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Guideline EFNS guideline on the drug treatment of migraine - report of an EFNS task force. 2006
Anonymous00234, Evers S, Afra J, Frese A, Goadsby PJ, Linde M, May A, Sándor PS. · Department of Neurology, University of Münster, Germany. European Federation of NeurologicalSocieties · Eur J Neurol. · Pubmed #16796580 No free full text.
Abstract: 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 of the different migraine syndromes based on a literature search and an consensus in an expert panel. All available medical reference systems were screened for all kinds 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 EFNS resulting in level A,B, or C recommendations and good practice points. For the acute treatment of migraine attacks, oral non-steroidal anti-inflammatory drugs (NSAIDs) and triptans are recommended. The administration should follow the concept of stratified treatment. Before intake of NSAIDs and triptans, oral metoclopramide or domperidon is recommended. In very severe attacks, intravenous acetylsalicylic acid or subcutaneous sumatriptan are drugs of first choice. A status migrainosus can probably be treated by steroids. 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 are amitriptyline, naproxen, petasites, and bisoprolol.
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Editorial [The future of headaches] 2004
May A. · No affiliation provided · Schmerz. · Pubmed #15449165 No free full text.
This publication has no abstract.
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Review Morphing voxels: the hype around structural imaging of headache patients. 2009
May A. · Department of Systems Neuroscience, Universitäts-Krankenhaus Eppendorf , Martinistrasse 52, Hamburg, Germany. · Brain. · Pubmed #19443629 No free full text.
Abstract: Neuroimaging analysis using structural data has begun to provide insights into the pathophysiology of headache syndromes. Several independent studies have suggested a decrease in grey matter in pain-transmitting areas in migraine patients. Most of these data are discussed as damage or loss of brain grey matter, reinforcing the idea of migraine as a progressive disease. However, given what we know about the nature of morphometric changes detectable by the methods we have to date, this interpretation is highly speculative and not supported by the data. It is likely that these changes are the consequence and not the cause of the respective headache syndromes, as they are probably not irreversible and only mirror the proportion or duration of pain suffered. Moreover, structural changes are not headache specific and have to be seen in the light of a wealth of pain studies using these methods. The studies in cluster headache patients prompted the use of stereotactic stimulation of the hypothalamic target point identified by functional and structural neuroimaging. Due to the nature of the methods used and due to a high anatomical variance it is more than questionable to use this point as a definite answer to the source of the headache in clusters and even more so when it is uncritically used in individuals. We need a way to study each patient individually using the functional imaging method with the highest spatial and temporal resolution available to enable us to target the seed point for deep brain stimulation on this individual basis. One of the major future challenges is to understand the behavioural consequences and cellular mechanisms underlying neuroanatomic changes in pain and headache.
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Review [Therapy of primary chronic headache: chronic migraine, chronic tension type headache and other forms of daily chronic headache] 2008
Straube A, May A, Kropp P, Katsarava Z, Haag G, Lampl C, Sándor PS, Diener HC, Evers S. · Neurologische Klinik, Klinikum Grosshadern der Ludwig-Maximilians-Universität München, Marchioninistr. 15, 81377 München, Deutschland. · Schmerz. · Pubmed #18483751 No free full text.
Abstract: The criteria of the International Headache Society (IHS) define four different primary headache syndromes with daily chronic headaches: chronic migraine, episodic and chronic tension type headache, hemicrania continua, new daily persisting headache. A further important differential diagnosis is medication overuse headache (previously known as analgesia headache). The German, Austrian, and Swiss headache societies now present the first joint guidelines for therapy of these headache syndromes. The current literature was reviewed and a summary is presented. The therapy recommendations do not only include the scientific evidence but also the practical relevance.
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Review [Cortical dysbalance in the brain in migraineurs--hyperexcitability as the result of sensitisation?] 2008
Stankewitz A, May A. · Institut für systemische Neurowissenschaften, Universitätsklinikum Hamburg-Eppendorf, Martinistrasse 52, 20246, Hamburg, Germany. · Schmerz. · Pubmed #18228046 No free full text.
Abstract: A cortical dysbalance has a pivotal role in the pathophysiology of migraine. Numerous electrophysiological and transcranial magnetic stimulation (TMS) studies have investigated the interictal excitability level in migraineurs and have shown a consistent lack of habituation during repetitive stimulation. There is some controversy in the current literature over whether this deficit is based on a lowered or an elevated preactivation level. However, the current discussion may be misguided. It seems that multiple external and intrinsic factors influence the level of cortical excitability and the frequency and intensity of attacks: Habituation is specific neither to migraine nor even to pain; the same phenomenon is found in tinnitus patients, for example. Cortical hyperexcitability is presumably the result of chronicity and the concomitant central sensitisation process.
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Review Cortical excitability and migraine. 2007
Stankewitz A, May A. · Department of Systems Neuroscience, University of Hamburg, Germany. · Cephalalgia. · Pubmed #18034689 No free full text.
This publication has no abstract.
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Review Evaluation and proposal for optimization of neurophysiological tests in migraine: part 2--neuroimaging and the nitroglycerin test. 2007
Magis D, Bendtsen L, Goadsby PJ, May A, Sánchez del Rio M, Sandór PS, Kaube H, Sandrini G, Schoonman GG, Schoenen J, Anonymous00021. · Headache Research Unit, Department of Neurology, University of Liège, Liège, Belgium. · Cephalalgia. · Pubmed #17970767 No free full text.
Abstract: Neuroimaging methods have been widely used in headache and migraine research. They have provided invaluable information on brain perfusion, metabolism and structure during and outside of migraine attacks, contributing to an improved understanding of the pathophysiology of the disorder. Human models of migraine attacks are indispensable tools in pathophysiological and therapeutic research. This review of neuroimaging methods and the attack-provoking nitroglycerin test is part an initiative by a task force within the EUROHEAD project (EU Strep LSHM-CT-2004-5044837-Workpackage 9) with the objective of critically evaluating neurophysiological tests used in migraine. The first part, presented in a companion paper, is devoted to electrophysiological methods, this second part to neuroimaging methods such as functional magnetic resonance imaging, positron emission tomography and voxel-based morphometry, as well as the nitroglycerin test. For each of these methods, we summarize the results, analyse the methodological limitations and propose recommendations for improved methodology and standardization of research protocols.
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Review New insights into migraine: application of functional and structural imaging. 2007
May A, Matharu M. · Department of Systems Neuroscience, University of Hamburg, Germany. · Curr Opin Neurol. · Pubmed #17495625 No free full text.
Abstract: PURPOSE OF REVIEW: Functional neuroimaging in headache patients has revolutionized our understanding of these syndromes. Further insights into the pathophysiology of headache syndromes have been provided by innovative neuroimaging analysis using structural data. This review highlights the recent advances made in studying migraine using neuroimaging techniques. RECENT FINDINGS: Several independent studies have reinforced the crucial role for the brainstem in acute and probably also chronic migraine. Recently described structural abnormalities in the visual network of motion-processing areas could account for, or be caused by, the cortical hyperexcitability observed in migraineurs. Although data from morphometric studies are heterogeneous, a recent study suggests an increased density of brainstem structures and decreased grey matter in pain-transmitting areas in migraine patients. SUMMARY: Given the rapid advances in functional neuroimaging, in particular newer techniques such as voxel-based morphometry and magnetic resonance spectrometry, functional imaging continues to play a significant role and opens new avenues in targeting the neural substrates in individual primary headache syndromes.
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Review A review of diagnostic and functional imaging in headache. 2006
May A. · Department of Systems Neuroscience, Universitäts-Krankenhaus Eppendorf, Martinistr. 52, D-20246, Hamburg, Germany. · J Headache Pain. · Pubmed #16897620 No free full text.
Abstract: The neuroimaging of headache patients has revolutionised our understanding of the pathophysiology of primary headaches and provided unique insights into these syndromes. Modern imaging studies point, together with the clinical picture, towards a central triggering cause. The early functional imaging work using positron emission tomography shed light on the genesis of some syndromes, and has recently been refined, implying that the observed activation in migraine (brainstem) and in several trigeminal-autonomic headaches (hypothalamic grey) is involved in the pain process in either a permissive or triggering manner rather than simply as a response to first-division nociception per se. Using the advanced method of voxel-based morphometry, it has been suggested that there is a correlation between the brain area activated specifically in acute cluster headache--the posterior hypothalamic grey matter--and an increase in grey matter in the same region. No structural changes have been found for migraine and medication overuse headache, whereas patients with chronic tension-type headache demonstrated a significant grey matter decrease in regions known to be involved in pain processing. Modern neuroimaging thus clearly suggests that most primary headache syndromes are predominantly driven from the brain, activating the trigeminovascular reflex and needing therapeutics that act on both sides: centrally and peripherally.
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Review The contribution of functional neuroimaging to primary headaches. 2004
May A. · Department of Neurology, Universitäts-Krankenhaus Eppendorf, Martinstr. 52, D-20246 Hamburg, Germany. · Neurol Sci. · Pubmed #15549576 No free full text.
Abstract: Functional imaging techniques have begun to provide considerable insight into the pathophysiology of primary headache syndromes. PET and f-MRI have allowed to to monitor the physiological cortical reaction and nociceptor transmission of head-pain, but more importantly have identified pathophysiological abnormalities and even the "motor" in migraine and cluster headache attacks. This has even prompted new treatment options such as DBS in cluster headache and will undoubtly change the way we see headache. Innovative techniques such as voxel- and deformation-based morphometry have just started to unravel the structural consequences of chronic pain. Functional imaging will undoubtedly provide further opportunities to study and compare metabolic, haemodynamic and structural parameters in headache sufferers' brains.
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Review [The trigeminovascular system in the human. Cerebral blood flow, functional imaging and primary headache] 2003
May A. · Klinik und Poliklinik für Neurologie im BKR, Universitätsklinkum Regensburg. · Nervenarzt. · Pubmed #14647907 No free full text.
Abstract: Primary headache syndromes, such as cluster and migraine, are widely described as vascular headaches, even though there is considerable clinical evidence to suggest that both conditions are primarily central, that is regulated by the brain. The shared anatomical and physiological substrate for both clinical syndromes is the neural innervation of the cranial circulation. Early functional imaging using PET has shed light on the genesis of both syndromes, documenting activation in the midbrain and pons in migraine and in the hypothalamic gray in cluster headache. These areas are involved in the pain process in a permissive or triggering manner rather than simply as a response to first-division nociceptive pain impulses. This article reviews findings in the physiology of the trigeminovascular system which demand renewed consideration of the neural influences in many primary headaches and the physiology of the neural innervation of cranial circulation. Primary headaches should thus be regarded as neurovascular headaches to emphasize the interaction between nerves and vessels which is their underlying characteristic.
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Review Ethical aspects of placebo in migraine research. 2003
Linde M, May A, Limmroth V, Dahlöf C, Anonymous00332. · Gothenburg Migraine Clinic and Institute of Clinical Neuroscience, Sahlgrenska University Hospital, Göteborg, Sweden. · Cephalalgia. · Pubmed #12950373 No free full text.
Abstract: Randomized placebo-controlled clinical trials have been the 'golden standard' during the last decades in the development of new drug therapies. This scientifically valid approach has recently been questioned in the fifth revised version of the Declaration of Helsinki, which states that the use of placebo-controlled clinical trials is only acceptable when no proven treatment exists for the studied disease. The World Medical Association further claims that no national ethical, legal or regulatory requirements should be allowed to reduce or eliminate any of the statements in the declaration. In spite of this, the document is not generally accepted as the world ethical standard, as demonstrated by its lack of adoption by many professional associations. In the evaluation process for a drug to be approved in many countries today, clinical investigators at the hospitals and researchers at the pharmaceutical companies are obliged to use study protocols that would be rejected if the new declaration were to be fully adopted. Adherence to the clinical trial guidelines of the International Headache Society could also mean violation of the new Helsinki declaration of ethics. Some ethics committees have already adopted the new declaration, which has caused concern among clinical investigators, who find this document to be vastly out of the line with common practice. At the moment, the situation is unclear and debated with increasing polarity concerning the scientific and ethical issues regarding the use of placebo in clinical trials.
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Review Headache: lessons learned from functional imaging. 2003
May A. · Department of Neurology, University of Regensburg, Germany. · Br Med Bull. · Pubmed #12697628 No free full text.
Abstract: Most idiopathic headache syndromes are still recognized as vascular headaches although the clinical picture points towards a central triggering cause. The early functional imaging work using PET shed light on the genesis of some syndromes, implying that the observed activation in migraine (brainstem) and in cluster headache (hypothalamic grey) is involved in the pain process in a permissive or triggering manner rather than simply as a response to first division nociception per se. Using the advanced method of voxel-based morphometry (VBM), it has been suggested that there is a correlation between the brain area activated particularly in acute cluster headache, the posterior hypothalamic grey matter, and some change in grey matter in the same region. Moreover, also in a PET study in cluster headache and experimental headache, a vasodilation of major basal vessels has been observed which is non-specific to the cause and most likely the effect of a trigemino-parasympathetic reflex. Taken together, functional neuroimaging in headache patients has revolutionised this area of study and provided unique insights into some of the commonest maladies in man, suggesting that migraine and cluster headache are primarily driven from the brain.
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Review [Therapy and prophylaxis of facial neuralgias and other forms of facial pain syndromes -- revised recommendations of the German Society of Migraine and Headache] 2003
Paulus W, Evers S, May A, Steude U, Wolowski A, Pfaffenrath V, Anonymous00002. · Abteilung Klinische Neurophysiologie der Universität Göttingen. · Schmerz. · Pubmed #12579391 No free full text.
Abstract: Trigeminal neuralgia and postherpetic neuralgia are the most relevant neuralgiform facial pain syndromes. Trigeminal neuralgia is characterized by lancinating intensive pain attacks of very short duration, triggered by external cues,whereas postherpetic neuralgia consists predominantly of long-lasting burning pain. Sodium channel blocking drugs are first choice in treatment of trigeminal neuralgia, operative procedures encompass microvascular decompression,thermocoagulation and percutaneous retrogasserian glycerol rhizotomy. In the acute stage postherpetic neuralgia is treated antivirally and analgesically, in the chronic stage by tricyclic antidepressive substances. Other pain syndromes described encompass the Tolosa-Hunt-syndrome, cervicogenic headache, craniomandibular dysfunction syndrome, atypical facial pain and rarer syndromes. Therapeutic recommendations are based on evidence based medicine criteria (EBM).
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Review Pharmacological opportunities and pitfalls in the therapy of migraine. 2001
May A, Goadsby PJ. · Department of Neurology, University of Regensburg, Regensburg, Germany. · Curr Opin Neurol. · Pubmed #11371757 No free full text.
Abstract: The mild vasoconstrictor effects of modern antimigraine drugs, such as serotonin (5-HT; 5-hydroxytryptamine)1B/D agonists, have led to a search for nonvasoconstrictor approaches to therapy. Such approaches have included substance P (neurokinin I) antagonists, endothelin antagonists and highly specific 5HT1D agonists. All of these substances are effective in animal models and have no significant vasoconstrictive effects. However, all of them failed to demonstrate any antimigraine effects. Current clinical and experimental evidence therefore supports the view that isolated peripheral trigeminal nerve inhibition is insufficient to relieve acute migraine.
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Review Substance P receptor antagonists in the therapy of migraine. 2001
May A, Goadsby PJ. · Department of Neurology, University of Regensburg, 93053 Regensburg, Germany. · Expert Opin Investig Drugs. · Pubmed #11281817 No free full text.
Abstract: Clinical observations, the vascular component of migraine pain, its pulsating or throbbing pain character, have focused attention on the trigeminal innervation of pain-sensitive intracranial structures, such as the dura mater and large vessels. These intracranial structures are innervated by the ophthalmic branch of the trigeminal nerve, which is marked by the presence of vasoactive peptides, such as substance P and calcitonin gene-related peptide. Substance P is a mediator of the sterile inflammation of the dura mater, which has been considered to be the source of migraine pain. Modern antimigraine drugs, such as 5-HT(1B/D) agonists (triptans), block this dural neurogenic inflammation dose-dependently in an animal model but their vasoconstrictor effects have led to a search for non-vasoconstrictor approaches. One such approach has been substance P (neurokinin-1) antagonists. These are highly effective in animal models of dural inflammation and have no significant vasoconstrictive effect. However, several NK(1) antagonists failed to demonstrate any effect in acute migraine. Current clinical and experimental evidence therefore supports the view that NK(1) receptor antagonists may have no significant antimigraine properties.
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Review The trigeminovascular system in humans: pathophysiologic implications for primary headache syndromes of the neural influences on the cerebral circulation. free! 1999
May A, Goadsby PJ. · University Department of Clinical Neurology, Institute of Neurology, The National Hospital for Neurology and Neurosurgery, London, UK. · J Cereb Blood Flow Metab. · Pubmed #10027765 links to free full text
Abstract: Primary headache syndromes, such as cluster headache and migraine, are widely described as vascular headaches, although considerable clinical evidence suggests that both are primarily driven from the brain. The shared anatomical and physiologic substrate for both of these clinical problems is the neural innervation of the cranial circulation. Functional imaging with positron emission tomography has shed light on the genesis of both syndromes, documenting activation in the midbrain and pons in migraine and in the hypothalamic gray in cluster headache. These areas are involved in the pain process in a permissive or triggering manner rather than as a response to first-division nociceptive pain impulses. In a positron emission tomography study in cluster headache, however, activation in the region of the major basal arteries was observed. This is likely to result from vasodilation of these vessels during the acute pain attack as opposed to the rest state in cluster headache, and represents the first convincing activation of neural vasodilator mechanisms in humans. The observation of vasodilation was also made in an experimental trigeminal pain study, which concluded that the observed dilation of these vessels in trigeminal pain is not inherent to a specific headache syndrome, but rather is a feature of the trigeminal neural innervation of the cranial circulation. Clinical and animal data suggest that the observed vasodilation is, in part, an effect of a trigeminoparasympathetic reflex. The data presented here review these developments in the physiology of the trigeminovascular system, which demand renewed consideration of the neural influences at work in many primary headaches and, thus, further consideration of the physiology of the neural innervation of the cranial circulation. We take the view that the known physiologic and pathophysiologic mechanisms of the systems involved dictate that these disorders should be collectively regarded as neurovascular headaches to emphasize the interaction between nerves and vessels, which is the underlying characteristic of these syndromes. Moreover, the syndromes can be understood only by a detailed study of the cerebrovascular physiologic mechanisms that underpin their expression.
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Clinical Conference Sumatriptan and corneal reflexes in headache-free migraine patients: a randomized and placebo-controlled crossover study. 2007
Busch V, Kaube S, Schulte-Mattler W, Kaube H, May A. · Department of Neurology, University of Regensburg, Universitätsstr. 84, 93053 Regensburg, Germany. · Cephalalgia. · Pubmed #17257238 No free full text.
Abstract: A temporary sensitization of central trigeminal neurones in migraine patients during acute attacks has been described in previous studies using the electrically evoked nociceptive blink reflex. The cornea is innervated by small myelinated A-delta and unmyelinated C-fibres only. Stimulation with air puffs activates peripheral nociceptors and allows the investigation of peripheral trigeminal nerve structures. Our objective was to investigate whether corneal reflex examinations with air puff stimulation detect abnormalities in migraineurs during their pain-free interval and if the corneal reflex may be modulated by the administration of an oral triptan. After validation of the nociceptive air puff technique by investigating the corneal reflexes before and after a local anaesthesia of the cornea, we recorded corneal reflexes in 25 migraineurs during their pain-free period and 25 healthy controls before and after the oral administration of 100 mg sumatriptan in a randomized, placebo-controlled, crossover study. Baseline response areas under the curve (AUCs) and latencies of the R2 components of the corneal reflexes did not show any significant differences between patients and controls. Patients did not show any significant differences regarding their headache and non-headache side. The use of an oral triptan had no significant influence on latencies or AUCs in both patients and controls. Our data suggest that there is no facilitation of the trigeminal system in the headache-free interval among patients with migraine. The stable corneal reflexes after the oral administration of 100 mg sumatriptan suggest that there was no inhibition of the trigeminal system, both in patients during their headache-free period and in healthy controls.
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Clinical Conference Treatment satisfaction with zolmitriptan nasal spray for migraine in a real life setting: results from phase two of the REALIZE study. 2005
Gawel M, Aschoff J, May A, Charlesworth BR, Anonymous00214. · Department of Medicine (Neurology), Sunnybrook and Women's Health Sciences Centre, Suite 515, 60 Grosvenor Street, Toronto, Ontario M5S 1B6, Canada. · J Headache Pain. · Pubmed #16362714 No free full text.
Abstract: In phase one of the REALIZE study, zolmitriptan nasal spray demonstrated a significant headache response from 10 min post-dose and total symptom relief from 30 min post-dose. The objective of phase two was to investigate patients' dosing patterns, satisfaction and preference following open-label treatment with the nasal spray. Up to 3 attacks were treated. The ITT population consisted of 851 patients. The median time from onset of symptoms to treatment was 1 h 15 min (primary endpoint). Most patients reported being satisfied or very satisfied with zolmitriptan nasal spray (75.7%). Furthermore, the majority of patients would be willing to use zolmitriptan nasal spray in the future (59.8%) and preferred zolmitriptan nasal spray over previous therapies (57.8%). Zolmitriptan nasal spray was well tolerated. Most patients were satisfied with zolmitriptan nasal spray, were willing to continue using it and preferred it to previous therapies.
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Clinical Conference Zolmitriptan 5 mg nasal spray: efficacy and onset of action in the acute treatment of migraine--results from phase 1 of the REALIZE Study. 2005
Gawel M, Aschoff J, May A, Charlesworth BR, Anonymous00024. · Department of Sunnybrook and Women's College Health Sciences Centre, Toronto, Canada. · Headache. · Pubmed #15663607 No free full text.
Abstract: OBJECTIVES: The objective of phase 1 (reported here) of this two-phase study was to assess the efficacy of zolmitriptan 5 mg nasal spray, in terms of ability to provide relief from all migraine symptoms, in a controlled setting, designed to replicate clinical practice. BACKGROUND: Zolmitriptan nasal spray has been shown to be fast acting and highly effective in the treatment of migraine, as assessed using standard endpoints, such as headache response and pain-free rates. METHODS: In the double-blind first phase of the study, patients with migraine were randomized to receive zolmitriptan 5 mg nasal spray or placebo to treat a single migraine attack. Attacks were treated according to patients' normal patterns of use, in order to closely reflect clinical practice; that is, no specific regimen was dictated in terms of time to treatment or at what level of pain intensity the headache should be treated. Patients could take a second dose of study medication or an agreed escape medication if adequate pain relief had not been achieved 2 hours after the first dose. The primary efficacy endpoint was total symptom relief (freedom from pain, nausea, photophobia, and phonophobia) 1 hour after the first dose. Secondary efficacy endpoints included headache response, pain-free status and sustained pain-free status, and ability to perform normal activities. RESULTS: The intention-to-treat population comprised 461 zolmitriptan nasal spray recipients and 451 placebo recipients. The total symptom relief rate 1 hour post-dose was significantly higher in the zolmitriptan 5 mg nasal spray group than in the placebo group (14.5% vs. 5.1%; P < .0001); the difference between the groups was significant from 30 minutes post-dose. Treatment with zolmitriptan nasal spray, compared with placebo, also produced a higher headache response rate from 10 minutes post-dose (15.1% vs. 9.1%; P = .0079) and a higher pain-free rate from 30 minutes post-dose (7.7% vs. 3.2%; P = .0039). Zolmitriptan nasal spray was also significantly superior to placebo in terms of sustained pain-free status and patients' ability to perform normal activities. Zolmitriptan nasal spray was well tolerated. CONCLUSIONS: These findings confirm the efficacy demonstrated by zolmitriptan nasal spray in previous clinical trials.
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Clinical Conference Efficacy of 1,000 mg effervescent acetylsalicylic acid and sumatriptan in treating associated migraine symptoms. 2004
Diener HC, Eikermann A, Gessner U, Göbel H, Haag G, Lange R, May A, Müller-Schwefe G, Voelker M. · Department of Neurology, University of Essen, Hufelandstrasse 55, DE-45147 Essen, Germany. · Eur Neurol. · Pubmed #15240983 No free full text.
Abstract: Recently a new effervescent acetylsalicylic acid (ASA) tablet with high buffering capacity has been developed. In this double-blind, 3-arm, multicenter, parallel-group study, 433 patients were treated either with 1,000 mg effervescent ASA or 50 mg encapsulated sumatriptan or placebo. The primary endpoint was the percentage of patients with complete remission of the 3 accompanying symptoms nausea, photophobia and phonophobia within 2 h after intake of the study drug. 43.8% of patients treated with ASA, 43.7% of patients treated with sumatriptan and 30.9% of patients treated with placebo showed complete remission of all 3 accompanying symptoms (p < 0.05 for ASA and sumatriptan vs. placebo). Both active treatments were superior to placebo regarding the individual symptoms photophobia and phonophobia, but not for nausea. The percentage of patients with reduction in headache severity from moderate or severe to mild or no pain (secondary objective) was 49.3% for ASA, 48.8% for sumatriptan and 32.9% for placebo. All active treatments were superior to placebo (p < 0.05). 25.3, 24.4 and 14.5% of patients treated with ASA, sumatriptan or placebo were pain free at 2 h. Drug-related adverse events were reported in 3.9, 4.7 and 6.7% of patients treated with placebo, ASA or sumatriptan. The study showed that administration of effervescent ASA leads to remission of the migraine symptoms nausea, photophobia and phonophobia, reduces migraine headache and is comparable to sumatriptan.
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Clinical Conference Lysine-acetylsalicylic acid in acute migraine attacks. 1999
Limmroth V, May A, Diener H. · Neurologische Universitätsklinik Essen, Germany. · Eur Neurol. · Pubmed #10023111 No free full text.
Abstract: Vasoconstrictive agents have been widely used in the treatment of migraine. These types of drugs have various side effects and are not suitable for many patients. Due to nausea or vomiting, nonoral treatment is often required, but only a few nonvasoconstrictive drugs exist in a parenteral form and are suitable for the treatment of acute migraine in the emergency setting. In a randomized, double-blind, crossover trial we evaluated the efficacy of 1,000 mg lysine-acetylsalicylic acid i.v. (LAS) compared to 0.5 mg ergotamine s.c. in 56 patients (112 attacks) with acute migraine. To gain further insight into the possible role of vasoconstriction, blood flow velocities (BFV) were measured in intra- and extracranial arteries using duplex sonography and transcranial Doppler sonography. Both agents were equally potent in relieving headache. Intravenous LAS resulted in a significantly faster relief and had fewer side effects. LAS had no effect on BFV. Ergotamine increased BFV in the middle cerebral artery only. No correlation was found between changes in BFV and the relief of headache. This is the first trial to compare the intravenous formulation of LAS in the treatment of migraine with another antimigraine medication and suggests that it is an effective and safe drug for the parenteral treatment of acute migraine attacks.
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Article Are cortical spreading depression and headache in migraine causally linked? 2009
Wolthausen J, Sternberg S, Gerloff C, May A. · Department of Neurology, University of Hamburg, Hamburg, Germany. · Cephalalgia. · Pubmed #19025548 No free full text.
Abstract: During the past few decades, much controversy has surrounded the pathophysiology of migraine. Cortical spreading depression (CSD) is widely accepted as the neuronal process underlying visual auras. It has been proposed that CSD can also cause the headaches, at least in migraine with aura. We describe three patients, each fulfilling the International Headache Society criteria for migraine with aura, who suffered from headaches 6-10 days per month. Two patients were treated with flunarizine and the third patient with topiramate for the duration of 4 months. All patients reported that aura symptoms resolved completely, whereas the migraine headache attacks persisted or even increased. These observations question the theory that CSD (silent or not) is a prerequisite for migraine headaches.
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Article Migraine-like headache in intracranial haemorrhage is alleviated by sumatriptan and almotriptan. 2008
Jürgens TP, Busch V, Schmidt-Wilcke T, Schuierer G, Leinisch E, May A. · Department of Neurology, University of Regensburg, Regensburg, Germany. · Cephalalgia. · Pubmed #18201253 No free full text.
This publication has no abstract.
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Article Subtle grey matter changes between migraine patients and healthy controls. 2008
Schmidt-Wilcke T, Gänssbauer S, Neuner T, Bogdahn U, May A. · Department of Neurology, University of Regensburg, Regensburg, Germany. · Cephalalgia. · Pubmed #17986275 No free full text.
Abstract: Local morphological alterations of the brain have recently been detected in cluster headache and chronic tension-type headache, but not in migraine. We investigated 35 patients suffering from migraine and compared them with 31 healthy controls with no headache history. Using magnetic resonance imaging and voxel based morphometry, we found a significant decrease of grey matter in areas ascribable to the transmission of pain (cingulate cortex), but not in areas specific for migraine, such as the brainstem. Our data are in line with recent findings in chronic pain states, such as chronic phantom pain and chronic back pain. We suggest that the grey matter change in migraine patients is the consequence of frequent nociceptive input and should thus be reversible when migraine attacks cease.
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