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Peer Tfelt-Hansen

Bio: Peer Tfelt-Hansen is an academic researcher from University of Copenhagen. The author has contributed to research in topics: Migraine & Sumatriptan. The author has an hindex of 46, co-authored 236 publications receiving 14422 citations. Previous affiliations of Peer Tfelt-Hansen include University of Duisburg-Essen & Bispebjerg Hospital.
Topics: Migraine, Sumatriptan, Triptans, Placebo, Rizatriptan


Papers
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Journal ArticleDOI
Jes Olesen, André Bes, Robert S. Kunkel, James W. Lance, Giuseppe Nappi, V Pfaffenrath, Frank Clifford Rose, Bruce S. Schoenberg, D. Soyka, Peer Tfelt-Hansen, K. Michael A. Welch, Marica Wilkinson, Marie-Germaine Bousser, Hans-Christoph Diener, David W. Dodick, Michael First, Peter J. Goadsby, Hartmut Göbel, Miguel J. A. Láinez, Richard B. Lipton, Fumihiko Sakai, Jean Schoenen, Stephen D. Silberstein, Timothy J. Steiner, Lars Bendtsen, Anne Ducros, Stefan Evers, Andrew D. Hershey, Zaza Katsarava, Morris Levin, Julio Pascual, Michael Bjørn Russell, Todd J. Schwedt, Cristina Tassorelli, Gisela M. Terwindt, Maurice Vincent, Shuu Jiun Wang, Andrew Charles, R. Lipton, Hayrunnisa Bolay, Michel Lantéri-Minet, E. A. Macgregor, T. Takeshima, Henrik Winther Schytz, S. Ashina, M. T. Goicochea, K. Hirata, Kenneth A. Holroyd, Christian Lampl, Dimos-Dimitrios Mitsikostas, P. Goadsby, C. Boes, C. Bordini, E. Cittadini, Andrew I. Cohen, M. Leone, A. May, L. Newman, J. Pareja, J. W. Park, T. Rozen, E. Waldenlind, Jong Ling Fuh, Aynur Özge, J. A. Pareja, Mario Fernando Prieto Peres, William B. Young, S. Y. Yu, Ishaq Abu-Arafeh, J. Gladstone, S. J. Huang, Rigmor Jensen, J.M. Láinez, D. Obelieniene, Peter S. Sandor, A. I. Scher, Marcel Arnold, Martin Dichgans, E. Houdart, José M. Ferro, Elizabeth Leroux, Y. S. Li, Aneesh B. Singhal, Gretchen E. Tietjen, Deborah I. Friedman, S. Kirby, B. Mokri, A. Purdy, K. Ravishankar, W. Schievink, R. Stark, F. Taylor, A. V. Krymchantowski, A. Tugrul, N. J. Wiendels, E. Marchioni, V. V. Osipova, Lidia Savi, J. R. Berger, Marcelo E. Bigal, J. González Menacho, Federico Mainardi, J. Pereira-Monteiro, M. Serrano-Dueñas, Roger Cady, C. Fernandez de las Peñas, Vincenzo Guidetti, J. Lance, Peter Svensson, Elizabeth Loder, A. E. Lake, Françoise Radat, J. I. Escobar, R. Benoliel, Claudia Sommer, A. Woda, Joanna M Zakrzewska, V. Aggarwal, L. Bonamico, Dominik A Ettlin, S. Graff-Radford, Jean-Paul Goulet, S. Jääskeläinen, Volker Limmroth, Ambra Michelotti, Donald R. Nixdorf, Mark Obermann, Richard Ohrbach, Paul Pionchon, Tara Renton, S. De Siqueira, Çiçek Wöber-Bingöl 
TL;DR: The International Classification of Headache Disorders, 3 edition (beta version), may be reproduced freely for scientific, educational or clinical uses by institutions, societies or individuals as mentioned in this paper. But the authors require the permission of the International Headache Society.
Abstract: The International Classification of Headache Disorders, 3 edition (beta version), may be reproduced freely for scientific, educational or clinical uses by institutions, societies or individuals. Otherwise, copyright belongs exclusively to the International Headache Society. Reproduction of any part or parts in any manner for commercial uses requires the Society’s permission, which will be granted on payment of a fee. Please contact the publisher at the address below. International Headache Society 2013. Applications for copyright permissions should be submitted to Sage Publications Ltd, 1 Oliver’s Yard, 55 City Road, London EC1Y 1SP, United Kingdom (tel: þ44 (0) 20 7324 8500; fax: þ44 (0) 207 324 8600) (www.sagepub.co.uk). Translations

6,519 citations

Journal ArticleDOI
TL;DR: It is suggested that migraine can be explained to patients as a disorder of the brain, and that the headache originates in the sensory fibres that convey pain signals from intracranial and extracranial blood vessels.
Abstract: Summary Migraine is the most common neurological disorder, and much has been learned about its mechanisms in recent years. However, the origin of painful impulses in the trigeminal nerve is still uncertain. Despite the attention paid recently to the role of central sensitisation in migraine pathophysiology, in our view, neuronal hyperexcitability depends on activation of peripheral nociceptors. Although the onset of a migraine attack might take place in deep-brain structures, some evidence indicates that the headache phase depends on nociceptive input from perivascular sensory nerve terminals. The input from arteries is probably more important than the input from veins. Several studies provide evidence for input from extracranial, dural, and pial arteries but, likewise, there is also evidence against all three of these locations. On balance, afferents are most probably excited in all three territories or the importance of individual territories varies from patient to patient. We suggest that migraine can be explained to patients as a disorder of the brain, and that the headache originates in the sensory fibres that convey pain signals from intracranial and extracranial blood vessels.

476 citations

Journal ArticleDOI
01 Dec 2000-Drugs
TL;DR: Rizatriptan with its shorter time to maximum concentration (tmax) tended to produce a quicker onset of headache relief than sum atriptan and zolmitriptan, and the place of triptans compared with non-triptan drugs in migraine therapy remains to be established and further RCTs are required.
Abstract: Triptans are a new class of compounds developed for the treatment of migraine attacks. The first of the class, sumatriptan, and the newer triptans (zolmitriptan, naratriptan, rizatriptan, eletriptan, almotriptan and frovatriptan) display high agonist activity at mainly the serotonin 5-HT1b and 5-HT1d receptor subtypes. As expected for a class of compounds developed for affinity at a specific receptor, there are minor pharmacodynamic differences between the triptans.

459 citations

Journal ArticleDOI
01 Jul 1989-Pain
TL;DR: NTG is suitable as an experimental headache model, suitable for studies of arterial diameter, pulsations, blood flow, etc, and Comparative studies of sensitivity should use the present infusion schedule but with the two highest doses substituted by 0.06 and 0.125.
Abstract: To develop a reliable experimental model of vascular headache, we studied the dose-response relationship between headache and i.v. nitroglycerin (NTG) in 10 healthy subjects. NTG was infused intravenously over periods of 10 min separated by wash-out periods. Doses of 0.25, 0.50, 1.00 and 2.00 micrograms/kg/min were applied successively with one placebo infusion and wash-out period inserted randomly and double blindly. The subjects scored their headache intensity on a scale 0-10. After 1-8 weeks a retest was performed. Nine subjects developed headache already at 0.25 microgram/kg/min, whereas one had no headache at any dose. Headache severity did not increase with doses above 0.5 microgram/kg/min. This ceiling effect was reproducible. The headache was moderate, usually throbbing, bifrontal and not associated with other migrainous features. It reached maximum within 2.5-5.5 min (medians) at various doses and declined rapidly after NTG discontinuation. Wash-out periods of 10-20 min were sufficient. The reproducibility of headache intensity and character was satisfactory in the retest experiment. There were no unpleasant side effects and no visible flushing. Thus blindness was maintained. I.v. NTG is suitable as an experimental headache model. A constant infusion of 0.5 microgram/kg/min will be suitable for studies of arterial diameter, pulsations, blood flow, etc. Comparative studies of sensitivity should use the present infusion schedule but with the two highest doses substituted by 0.06 and 0.125 microgram/kg/min.

357 citations


Cited by
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Journal ArticleDOI
01 Jan 2018
TL;DR: The 3rd edition of the International Classification of Headache Disorders (ICHD-3) may be reproduced freely for scientific, educational or clinical uses by institutions, societies or individuals if the Society’s permission is granted.
Abstract: The 3rd edition of the International Classification of Headache Disorders (ICHD-3) may be reproduced freely for scientific, educational or clinical uses by institutions, societies or individuals. Otherwise, copyright belongs exclusively to the International Headache Society. Reproduction of any part or parts in any manner for commercial uses requires the Society’s permission, which will be granted on payment of a fee. Please contact the publisher at the address below. International Headache Society 2013–2018. Applications for copyright permissions should be submitted to Sage Publications Ltd, 1 Oliver’s Yard, 55 City Road, London EC1Y 1SP, United Kingdom (tel: þ44 (0) 207 324 8500; fax: þ44 (0) 207 324 8600; permissions@sagepub.co.uk) (www.uk.sagepub.com). Translations

6,269 citations

Journal ArticleDOI
01 Dec 1941-Nature
TL;DR: The Pharmacological Basis of Therapeutics, by Prof. Louis Goodman and Prof. Alfred Gilman, New York: The Macmillan Company, 1941, p.
Abstract: The Pharmacological Basis of Therapeutics A Textbook of Pharmacology, Toxicology and Therapeutics for Physicians and Medical Students. By Prof. Louis Goodman and Prof. Alfred Gilman. Pp. xiii + 1383. (New York: The Macmillan Company, 1941.) 50s. net.

2,686 citations

Journal ArticleDOI
TL;DR: The newly recommended evidence-based new DC/TMD protocol is appropriate for use in both clinical and research settings and includes both a valid screener for detecting any pain-related TMD as well as valid diagnostic criteria for differentiating the most common pain- related TMD.
Abstract: Temporomandibular disorders (TMD) are a significant public health problem affecting approximately 5% to 12% of the population.1 TMD is the second most common musculoskeletal condition (after chronic low back pain) resulting in pain and disability.1 Pain-related TMD can impact the individual's daily activities, psychosocial functioning, and quality of life. Overall, the annual TMD management cost in the USA, not including imaging, has doubled in the last decade to $4 billion.1 Patients often seek consultation with dentists for their TMD, especially for pain-related TMD. Diagnostic criteria for TMD with simple, clear, reliable, and valid operational definitions for the history, examination, and imaging procedures are needed to render physical diagnoses in both clinical and research settings. In addition, biobehavioral assessment of pain-related behavior and psychosocial functioning—an essential part of the diagnostic process—is required and provides the minimal information whereby one can determine whether the patient's pain disorder, especially when chronic, warrants further multidisciplinary assessment. Taken together, a new dual-axis Diagnostic Criteria for TMD (DC/TMD) will provide evidence-based criteria for the clinician to use when assessing patients, and will facilitate communication regarding consultations, referrals, and prognosis.2 The research community benefits from the ability to use well-defined and clinically relevant characteristics associated with the phenotype in order to facilitate more generalizable research. When clinicians and researchers use the same criteria, taxonomy, and nomenclature, then clinical questions and experience can be more easily transferred into relevant research questions, and research findings are more accessible to clinicians to better diagnose and manage their patients. The Research Diagnostic Criteria for Temporomandibular Disorders (RDC/TMD) have been the most widely employed diagnostic protocol for TMD research since its publication in 1992.3 This classification system was based on the biopsychosocial model of pain4 that included an Axis I physical assessment, using reliable and well-operationalized diagnostic criteria, and an Axis II assessment of psychosocial status and pain-related disability. The intent was to simultaneously provide a physical diagnosis and identify other relevant characteristics of the patient that could influence the expression and thus management of their TMD. Indeed, the longer the pain persists, the greater the potential for emergence and amplification of cognitive, psychosocial, and behavioral risk factors, with resultant enhanced pain sensitivity, greater likelihood of additional pain persistence, and reduced probability of success from standard treatments.5 The RDC/TMD (1992) was intended to be only a first step toward improved TMD classification, and the authors stated the need for future investigation of the accuracy of the Axis I diagnostic algorithms in terms of reliability and criterion validity—the latter involving the use of credible reference standard diagnoses. Also recommended was further assessment of the clinical utility of the Axis II instruments. The original RDC/TMD Axis I physical diagnoses have content validity based on the critical review by experts of the published diagnostic approach in use at that time and were tested using population-based epidemiologic data.6 Subsequently, a multicenter study showed that, for the most common TMD, the original RDC/TMD diagnoses exhibited sufficient reliability for clinical use.7 While the validity of the individual RDC/TMD diagnoses has been extensively investigated, assessment of the criterion validity for the complete spectrum of RDC/TMD diagnoses had been absent until recently.8 For the original RDC/TMD Axis II instruments, good evidence for their reliability and validity for measuring psychosocial status and pain-related disability already existed when the classification system was published.9–13 Subsequently, a variety of studies have demonstrated the significance and utility of the original RDC/TMD biobehavioral measures in such areas as predicting outcomes of clinical trials, escalation from acute to chronic pain, and experimental laboratory settings.14–20 Other studies have shown that the original RDC/TMD biobehavioral measures are incomplete in terms of prediction of disease course.21–23 The overall utility of the biobehavioral measures in routine clinical settings has, however, yet to be demonstrated, in part because most studies have to date focused on Axis I diagnoses rather than Axis II biobehavioral factors.24 The aims of this article are to present the evidence-based new Axis I and Axis II DC/TMD to be used in both clinical and research settings, as well as present the processes related to their development.

2,283 citations