Peter J Goadsby

King's College London, Londinium, England, United Kingdom

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Publications (252)1626.47 Total impact

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    ABSTRACT: Nausea is a common and disabling symptom of migraine. The origin of nausea is not well understood although functional connections between trigeminal neurons and the nucleus tractus solitarius may explain occurrence of nausea with pain. However, nausea occurs as a premonitory symptom in about a quarter of patients, suggesting that a primary brain alteration unrelated to the experience of pain may be the reason for nausea. We performed positron emission tomography scans with H215O PET in premonitory phase of nitroglycerin-induced migraine and compared patients with and without nausea. The results showed activation in rostral dorsal medulla and periaqueductal grey (PAG) in the nausea group, which was absent in the no nausea group. The rostral dorsal medullary area included the nucleus tractus solitarius, dorsal motor nucleus of the vagus nerve and the nucleus ambiguus, all of which are thought to be involved in brain circuits mediating nausea. The results demonstrate that nausea can occur as a premonitory symptom in migraine, independent of pain and trigeminal activation. This is associated with activation of brain structures known to be involved in nausea. We conclude that nausea is a centrally driven symptom in migraine.
    The journal of headache and pain. 12/2014; 15(1):84.
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    ABSTRACT: To examine the effect of the orexinergic blockade with a dual orexin receptor antagonist (DORA) on experimental models of peripheral and central trigeminal as well as cortical activation relevant to migraine and migraine aura. In this study we used a precursor of suvorexant, a dual orexin receptor antagonist #12 (DORA-12) in established experimental in vivo models of dural trigeminovascular nociception in rat. Neurogenic dural vasodilation and electrophysiological recordings of second order trigeminocervical neurons were used to study trigeminal nociceptive mechanisms directly. KCl-evoked cortical spreading depression was also used as a surrogate for migraine aura. Neurogenically-induced vasodilation of the middle meningeal artery, caused by nociceptive activation of peripheral afferent projections of the trigeminal nerve, was attenuated by intravenous DORA-12 (1mgkg(-1)). Second-order trigeminocervical complex neuronal activity was significantly inhibited by intravenous DORA-12 (1mgkg(-1)). DORA-12 significantly reduced susceptibility to KCl-evoked cortical spreading depression. The study provides the first direct evidence, that simultaneous antagonism on both orexin receptors is able to attenuate trigeminal nociceptive activity as well as to induce an elevation of the threshold for the induction of a cortical spreading depression (CSD). In the clinical context, these data imply that targeting the hypothalamic orexinergic system may offer an entirely novel mechanism for the preventive treatment of migraine with and without aura. Copyright © 2014. Published by Elsevier Inc.
    Neurobiology of Disease 11/2014; · 5.62 Impact Factor
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    ABSTRACT: Background Calcitonin gene-related peptide (CGRP) is crucial in the pathophysiology of migraine. We assessed the safety, tolerability, and efficacy of ALD403, a genetically engineered humanised anti-CGRP antibody, for migraine prevention. Methods In this randomised, double-blind, placebo-controlled, exploratory, proof-of-concept phase 2 trial, patients aged 18–55 years with five to 14 migraine days per 28-day period were randomly assigned (1:1) via an interactive web response system to receive an intravenous dose of ALD403 1000 mg or placebo. Site investigators, patients, and the sponsor were masked to treatment allocation during the study. The primary objective was to assess safety at 12 weeks after infusion. The primary efficacy endpoint was the change from baseline to weeks 5–8 in the frequency of migraine days, as recorded in patient electronic diaries. Patients were followed up until 24 weeks for exploratory safety and efficacy analyses. Safety and efficacy analyses were done by intention to treat. This study is registered with, NCT01772524. Findings Between Jan 28, 2013, and Dec 23, 2013, of 174 patients randomly assigned at 26 centres in the USA, 163 received either ALD403 (n=81) or placebo (n=82). Adverse events were experienced by 46 (57%) of 81 patients in the ALD403 group and 43 (52%) of 82 in the placebo group. The most frequent adverse events were upper respiratory tract infection (placebo 6 [7%] patients vs ALD403 7 [9%] patients), urinary tract infection (4 [5%] vs 1 [1%]), fatigue (3 [4%] vs 3 [4%]), back pain (4 [5%] vs 3 [4%]), arthralgia (4 [5%] vs 1 [1%]), and nausea and vomiting (2 [2%] vs 3 [4%]). Six serious adverse events were reported by three patients and were judged to be unrelated to study drug: in the ALD403 group, one patient had four serious adverse events and one had one serious adverse event, and in the placebo group, one patient had one serious adverse event. There were no differences in vital signs or laboratory safety data between the two treatment groups. The mean change in migraine days between baseline and weeks 5–8 was −5·6 (SD 3·0) for the ALD403 group compared with −4·6 (3·6) for the placebo group (difference −1·0, 95% CI −2·0 to 0·1; one-sided p=0·0306). Interpretation No safety concerns were noted with an intravenous dose of ALD403 1000 mg. This study also provides preliminary evidence for the efficacy of ALD403 in the preventive treatment of migraine in patients with a high monthly frequency of migraine days. Funding Alder Biopharmaceuticals.
    The Lancet. Neurology. 10/2014;
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    ABSTRACT: Background Migraine remains poorly treated, with few effective preventive drugs available. We assessed the safety and efficacy of LY2951742, a fully humanised monoclonal antibody to calcitonin gene-related peptide, for migraine prevention. Methods We did a randomised, double-blind, placebo-controlled, phase 2 proof-of-concept study at 35 centres in the USA. Patients aged 18–65 years with four to 14 migraine headache days per month were randomly assigned (1:1) to LY2951742 or placebo by a computerised randomisation scheme. LY2951742 (150 mg) or placebo were given as a subcutaneous injection once every 2 weeks for 12 weeks. The primary endpoint was the mean change in number of migraine headache days per 28-day period assessed at 9–12 weeks. Safety was assessed over 24 weeks, including the 12-week treatment period and the subsequent 12 weeks after study drug administration. Patients and treating investigators were masked to treatment allocation. Analyses were by intention to treat. A mixed-effects model of repeated measures was used, including patient baseline value, treatment, visit, and treatment-by-visit interaction as fixed effects, and patients as random effects. Safety measures were analysed according to the treatment received. This study has been completed and is registered with, NCT01625988. Findings Between July 31, 2012, and Sept 18, 2013, 218 patients were randomly assigned to LY2951742 (n=108, but one patient withdrew before treatment) or placebo (n=110). The mean change from baseline to week 12 in the number of migraine headache days was −4·2 (SD 3·1; 62·5% decrease) in the LY2951742 group compared with −3·0 (SD 3·0; 42·3% decrease) in the placebo group (least-squares mean difference −1·2, 90% CI −1·9 to −0·6; p=0·0030). Adverse events that occurred more frequently with LY2951742 than with placebo included injection site pain, erythema, or both (21 [20%] of 107 vs seven [6%] of 110), upper respiratory tract infections (18 [17%] vs ten [9%]), and abdominal pain (six [6%] vs three [3%]). There were two serious adverse events reported in the treatment arm and four in the placebo arm, none of which were deemed to be related to the study drug. Interpretation These results provide preliminary evidence that LY2951742 might be beneficial in migraine prevention and provide support for the role of calcitonin gene-related peptide in the pathogenesis of migraine. Further controlled studies are needed to assess the safety and efficacy of monoclonal calcitonin gene-related peptide antibodies for the preventive treatment of migraine. Funding Arteaus Therapeutics.
    The Lancet Neurology 09/2014; · 23.92 Impact Factor
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    ABSTRACT: Pituitary adenylate cyclase activating peptide (PACAP) is found in human trigeminocervical complex and can trigger migraine. PACAP levels were measured using a sensitive radioimmunoassay. Stimulation of the superior sagittal sinus (SSS) in cat elevated PACAP levels in cranial blood. Patients with moderate or severe migraine headache had elevated PACAP in the external jugular vein during headache (n = 15), that was reduced 1 h after treatment with sumatriptan 6 mg (n = 11), and further reduced interictally (n = 9). The data suggest PACAP, or its receptors, are a promising target for migraine therapeutics.
    Annals of Clinical and Translational Neurology. 09/2014;
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    Peter J Goadsby
    The journal of headache and pain. 08/2014; 15(1):53.
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    ABSTRACT: To evaluate whether the calcitonin gene-related peptide (CGRP) receptor antagonist telcagepant might be effective for migraine prevention.
    Neurology 08/2014; · 8.30 Impact Factor
  • Amy A Gelfand, Peter J Goadsby
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    ABSTRACT: Medication overuse is not uncommon among children and adolescents with primary headache disorders. Medication overuse in adults is associated with increased headache frequency and reduced effectiveness of acute and preventive medications. These issues probably exist in children. While withdrawal of overused medications is generally recommended, it may not result in improved headache frequency in all patients. This review summarizes what is known about predicting the response to medication withdrawal. Strategies for managing children and adolescents with medication overuse are also offered.
    Current Pain and Headache Reports 07/2014; 18(7):428. · 1.67 Impact Factor
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    ABSTRACT: Objective To assess the relationship between the phenotype of the “visual snow” syndrome, comorbid migraine, and typical migraine aura on a clinical basis and using functional brain imaging.Background Patients with “visual snow” suffer from continuous TV-static-like tiny flickering dots in the entire visual field. Most patients describe a syndrome with additional visual symptoms of the following categories: palinopsia (“afterimages” and “trailing”), entopic phenomena arising from the optic apparatus itself (floaters, blue field entoptic phenomenon, photopsia, self-light of the eye), photophobia, nyctalopia (impaired night vision), as well as the non-visual symptom tinnitus. The high prevalence of migraine and typical migraine aura in this population has led to the assumption that “visual snow” is caused by persistent migraine aura. Due to the lack of objective measures, alternative diagnoses are malingering or a psychogenic disorder.Methods(1) The prevalence of additional visual symptoms, tinnitus, and comorbid migraine as well as typical migraine aura was assessed in a prospective semi-structured telephone interview of patients with “visual snow.” Correlations were calculated using standard statistics with P < .05 being considered statistically significant. (2) Areas with increased brain metabolism in a group of “visual snow” patients in comparison to healthy controls were identified using [18F]-2-fluoro-2-deoxy-D-glucose positron emission tomography and statistical parametric mapping (SPM8 with whole brain analysis; statistical significance was defined by P < .001 uncorrected for multiple comparisons).Results(1) Of 120 patients with “visual snow,” 70 patients also had migraine and 37 had typical migraine aura. Having comorbid migraine was associated with an increased likelihood of having palinopsia (odds ratio [OR] 2.8; P = .04 for “afterimages” and OR 2.6; P = .01 for “trailing”), spontaneous photopsia (OR 2.9; P = .004), photophobia (OR 3.2; P = .005), nyctalopia (OR 2.7; P = .01), and tinnitus (OR 2.9; P = .006). Typical migraine aura was associated with an increased likelihood of spontaneous photopsia (OR 2.4; P = .04). (2) After adjusting for typical migraine aura, comparison of 17 “visual snow” patients with 17 age and gender matched controls showed brain hypermetabolism in the right lingual gyrus (Montreal Neurological Institute coordinates 16-78-5; kE = 101; ZE = 3.41; P < .001) and the left cerebellar anterior lobe adjacent to the left lingual gyrus (Montreal Neurological Institute coordinates -12-62-9; kE = 152; ZE = 3.28; P = .001).Conclusions—Comorbid migraine aggravates the clinical phenotype of the “visual snow” syndrome by worsening some of the additional visual symptoms and tinnitus. This might bias studies on “visual snow” by migraineurs offering study participation more likely than non-migraineurs due to a more severe clinical presentation. The independence of entoptic phenomena from comorbid migraine indicates “visual snow” is the main determinant. The hypermetabolic lingual gyrus confirms a brain dysfunction in patients with “visual snow.” The metabolic pattern differs from interictal migraine with some similarities to migrainous photophobia. The findings support the view that “visual snow,” migraine, and typical migraine aura are distinct syndromes with shared pathophysiological mechanisms that need to be addressed in order to develop rational treatment strategies for this disabling condition.
    Headache The Journal of Head and Face Pain 06/2014; · 2.94 Impact Factor
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    ABSTRACT: Background Crowned dens syndrome (CDS) is a clinical-radiological entity characterized by acute attacks of neck pain with fever, rigidity, general signs of inflammation, and calcification of the periodontoid articular structures.Methods Case report with 42 months follow-up.Case descriptionAn 81-year-old man, who had never suffered from headache before July 2010, developed strictly left-sided headaches. The pain was restricted to the left side of the scalp and felt more intense in the frontal area. The intensity was moderate to high with a throbbing quality. The pain had an orthostatic component and was worsened by neck hyperextension and Valsalva maneuvers. Neurological and general examinations were normal, except for a reduced range of motion of the neck. He was prescribed indomethacin orally 25 mg t.i.d. and had a partial response. After a week, he was given a dosage of 50 mg t.i.d. with complete remission of the pain. Brain magnetic resonance imaging was normal, while an magnetic resonance imaging of the cervical spine showed a non-homogeneous mass behind the odontoid process of C2, narrowing the subarachnoid space in C1, stretching the posterior longitudinal ligament, and touching the left vertebral artery. A computed tomography scan showed calcification of the soft tissue around the odontoid process and a thickening of the left C2 root. After 4 months, the indomethacin dosage was reduced step-by-step. Indomethacin was discontinued in March 2012. Since then, the headache has not recurred.DiscussionWe here present the case of a patient with headache and radiological findings of crowned dens. However, the clinical presentation differed from previous CDS cases in the literature in that the pain was unilateral with frontal localization and throbbing quality, as well as an orthostatic component and lack of either fever or inflammatory signs. The differential diagnosis also includes a remitting form of hemicrania continua, presenting with an atypical presentation, with neuroimaging incidental finding of CDS.Conclusion This case widens the spectrum of the clinical presentation of crowned dens, a condition that should be kept in mind in cases of unilateral headache in older patients.
    Headache The Journal of Head and Face Pain 06/2014; · 2.94 Impact Factor
  • Amy A Gelfand, Peter J Goadsby, I Elaine Allen
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    ABSTRACT: Infant colic is a common and distressing disorder of early infancy. Its etiology is unknown, making treatment challenging. Several articles have suggested a link to migraine.
    Cephalalgia : an international journal of headache. 05/2014;
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    ABSTRACT: Medical students routinely have triggers, notably stress and irregular sleep, which are typically associated with migraine. We hypothesized that they may be at higher risk to manifest migraine. We aimed to determine the prevalence of migraine among medical students in Kuwait University.
    The journal of headache and pain. 05/2014; 15(1):26.
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    ABSTRACT: Patients with 'visual snow' report continuous tiny dots in the entire visual field similar to the noise of an analogue television. As they frequently have migraine as a comorbidity with ophthalmological, neurological and radiological studies being normal, they are offered various diagnoses, including persistent migraine aura, post-hallucinogen flashback, or psychogenic disorder. Our aim was to study patients with 'visual snow' to characterize the phenotype. A three-step approach was followed: (i) a chart review of patients referred to us identified 22 patients with 'visual snow'. Fifteen had additional visual symptoms, and 20 patients had comorbid migraine, five with aura; (ii) to identify systematically additional visual symptoms, an internet survey (n = 275) of self-assessed 'visual snow' subjects done by Eye On Vision Foundation was analysed. In two random samples from 235 complete data sets, the same eight additional visual symptoms were present in >33% of patients: palinopsia (trailing and afterimages), entoptic phenomena (floaters, blue field entoptic phenomenon, spontaneous photopsia, self-light of the eye), photophobia, and nyctalopia (impaired night vision); and (iii) a prospective semi-structured telephone interview in a further 142 patients identified 78 (41 female) with confirmed 'visual snow' and normal ophthalmological exams. Of these, 72 had at least three of the additional visual symptoms from step (ii). One-quarter of patients had 'visual snow' as long as they could remember, whereas for the others the mean age of onset was 21 ± 9 years. Thirty-two patients had constant visual symptoms, whereas the remainder experienced either progressive or stepwise worsening. Headache was the most frequent symptom associated with the beginning or a worsening of the visual disturbance (36%), whereas migraine aura (seven patients) and consumption of illicit drugs (five, no hallucinogens) were rare. Migraine (59%), migraine with aura (27%), anxiety and depression were common comorbidities over time. Eight patients had first degree relatives with visual snow. Clinical investigations were not contributory. Only a few treatment trials have been successful in individual patients. Our data suggest that 'visual snow' is a unique visual disturbance clinically distinct from migraine aura that can be disabling for patients. Migraine is a common concomitant although standard migraine treatments are often unhelpful. 'Visual snow' should be considered a distinct disorder and systematic studies of its clinical features, biology and treatment responses need to be commenced to begin to understand what has been an almost completely ignored problem.
    Brain 03/2014; · 10.23 Impact Factor
  • Peter J. Goadsby
    Headache The Journal of Head and Face Pain 03/2014; 54(3). · 2.94 Impact Factor
  • Jan Hoffmann, Simon Akerman, Peter J Goadsby
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    ABSTRACT: Anticonvulsants represent one of the main substance classes used for the preventive treatment of migraine. Efficacy has been demonstrated in randomized placebo-controlled trials for topiramate and valproic acid including divalproex sodium. In the case of topiramate, efficacy has recently been proven for chronic migraine and even medication overuse headache, questioning the established concept of medication withdrawal. However, preventive treatment with anticonvulsants is frequently hampered by side effects that occasionally require treatment discontinuation. In addition, these data indicate that some anticonvulsant drugs are effective in migraine, while a number are clearly not useful. Effective anticonvulsants, such as topiramate and valproate, target nociceptive trigeminovascular and trigeminothalamic dural pathways or mechanisms involved in cortical spreading depression. Dissecting out how the anticonvulsants that do not work differ mechanistically from those that do will almost certainly provide avenues through which one can develop new treatments to bring to patients with migraine.
    Expert Review of Clinical Pharmacology 02/2014;
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    ABSTRACT: Migraine patients have an increased photic-driving response. This 'H-response' (HR) has potential diagnostic value but it is time consuming. The aim of the study was to establish a fast and standardized test for the study of migraine biology and treatment. We studied 11 migraine patients and 11 matched control participants. We used stroboscope flashes with a 'chirp'-like linear frequency-increase from 10 to 40 Hz. EEG was recorded from occipital electrodes. Power spectral density was calculated for the stimulus response and corrected for baseline. An HR-estimator was calculated as the average power between 18 and 26 Hz in the stimulation-frequency window. There was a significant difference for single ( P < 0.05) and for 10 averaged recordings ( P < 0.01) between migraineurs and controls, and a high inter-test reliability (Cronbach's alpha = 0.94). Chirp-like stimulation to study the H-response is reliable and efficient and might therefore have a potential for acute interventional studies in migraine research.
    Cephalalgia 01/2014; · 3.49 Impact Factor
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    ABSTRACT: This study was designed to evaluate the traditional advice to headache sufferers to avoid all triggers (‘Avoidance’), and a novel approach to trigger management (Learning to Cope with Triggers – ‘LCT’) that included graduated exposure to selected triggers to promote desensitization. Individuals (84F, 43M) with migraine and/or tension-type headache were assigned randomly to one of four groups: Waiting-list (Waitlist); Avoidance; Avoidance combined with cognitive behavior therapy (Avoid + CBT); and LCT. Changes in headaches and medication consumption (in parentheses) from pre- to post-treatment were (a minus sign indicates improvement): Waitlist, +11.0% (+15.4%); Avoidance, -13.2% (-9.0%); Avoid + CBT, -30.0% (-19.4%); and LCT, -35.9% (-27.9%). Avoidance did not differ significantly from Waitlist on headaches or medication use, but LCT differed significantly from Waitlist on both measures. Avoid + CBT significantly differed from Waitlist on headaches but not medication consumption. In summary, the study failed to find support for the standard approach to trigger management of advising avoidance, but LCT emerged as a promising strategy. LCT resulted in greater improvement than the other three conditions on all measures of headaches and medication consumption, and was the only treatment condition that significantly differed from the waiting-list control condition in terms of treatment responder rate (50% or greater reduction in headaches) and medication consumption.
    Behaviour Research and Therapy. 01/2014;
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    ABSTRACT: Familial hemiplegic migraine type 1 (FHM-1) is a monogenic subtype of migraine with aura caused by missense mutations in the CACNA1A gene, which encodes the pore-forming α1 subunit of voltage-gated neuronal CaV2.1 (P/Q-type) calcium channels. Transgenic knock-in mice expressing the CACNA1A R192Q mutation that causes FHM-1 in patients show a greater susceptibility to cortical spreading depression, the likely underlying mechanism of human migraine aura. The aim of this study was to compare neuronal activation within the trigeminal pain pathways in response to nociceptive trigeminovascular stimulation in wild-type and R192Q knock-in mice. After sham surgery or electrical stimulation of the superior sagittal sinus for two hours, or stimulation preceded by treatment with naratriptan, mice underwent intracardiac perfusion, and the brain, including the brainstem, was removed. Fos expression was measured in the trigeminocervical complex (TCC) and the lateral (ventroposteromedial, ventrolateral), medial (parafascicular, centromedian) and posterior thalamic nuclei. In the TCC of wild-type animals, the number of Fos-positive cells increased significantly following dural stimulation compared to the sham control group (P<0.001) and decreased after naratriptan treatment (P<0.05). In R192Q knock-in mice, there was no significant difference between the stimulated and sham (P=0.10) or naratriptan pre-treated groups (P=0.15). The number of Fos-positive cells in the R192Q stimulated group was significantly lower compared to the wild-type stimulated mice (P<0.05). In the thalamus, R192Q mice tended to be more sensitive to stimulation compared to the sham control in the medial and posterior nucleus, and between the two strains of stimulated animals there was a significant difference in the centromedian (P<0.005), and posterior nuclei (P<0.05). The present study suggests that the FHM-1 mutation affects more rostral brain structures in this experimental paradigm, which may offer a novel perspective on possible differential effects of mutations causing migraine in terms of phenotype-genotype correlations.
    Neurobiology of Disease 12/2013; · 5.62 Impact Factor
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    ABSTRACT: Sinusitis is the most frequent misdiagnosis given to patients with migraine.Therefore we decided to estimate the frequency of misdiagnosis of sinusitis among migraine patients. The study included migraine patients with a past history of sinusitis. All included cases fulfilled the International Classification of Headache Disorders, 3rd edition (ICHD-III- beta) criteria. We excluded patients with evidence of sinusitis within the past 6 months of evaluation. Demographic data, headache history, medical consultation, and medication intake for headache and effectiveness of therapy before and after diagnosis were collected. A total of 130 migraine patients were recruited. Of these patients 106 (81.5%) were misdiagnosed as sinusitis. The mean time delay of migraine diagnosis was (7.75 +/- 6.29, range 1 to 38 years). Chronic migraine was significantly higher (p < 0.02) in misdiagnosed patients than in patients with proper diagnosis. Medication overuse headache (MOH) was reported only in patients misdiagnosed as sinusitis. The misdiagnosed patients were treated either medically 87.7%, or surgically12.3% without relieve of their symptoms in 84.9% and 76.9% respectively. However, migraine headache improved in 68.9% after proper diagnosis and treatment. Many migraine patients were misdiagnosed as sinusitis. Strict adherence to the diagnostic criteria will prevent the delay in migraine diagnosis and help to prevent chronification of the headache and possible MOH.
    The Journal of Headache and Pain 12/2013; 14(1):97. · 2.78 Impact Factor
  • Jan Hoffmann, Peter J Goadsby
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    ABSTRACT: Migraine is a common and highly disabling neurological disorder. Despite the complexity of its pathophysiology, substantial advances have been achieved over the past 20 years in its understanding, as well as the development of pharmacological treatment options. The development of serotonin 5-HT1B/1D receptor agonists ("triptans") substantially improved the acute treatment of migraine attacks. However, many migraineurs do not respond satisfactorily to triptans and cardiovascular co-morbidities limit their use in a significant number of patients. As migraine is increasingly considered to be a disorder of the brain, and preclinical and clinical data indicate that the observed vasodilation is merely an epiphenomenon, research has recently focused on the development of neurally acting compounds that lack vasoconstrictor properties. This review highlights the most important pharmacological targets for which compounds have been developed that are highly likely to enter or have already advanced into clinical trials for the acute and preventive treatment of migraine. In this context, preclinical and clinical data on compounds acting on calcitonin gene-related peptide or its receptor, the 5-HT1F receptor, nitric oxide synthase, and acid-sensing ion channel blockers are discussed.
    CNS Drugs 12/2013; · 4.38 Impact Factor

Publication Stats

7k Citations
1,626.47 Total Impact Points


  • 2014
    • King's College London
      Londinium, England, United Kingdom
    • ICL
      Londinium, England, United Kingdom
  • 2008–2014
    • University of California, San Francisco
      • Department of Neurology
      San Francisco, California, United States
    • University of Bristol
      • School of Social and Community Medicine
      Bristol, England, United Kingdom
    • The Bracton Centre, Oxleas NHS Trust
      Дартфорде, England, United Kingdom
  • 2013
    • IRCCS Fondazione Istituto Neurologico Nazionale C. Mondino
      • Headache Science Center
      Ticinum, Lombardy, Italy
    • SwedishAmerican
      Rockford, Illinois, United States
    • Thomas Jefferson University
      • Department of Neurology
      Philadelphia, PA, United States
    • Children's Hospital of Michigan
      Detroit, Michigan, United States
  • 2012
    • SickKids
      Toronto, Ontario, Canada
    • University Hospital Essen
      Essen, North Rhine-Westphalia, Germany
    • University of Surrey
      • Surrey Sleep Research Centre (SSRC)
      Guildford, ENG, United Kingdom
  • 2010–2012
    • CSU Mentor
      • Department of Neurology
      Long Beach, California, United States
    • Washington University in St. Louis
      San Luis, Missouri, United States
    • University of Iowa
      Iowa City, Iowa, United States
    • University of Oxford
      Oxford, England, United Kingdom
    • Lund University
      Lund, Skåne, Sweden
  • 2011
    • University of Alberta
      • Division of Neurology
      Edmonton, Alberta, Canada
    • Michigan Headache and Neurological Institute
      Ann Arbor, Michigan, United States
    • UCL Eastman Dental Institute
      Londinium, England, United Kingdom
    • Cedars-Sinai Medical Center
      • Cedars Sinai Medical Center
      Los Angeles, CA, United States
  • 2009–2011
    • University Medical Center Schleswig-Holstein
      Kiel, Schleswig-Holstein, Germany
  • 2007–2010
    • Albert Einstein College of Medicine
      • Department of Neuroradiology
      New York City, NY, United States
  • 2006–2008
    • Ghent University
      • Neurology
      Gent, VLG, Belgium
  • 2002–2007
    • University College London
      • Institute of Neurology
      London, ENG, United Kingdom
    • Kansas City VA Medical Center
      Kansas City, Missouri, United States
  • 2003–2005
    • Mayo Foundation for Medical Education and Research
      • Department of Neurology
      Scottsdale, AZ, United States
    • University of Münster
      • Department of Neurology
      Münster, North Rhine-Westphalia, Germany
  • 2004
    • WWF United Kingdom
      Londinium, England, United Kingdom
      • Department of Neurology
      Athínai, Attica, Greece