board of Directors, National Headache Foundation

Clinical Procedures or Imaging Studies:

1. NONE

Research Support, Commercial Entities:

1. NONE

Research Support, Government Entities:

1. NONE

Research Support, Academic Entities:

1. NONE

Research Support, Foundations and Societies:

1. NONE

Stock/Stock Options/Board of Directors Compensation:

1. NONE

License Fee Payments, Technology or Inventions:

1. NONE

Royalty Payments, Technology or Inventions:

1. NONE

Stock/Stock Options, Research Sponsor:

1. NONE

Stock/Stock Options, Medical Equipment & Materials:

1. NONE

Legal Proceedings:

1. NONE

+ Author Disclosures: D.W. Dodick

Scientific Advisory Boards:

1. Within the past 3 years, serves or has served on advisory boards and has consulted for; Allergan; Pfizer; Merck; Coherex; Ferring; Neurocore; Neuralieve; Neuraxon; NuPathe Inc.; MAP; SmithKlineBeecham; Boston Scientific; Medtronic, Inc.; Nautilus; Eli Lilly and Company; Novartis; Colucid; GlaxoSmithKline; Autonomic Technologies; MAP Pharmaceuticals, Inc.; Zogenix, Inc.; Impax Laboratories, Inc.; Bristol Myers Squibb; Nevro Corp.; Atlas; Arteaus; Alder Pharmaceuticals

Gifts:

1. NONE

Funding for Travel or Speaker Honoraria:

1. Cognimed; Miller Medical; Annenberg Center for Health Sciences; Intramed; Scientiae

Editorial Boards:

1. Within the past 2 years, has received funding editorial activities, from the following:; SAGE Publishing; Lippincott Williams and Wilkins; Oxford University Press; Cambridge University Press. Serves as Editor- in-Chief and on the editorial boards of The Neurologist, Lancet Neurology, and Postgraduate Medicine; and has served as Editor-in-Chief of Headache Currents and as an Associate Editor of Headache

Patents:

1. NONE

Publishing Royalties:

1. Wolff’s Headache 8th edition, Oxford University Press, 2009; Handbook of Headache, Cambridge Univeristy Press, 2010

Employment, Commercial Entity:

1. NONE

Consultancies:

1. Allergan; Pfizer; Merck; Coherex; Ferring; Neurocore; Neuralieve; Neuraxon; NuPathe Inc.; MAP; SmithKlineBeecham; Boston Scientific; Medtronic, Inc.; Nautilus; Eli Lilly and Company; Novartis; Colucid; GlaxoSmithKline; Autonomic Technologies; MAP Pharmaceuticals, Inc.; Zogenix, Inc.; Impax Laboratories, Inc.; Bristol Myers Squibb

Speakers’ Bureaus:

1. NONE

Other Activities:

1. NONE

Clinical Procedures or Imaging Studies:

1. NONE

Research Support, Commercial Entities:

1. Boston Scientific; Medtronic; Advanced Neurostimulation Systems; St Jude; Mayo Clinic

Research Support, Government Entities:

1. NINDS-CRC, Co-PI, CMTT Trial

Research Support, Academic Entities:

1. NONE

Research Support, Foundations and Societies:

1. NONE

Stock/Stock Options/Board of Directors Compensation:

1. NONE

License Fee Payments, Technology or Inventions:

1. NONE

Royalty Payments, Technology or Inventions:

1. NONE

Stock/Stock Options, Research Sponsor:

1. NONE

Stock/Stock Options, Medical Equipment & Materials:

1. NONE

Legal Proceedings:

1. NONE

+ Author Disclosures: C. Argoff

Scientific Advisory Boards:

1. Department of Defense Grant Review 2011; DSMB for NIH study (PI: Know Todd, M.D.)

Gifts:

1. NONE

Funding for Travel or Speaker Honoraria:

1. Pfizer (King), speaker honoraria and related travel; Janssen (Pricara), speaker honoraria and related travel; Neurogesx, speaker honoraria and related travel; Forest Laboratories, speaker honoraria and related travel; Eli Lilly, speaker honoraria and related travel; Covidien, speaker honoraria and related travel; Endo Pharmaceuticals, speaker honoraria and related travel

Editorial Boards:

1. Pain Medicine, Neuropathic Pain Section Co-Editor, approximately 3 years; Clinical Journal of Pain, Editorial Board Member, over 5 years; Practical Neurology, Section Editor (Pain), approximately 5 years

Patents:

1. NONE

Publishing Royalties:

1. Pain Management Secrets 3rd edition, Elsevier, 2009; Raj’s Practical Management of Pain, 4th edition, Mosby Elsevier, 2008; Defeat Chronic Pain Now, Fairwinds Press, 2010

Employment, Commercial Entity:

1. NONE

Consultancies:

1. Forest Laboratories; Millenium Laboratories; Pfizer, Inc. (KING); Janssen (Pricara); Bristol Meyer Squibb; GlaxoSmithKline; Depomed; Abbott Labs; Endo Pharmaceuticals; Covidien; Nuvo Research; Gruenthal; Eli Lilly; Jazz Pharmaceuticals; Neurogesx; Sanofi Aventis Speakers’ Bureaus:; Pfizer (King); Endo Pharmaceuticals; Eli Lilly; Forest Laboratories; Millenium Laboratories; Covidien; Janssen (Pricara); Neurogesx

Speakers’ Bureaus:

1. NONE

Other Activities:

1. NONE

Clinical Procedures or Imaging Studies:

1. NONE

Research Support, Commercial Entities:

1. Investigaor Initiated Grant (Painful Diabetic Neuropathy): Endo Pharmaceuticals; Investigator Initiated Grant(Fibromyalgia): Forest Laboratories 3. Investigator Initiated Grant(Fibromyalgia): Eli Lilly 4. Phase III clinical trial (Post Herpetic Neuralgia): Neurogesx 5. Phase III clinical trial (Fibromyalgia); Pfizer

Research Support, Government Entities:

1. Co-PI NIH Funded Study (SBRT) re: Post Herpetic Neuralgia

Research Support, Academic Entities:

1. NONE

Research Support, Foundations and Societies:

1. NONE

Stock/Stock Options/Board of Directors Compensation:

1. NONE

License Fee Payments, Technology or Inventions:

1. NONE

Royalty Payments, Technology or Inventions:

1. NONE

Stock/Stock Options, Research Sponsor:

1. Pfizer Inc., at least 5 years

Stock/Stock Options, Medical Equipment & Materials:

1. NONE

Legal Proceedings:

1. NONE

+ Author Disclosures: E. Ashman

Scientific Advisory Boards:

1. NONE

Gifts:

1. NONE

Funding for Travel or Speaker Honoraria:

1. NONE

Editorial Boards:

1. Neurology, Associate Editor, Level of Evidence

Patents:

1. NONE

Publishing Royalties:

1. NONE

Employment, Commercial Entity:

1. NONE

Consultancies:

1. NONE

Speakers’ Bureaus:

1. NONE

Other Activities:

1. Member of Guideline Development Subcommittee of the AAN

Clinical Procedures or Imaging Studies:

1. NONE

Research Support, Commercial Entities:

1. NONE

Research Support, Government Entities:

1. NONE

Research Support, Academic Entities:

1. NONE

Research Support, Foundations and Societies:

1. NONE

Stock/Stock Options/Board of Directors Compensation:

1. NONE

License Fee Payments, Technology or Inventions:

1. NONE

Royalty Payments, Technology or Inventions:

1. NONE

Stock/Stock Options, Research Sponsor:

1. NONE

Stock/Stock Options, Medical Equipment & Materials:

1. NONE

Legal Proceedings:

1. NONE

View Complete Disclosures

Next Section

Abstract

Objective: 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?

Methods: 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.

Results and Recommendations: 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).

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GLOSSARY

AAN=

American Academy of Neurology;

AE=

adverse event;

CI=

confidence interval;

ER=

extended-release;

MAM=

menstrually associated migraine;

PMP=

perimenstrual period;

RCT=

randomized controlled trial

Epidemiologic studies suggest approximately 38% of migraineurs need preventive therapy, but only 3%–13% currently use it.¹ In 2000, the American Academy of Neurology (AAN) published guidelines for migraine prevention.^2,3 Since then, new clinical studies have been published on the efficacy and safety of migraine preventive therapies. This guideline seeks to assess this new evidence to answer the following clinical question: For patients with migraine, which pharmacologic therapies are proven effective for prevention, as measured by reduced migraine attack frequency, reduced number of migraine days, or reduced attack severity? This article addresses the safety and efficacy of pharmacologic therapies for migraine prevention.

Separate guidelines are available for botulinum toxin.⁴ The 2008 guideline included a Level B recommendation that botulinum toxin was probably ineffective for treatment of episodic migraine. A new guideline is in development. An updated guideline on nonsteroidal anti-inflammatory drugs⁵ and complementary alternative treatments has been approved for publication as a companion to this guideline.⁵

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DESCRIPTION OF THE ANALYTIC PROCESS

The AAN and the American Headache Society participated in the development process. An author panel of headache and methodologic experts was assembled to review the evidence. Computerized searches of the MEDLINE, PsycINFO, and CINAHL databases identified new studies (published in English). The search strategy used the MeSH term “headache” (exploded) and a published search strategy for identifying randomized controlled trials (RCTs) published between June 1999 and May 2007. Additional MEDLINE searches revealed studies published through May 2009, which were reviewed and included as supplemental articles.

Studies of pharmacologic agents available in the United States were included in the analysis if they randomized adult patients with migraine to the agent under study or a comparator drug (including placebo) and utilized masked outcome assessment. At least 2 panelists independently reviewed each study and rated it according to the AAN therapeutic classification of evidence scheme (appendix e-3 on the Neurology® Web site at www.neurology.org). Differences in ratings were resolved by author panel discussion.

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ANALYSIS OF EVIDENCE

The original search identified 179 articles. A supplemental search (2007–2009) yielded 105 additional articles. Of the total 284 articles, 29 were classified as Class I or Class II and are reviewed herein. Studies were excluded if they:

• Assessed the efficacy of therapeutic agents for headache other than episodic migraine in adults

• Assessed acute migraine treatment, migraine aura treatment/prevention, or nonpharmacologic treatments (e.g., behavioral approaches)

• Used quality of life measures, disability assessment, or nonstandardized outcomes as primary efficacy endpoints

• Tested the efficacy of drugs not available in the United States

Since the 2000 guideline publication, the AAN revised its evidence classification criteria to include study completion rates. Studies with completion rates below 80% were downgraded; several studies in the original guideline have thus been downgraded.

We found no new Class I or II studies published for acebutolol, atenolol, bisoprolol, carbamazepine, clonazepam, clonidine, clomipramine, fluvoxamine, guanfacine, nabumetone, nadolol, nicardipine, nifedipine, or protriptyline. Recommendations for these agents are based on the evidence reviewed in the original guideline (see table 1). Currently, no Class I or Class II studies exist for anticoagulants (limited Class III and IV studies were identified; table 1 includes anticoagulants).

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Table 1

Classification of migraine preventive therapies (available in the United States)

Angiotensin receptor blockers and angiotensin-converting-enzyme inhibitors.

In the 2000 guideline, there were no studies testing the efficacy of angiotensin receptor blockers or angiotensin-converting-enzyme (ACE) inhibitors for migraine prevention. Since that publication, 3 reports have been published.

Candesartan.

In a Class II crossover study (12-week treatment separated by 4-week washout), the mean number of headache days was 18.5 with placebo (26.3% reduction from baseline) vs 13.6 with candesartan (45.6% reduction from baseline; p = 0.001).⁶ Selected secondary endpoints also favored candesartan: headache hours (139 vs 95; p < 0.001), migraine days (12.6 vs 9.0; p < 0.001), migraine hours (92.2 vs 59.4; p < 0.001), and headache severity index (293 vs 191; p < 0.001). No serious adverse events (AEs) occurred. The most common AEs were dizziness (31%), “symptoms of the musculoskeletal system” (21%), and fatigue (14%); none occurred significantly more often than with placebo.

Lisinopril.

One Class II study reported significant reduction in all 3 primary endpoints with lisinopril vs placebo (headache hours: 129 vs 162 [mean change in hours 20, confidence interval (CI) 5–36]; headache days: 19.7 vs 23.7 [20, CI 5–30]; migraine days: 14.5 vs 18.5 [21, CI 9–34]).⁷ AEs included cough (26%; 10% discontinued treatment due to cough), dizziness (23%), and “tendency to faint” (10%). No serious AEs were reported.

Telmisartan.

In a single Class II placebo-controlled trial, telmisartan 80 mg did not show a significant difference from placebo for reduction in migraine days (−1.65 vs −1.14).⁸

Conclusions.

Lisinopril and candesartan are possibly effective for migraine prevention (1 Class II study each). Telmisartan is possibly ineffective for reducing the number of migraine days (1 negative Class II study).

Antiepileptic drugs.

Divalproex.

The original guideline found strong, consistent support (5 studies) for the efficacy of divalproex sodium and its corresponding compound, sodium valproate, for migraine prevention.

Since the 2000 publication, 1 double-blind, randomized, Class I placebo-controlled 12-week trial showed extended-release (ER) divalproex sodium 500–1,000 mg/day had a mean reduction in 4-week migraine headache rate from 4.4/week (baseline) to 3.2/week (−1.2 attacks/week) in the ER divalproex sodium group and from 4.2/week to 3.6/week (−0.6 attacks/week) in the placebo group (CI 0.2–1.2; p = 0.006).⁹ No significant differences were detected between groups in the number of treatment-emergent AEs.

Clinical context.

In most headache trials, patients taking divalproex sodium or sodium valproate reported no more AEs than those on placebo. However, weight gain has been clinically observed with divalproex sodium long-term use.^9,10 Treatment with these agents requires careful follow-up and testing because of pancreatitis, liver failure, and teratogenicity risks.¹¹

Gabapentin.

Since the 2000 publication, a Class III study¹² reported that a stable gabapentin dose (4-week titration phase to 2,400 mg/day; 8-week maintenance phase) significantly reduced the median monthly migraine rate vs placebo on the basis of a modified intention-to-treat analysis.

Lamotrigine.

The original guideline reported a single Class I lamotrigine study¹³ that failed to show a significant effect for migraine prevention. A second, new Class I study comparing lamotrigine 50 mg/day with placebo or topiramate 50 mg/day reported lamotrigine was not more effective than placebo (for both primary endpoints) and was less effective than topiramate in reducing migraine frequency and intensity.¹⁴ The primary outcome measure (responder rate: ≥50% monthly migraine frequency reduction) was 46% for lamotrigine vs 34% for placebo (p = 0.093, CI 0.02–0.26) and 63% for topiramate vs 46% for lamotrigine (p = 0.019, CI 0.03–0.31). Treatment-related AEs (rash, giddiness, sleepiness, and gastrointestinal intolerance) occurred in 10% of patients on lamotrigine.

Oxcarbazepine.

One Class II trial evaluated the efficacy of oxcarbazepine (1,200 mg/day) vs placebo.¹⁵ There was no difference between oxcarbazepine (−1.30 [SE 0.282]) and placebo for mean change in number of migraine attacks from baseline during the last 28 days of the double-blind 15-week treatment phase (−1.74 [SE 0.283]; p = 0.2274).

Topiramate.

Four Class I studies^14,16,–,18 and 7 Class II studies^19,–,25 report topiramate (50–200 mg/day) is effective in migraine prevention.

In a Class I placebo-controlled study (mean topiramate dose 125 mg/day [range 25–200 mg/day]), patients given topiramate experienced a significantly lower 28-day migraine frequency vs with placebo (3.31 ± 1.7 vs 3.83 ± 2.1; p = 0.002).¹⁸ In a second placebo-controlled Class I double-crossover study (reviewed above), topiramate was more effective than placebo and lamotrigine for primary efficacy measures.¹⁴ In the topiramate groups, 15% of patients experienced AEs, most commonly paresthesias, sleepiness, and gastrointestinal intolerance. The placebo group reported gastrointestinal intolerance (3%) and anorexia (3%).

Two additional Class I studies report topiramate is as effective as propranolol¹⁶ or sodium valproate,¹⁷ drugs previously established as effective for migraine prevention. In the first study, subjects given topiramate 50 mg/day had reduced mean migraine frequency (episodes/month) from baseline (6.07 ± 1.89 to 1.83 ± 1.39; p < 0.001) at 8 weeks, decreased headache intensity VAS score from 7.1 ± 1.45 to 3.67 ± 2.1 (p < 0.001), and decreased headache duration from 16.37 ± 7.26 hours to 6.23 ± 5.22 hours (p < 0.001).¹⁶ Subjects given topiramate reported paresthesias (23%), weight loss (16%), and somnolence (13%). In patients treated with propranolol 80 mg/day, mean headache frequency (episodes/month) decreased from 5.83 ± 1.98 to 2.2 ± 1.67 (p < 0.001) at 8 weeks, headache intensity VAS score decreased from 6.43 ± 1.6 to 4.13 ± 1.94 (p < 0.001), and headache duration decreased from 15.10 ± 6.84 hours to 7.27 ± 6.46 hours (p < 0.001). Although monthly headache frequency, intensity, and duration decreased in both groups, the topiramate group reported significantly greater mean reduction (topiramate frequency decrease 4.23 ± 1.2 vs propranolol 3.63 ± 0.96 [p = 0.036; CI 0.39–1.16]; topiramate intensity decrease 3.43 ± 1.38 vs propranolol 2.3 ± 1.2 [p = 0.001; CI 0.46–1.8]; topiramate duration decrease 10.1 ± 4.3 vs propranolol 7.83 ± 4.5 [p = 0.048; CI 0.17–4.6]).

In a crossover Class I trial (2-month washout between therapies) comparing topiramate 50 mg/day with sodium valproate 400 mg/day, both groups showed improvement from baseline in headache frequency, intensity, and duration.¹⁷ Average monthly migraine frequency decreased by 1.8 times with sodium valproate (baseline 5.4 ± 2.5; posttreatment 3.6 ± 2.1; CI 1.0–2.6; p < 0.001), as compared with a 3-time reduction with topiramate (baseline 5.4 ± 2.0; posttreatment 2.4 ± 2.4; CI 2.1–3.9; p < 0.001). Headache intensity decreased by 3.7 with sodium valproate (baseline 7.7 ± 1.2; treatment 4.0 ± 2.1; CI 2.9–4.6; p < 0.001), as compared with a reduction of 3.6 with topiramate (baseline 6.9 ± 1.2, treatment phase 3.3 ± 1.5; CI 2.9–4.3; p < 0.001). The average headache episode duration decreased by 13.4 hours from baseline with sodium valproate (baseline 21.3 ± 14.6; treatment 7.9 ± 7.7; CI 7.5–19.3; p < 0.001) as compared with an 11.9-hour reduction with topiramate (baseline 17.3 ± 8.4; treatment 5.4 ± 6.4; CI 8.2–15.6; p < 0.001). The overall analysis of repeated-measures analysis of variance demonstrated no differences in monthly headache frequency, intensity, or duration after the first or second treatment rounds. Topiramate AEs were weight loss (18.8%), paresthesias (9.4%), or both (25%). Sodium valproate AEs were weight gain (34.5%), hair loss (3.1%), and somnolence (3.1%).

Results of 5 Class II studies support those of the Class I studies showing topiramate as effective for migraine prevention.^19,–,25 Four studies demonstrated significant improvement over placebo^19,20,23,24; one included an active comparator arm, suggesting equivalence of topiramate (100, 200 mg/day) and propranolol (160 mg/day).²⁰ Two studies comparing topiramate and amitriptyline (25–150 mg/day) reported no difference in efficacy for primary endpoints; however, amitriptyline was associated with a significant AE increase, and the amitriptyline-topiramate combination suggested improvement in depression scores vs monotherapy.^21,22 In one of these studies,²¹ the most common AEs were similar to those previously reported. One Class II placebo-controlled 24-week pilot study failed to show a difference in efficacy between topiramate 200 mg and placebo.²⁶

Conclusions.

Divalproex sodium and sodium valproate are established as effective in migraine prevention (multiple Class I studies). Data are insufficient to determine the effectiveness of gabapentin (1 Class III study). Lamotrigine is established as ineffective for migraine prevention (2 Class I studies). Oxcarbazepine is possibly ineffective for migraine prevention (1 Class II study). Topiramate is established as effective for migraine prevention (4 Class I studies, multiple Class II studies; 1 negative Class II study). Topiramate is probably as effective for migraine prevention as propranolol (1 Class I study), sodium valproate (1 Class I study), and amitriptyline (2 Class II studies).

Antidepressants.

Fluoxetine.

In the original guideline, 1 Class II study²⁷ showed fluoxetine (racemic) was significantly better than placebo for migraine prevention, but the results were not duplicated in a second study.²⁸

Since the original guideline, a Class II study has shown fluoxetine 20 mg/day was more effective than placebo in reducing total pain index scores (calculated as [Dl × 1] + [D2 × 2] + [D3 × 3], where D1, D2, and D3 represent headache hours calculated in a month, with pain intensity shown by 1, 2, 3) at 6 months.²⁹ After the 6 months, pain index scores for the fluoxetine group decreased from 135 (baseline) to 41.3 (SD ± 63.8; p = 0.001). The placebo group pain index was 98 at baseline and 61.1 at 6 months (SD ± 57.7; p = 0.07); however, differences were noted between treatment groups for baseline measures.

Venlafaxine.

In a Class I study, venlafaxine XR 150 mg significantly reduced the number of headache days (median reduction in days: venlafaxine 150 mg −4 days; venlafaxine 75 mg −2 days; placebo −1 day; Kruskal-Wallis = 10.306, df = 2; p < 0.006).³⁰ All 3 groups showed decreased headache severity and duration from baseline; no differences were observed between treatment groups for these endpoints. The most common AEs were nausea (41%), vomiting (27%), and drowsiness (27%). Fourteen percent of patients receiving venlafaxine withdrew because of AEs.

A Class II trial assessed the efficacy of venlafaxine vs amitriptyline; both were effective in reducing attack frequency (venlafaxine: baseline = 4.15 [SD ± 2.24] vs 12 weeks = 1.77 [SD ± 1.39; p < 0.001]; amitriptyline: baseline = 3.27 [SD ± 1.61] vs 12 weeks 1.54 [SD ± 1.54; p < 0.001]).³¹ Patients taking venlafaxine experienced nausea/vomiting (23%) and tachycardia (15%); 1 patient withdrew because of AEs. Patients taking amitriptyline reported hypersomnolence (80%), dry mouth (69%), and concentration difficulties (54%).

Tricyclic antidepressants.

The original guideline concluded amitriptyline was established as effective for migraine prevention; that evidence has since been downgraded to Class II (all 3 studies had >20% dropout rates). Comparative studies of amitriptyline with topiramate^21,22 and venlafaxine³¹ (reviewed above) report similar efficacy at the doses tested.

Conclusions.

There is conflicting Class II evidence for use of fluoxetine. Venlafaxine is probably effective for migraine prevention (1 Class I study) and is possibly as effective as amitriptyline in migraine prevention (1 Class II study). Amitriptyline is probably effective for migraine prevention (multiple Class II studies); it is probably as effective as topiramate (2 Class II studies) and possibly as effective as venlafaxine (1 Class II study) for migraine prevention.

β-Blockers.

Metoprolol.

The original guideline concluded metoprolol was probably effective in migraine prevention. We reclassified these studies as Class I using the revised AAN criteria.

One new Class II study reported metoprolol (200 mg/day) was more effective than aspirin (300 mg/day) in achieving 50% migraine frequency reduction (responder rate metoprolol = 45.2%; aspirin = 29.6%; mean difference 15.65; CI 4.43–26.88).³² Attack frequencies (attacks/month) at placebo run-in and week 20 are 3.36 to 2.37, respectively, for aspirin and 3.55 to 1.82, respectively, for metoprolol. No significant AEs were reported.

A small Class II study reported metoprolol (47.5–142.5 mg/day) had similar efficacy to nebivolol 5 mg/day for migraine prevention (assessed by a decrease in mean migraine attacks).³³

Propranolol.

The original guideline concluded propranolol was established as effective for migraine prevention.

In a Class II study, propranolol (80 mg/day) was more effective than placebo and as effective as cyproheptadine (4 mg/day) in reducing migraine frequency, duration, and attack severity.³⁴ The difference in attack frequency reduction was significant between treatments: propranolol −2.85 ± 0.2 (SEM) vs cyproheptadine −3.09 ± 0.31 vs combination 3.12 ± 0.1 vs placebo −1.77 ± 0.44 (all p < 0.05 vs placebo). For attack frequency reduction, combination therapy was more effective than monotherapy (p < 0.05). AEs were drowsiness, sleep disturbance, weight gain, fatigue, and dry mouth; percentages of patients affected were not reported.

Conclusions.

Metoprolol is established as effective for migraine prevention (2 Class I studies) and is possibly as effective as nebivolol or aspirin for migraine prevention (1 Class II study each). Propranolol is established as effective for migraine prevention (multiple Class I studies) and is possibly as effective as cyproheptadine for migraine prevention (1 Class II study).

Calcium-channel blockers.

The original guideline concluded that verapamil and nimodipine were probably effective for migraine prevention. The original studies on verapamil and nimodipine were found to have conflicting Class III evidence on the basis of current classification criteria and were downgraded accordingly, yielding Level U recommendations.

Conclusions.

Data from older studies regarding verapamil and nimodipine are insufficient when current AAN classification criteria are applied.

Direct vascular smooth muscle relaxants.

The original guideline concluded cyclandelate was probably effective for migraine prevention.

Cyclandelate.

Two new Class II studies reported conflicting results. The first study showed cyclandelate to be no more effective than placebo in reducing migraine days, attacks, or duration.³⁵ The second study (smaller, underpowered; n = 25) found cyclandelate significantly reduced the number of migraine days and duration (assessed using a contingent negative variation measure).³⁶

Conclusions.

The efficacy of cyclandelate is unknown (conflicting Class II studies).

Triptans.

Since the original guideline, new Class I studies have assessed the efficacy of frovatriptan,^37,38 naratriptan,³⁹ and zolmitriptan⁴⁰ for short-term prevention of menstrually associated migraine (MAM).

Frovatriptan.

Frovatriptan 2.5 mg BID/qd was more effective than placebo in reducing migraine frequency.³⁷ The mean number of headache-free perimenstrual periods (PMPs) per patient (primary endpoint) was higher in the 2 frovatriptan groups (2.5 mg qd = 0.69 [SD ± 0.92; CI 1.14–2.73; p = 0.0091] vs 2.5 mg BID = 0.92 [SD 1.03; CI 1.84–4.28; p < 0.0001] vs placebo = 0.42 [SD ± 0.78]), representing 64% (2.5 mg/day) and 119% (5 mg/day) increases in the mean number of headache-free PMPs per patient over placebo. A second Class I study³⁸ also reports the MAM headache incidence during the 6-day PMP was 67% for placebo, 52% for frovatriptan 2.5 mg QD (p < 0.0001 vs placebo), and 41% for frovatriptan 2.5 mg BID (p < 0.0001 vs placebo; p < 0.0001 vs QD regimen). The AE incidence and type for both regimens were similar to those for placebo. The overall AE incidence for frovatriptan was 4.1% (2.5 mg BID) and 2.7% (2.5 mg qd) higher than during placebo treatment.

Naratriptan.

In a Class I study, 1 mg BID (given for 5 days, starting 2 days before menses onset) reduced the number of perimenstrual migraine attacks and migraine days.³⁹ Patients treated with naratriptan 1 mg experienced more headache-free PMPs than those on placebo (50% vs 25%, p = 0.003). Naratriptan 1 mg reduced the number of MAMs (2.0 vs 4.0, p < 0.05) and MAM days (4.2 vs 7.0, p < 0.01) vs placebo. The AE incidence and severity were similar to those of placebo; <10% of patients experienced dizziness, chest pain, or malaise.

Zolmitriptan.

One Class I study reported the efficacy of zolmitriptan 2.5 BID/TID vs placebo. Both zolmitriptan regimens demonstrated superior efficacy vs placebo: the proportion of patients with a ≥50% MAM attack frequency reduction (zolmitriptan 2.5 mg TID [58.6%], p = 0.0007 vs placebo; zolmitriptan 2.5 mg BID [54.7%], p = 0.002 vs placebo; placebo 37.8%).⁴⁰ AEs were considered possibly treatment-related in 28 patients (33.3%) in the zolmitriptan 2.5 mg TID group, 29 (36.3%) in the zolmitriptan 2.5 mg BID group, and 18 (22.0%) in the placebo group. The most common AEs were asthenia, headache, dizziness, and nausea.

Conclusions.

Frovatriptan is established as effective for the short-term prevention of MAMs (2 Class I studies). Zolmitriptan and naratriptan are probably effective for the short-term prevention of MAMs (1 Class I study each). The utility of these agents in receiving a separate indication for pure menstrual migraine is currently being deliberated by US regulatory authorities.

Other agents.

Since the original guideline, additional studies have been identified that assess the efficacy of a carbonic anhydrase inhibitor and a neurokinin inhibitor for migraine prevention.

Carbonic anhydrase inhibitor.

In a single Class II study, acetazolamide 250 mg BID was no more effective than placebo in reducing migraine frequency, duration, and severity.^e1 This trial (n = 53) was stopped prematurely because of a high number of withdrawals (34%), primarily due to acetazolamide-associated AEs, including paresthesias and asthenia.

Conclusions.

The efficacy of acetazolamide is unknown at this time (1 Class II study terminated early).

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RECOMMENDATIONS

Level A.

The following medications are established as effective and should be offered for migraine prevention:

• Antiepileptic drugs (AEDs): divalproex sodium, sodium valproate, topiramate

• β-Blockers: metoprolol, propranolol, timolol

• Triptans: frovatriptan for short-term MAMs prevention

Level B.

The following medications are probably effective and should be considered for migraine prevention:

• Antidepressants: amitriptyline, venlafaxine

• β-Blockers: atenolol, nadolol

• Triptans: naratriptan, zolmitriptan for short-term MAMs prevention

Level C.

The following medications are possibly effective and may be considered for migraine prevention:

• ACE inhibitors: lisinopril

• Angiotensin receptor blockers: candesartan

• α-Agonists: clonidine, guanfacine

• AEDs: carbamazepine

• β-Blockers: nebivolol, pindolol

Level U.

Evidence is conflicting or inadequate to support or refute the use of the following medications for migraine prevention:

• AEDs: gabapentin

• Antidepressants

  • Selective serotonin reuptake inhibitor/selective serotonin-norepinephrine reuptake inhibitors: fluoxetine, fluvoxamine

  • Tricyclics: protriptyline

• Antithrombotics: acenocoumarol, Coumadin, picotamide

• β-Blockers: bisoprolol

• Calcium-channel blockers: nicardipine, nifedipine, nimodipine, verapamil

• Acetazolamide

• Cyclandelate

Level A negative.

The following medication is established as ineffective and should not be offered for migraine prevention:

• Lamotrigine

Level B negative.

The following medication is probably ineffective and should not be considered for migraine prevention:

• Clomipramine

Level C negative.

The following medications are possibly ineffective and may not be considered for migraine prevention:

• Acebutolol

• Clonazepam

• Nabumetone

• Oxcarbazepine

• Telmisartan

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