50 results on '"Snoer, Agneta"'
Search Results
2. Compensated Hypogonadism Identified in Males with Cluster Headache: A Prospective Case‐Controlled Study
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Petersen, Anja S., primary, Kristensen, David M., additional, Westgate, Connar S. J., additional, Folkmann‐Hansen, Thomas, additional, Lund, Nunu, additional, Barloese, Mads, additional, Søborg, Marie‐Louise K., additional, Snoer, Agneta, additional, Johannsen, Trine H., additional, Frederiksen, Hanne, additional, Juul, Anders, additional, and Jensen, Rigmor H., additional
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- 2024
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3. Compensated Hypogonadism Identified in Males with Cluster Headache:A Prospective Case-Controlled Study
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Petersen, Anja S., Kristensen, David M., Westgate, Connar S. J., Folkmann-Hansen, Thomas, Lund, Nunu, Barloese, Mads, Søborg, Marie Louise K., Snoer, Agneta, Johannsen, Trine H., Frederiksen, Hanne, Juul, Anders, Jensen, Rigmor H., Petersen, Anja S., Kristensen, David M., Westgate, Connar S. J., Folkmann-Hansen, Thomas, Lund, Nunu, Barloese, Mads, Søborg, Marie Louise K., Snoer, Agneta, Johannsen, Trine H., Frederiksen, Hanne, Juul, Anders, and Jensen, Rigmor H.
- Abstract
Objective Androgens have been hypothesized to be involved in the pathophysiology of cluster headache due to the male predominance, but whether androgens are altered in patients with cluster headache remains unclear. Methods We performed a prospective, case-controlled study in adult males with cluster headache. Sera were measured for hormones including testosterone, luteinizing hormone (LH), and sex hormone-binding globulin in 60 participants with episodic cluster headache (during a bout and in remission), 60 participants with chronic cluster headache, and 60 age- and sex-matched healthy controls. Free testosterone (fT) was calculated according to the Vermeulen equation. Shared genetic risk variants were assessed between cluster headache and testosterone concentrations. Results The mean fT/LH ratio was reduced by 35% (95% confidence interval [CI]: 21%–47%, p < 0.0001) in patients with chronic cluster headache and by 24% (95% CI: 9%–37%, p = 0.004) in patients with episodic cluster headache compared to controls after adjusting for age, sleep duration, and use of acute medication. Androgen concentrations did not differ between bouts and remissions. Furthermore, a shared genetic risk allele, rs112572874 (located in the intron of the microtubule associated protein tau (MAPT) gene on chromosome 17), between fT and cluster headache was identified. Interpretation Our results demonstrate that the male endocrine system is altered in patients with cluster headache to a state of compensated hypogonadism, and this is not an epiphenomenon associated with sleep or the use of acute medication. Together with the identified shared genetic risk allele, this may suggest a pathophysiological link between cluster headache and fT. ANN NEUROL 2024, Objective: Androgens have been hypothesized to be involved in the pathophysiology of cluster headache due to the male predominance, but whether androgens are altered in patients with cluster headache remains unclear. Methods: We performed a prospective, case-controlled study in adult males with cluster headache. Sera were measured for hormones including testosterone, luteinizing hormone (LH), and sex hormone-binding globulin in 60 participants with episodic cluster headache (during a bout and in remission), 60 participants with chronic cluster headache, and 60 age- and sex-matched healthy controls. Free testosterone (fT) was calculated according to the Vermeulen equation. Shared genetic risk variants were assessed between cluster headache and testosterone concentrations. Results: The mean fT/LH ratio was reduced by 35% (95% confidence interval [CI]: 21%–47%, p < 0.0001) in patients with chronic cluster headache and by 24% (95% CI: 9%–37%, p = 0.004) in patients with episodic cluster headache compared to controls after adjusting for age, sleep duration, and use of acute medication. Androgen concentrations did not differ between bouts and remissions. Furthermore, a shared genetic risk allele, rs112572874 (located in the intron of the microtubule associated protein tau (MAPT) gene on chromosome 17), between fT and cluster headache was identified. Interpretation: Our results demonstrate that the male endocrine system is altered in patients with cluster headache to a state of compensated hypogonadism, and this is not an epiphenomenon associated with sleep or the use of acute medication. Together with the identified shared genetic risk allele, this may suggest a pathophysiological link between cluster headache and fT. ANN NEUROL 2024.
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- 2024
4. Plasma levels of VIP are not elevated during PACAP- and VIP-induced cluster headache attacks: an exploratory study
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Deligianni, Christina, primary, Pellesi, Lanfranco, additional, Chaudhry, Basit Ali, additional, Haulund Vollesen, Anne Luise, additional, Snoer, Agneta Henriette, additional, Hannibal, Jens, additional, Jensen, Rigmor Højland, additional, and Ashina, Messoud, additional
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- 2023
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5. Plasma levels of VIP are not elevated during PACAP- and VIP-induced cluster headache attacks:an exploratory study
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Deligianni, Christina, Pellesi, Lanfranco, Chaudhry, Basit Ali, Haulund Vollesen, Anne Luise, Snoer, Agneta Henriette, Hannibal, Jens, Jensen, Rigmor Højland, Ashina, Messoud, Deligianni, Christina, Pellesi, Lanfranco, Chaudhry, Basit Ali, Haulund Vollesen, Anne Luise, Snoer, Agneta Henriette, Hannibal, Jens, Jensen, Rigmor Højland, and Ashina, Messoud
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Background: Pituitary adenylate cyclase-activating peptide (PACAP) and vasoactive intestinal peptide (VIP) provoked cluster headache attacks in individuals with episodic cluster headache during their active phase and individuals with chronic cluster headache. In this study, we investigated whether infusions of PACAP and VIP caused alterations in plasma levels of VIP and their potential contribution to induced cluster headache attacks. Methods: Participants received either PACAP or VIP infusion for 20 min on 2 separate days with an interval of at least 7 days in between. Blood collection was performed at T0, T20, T30, and T90. Plasma levels of VIP were measured using a validated radioimmunoassay method. Results: Blood samples were collected from participants with episodic cluster headache in the active phase (eCHA, n = 14), remission (eCHR, n = 15), and from participants with chronic cluster headache (cCH, n = 15). Baseline levels of VIP did not differ among the three groups (p = 0.1161). During PACAP infusion, mixed-effects analysis revealed a significant increase in plasma levels of VIP in eCHA (p = 0.0300) and eCHR (p = 0.0058) but not in cCH (p = 0.2930). We found no difference in the increase of plasma VIP levels between patients who developed PACAP38- or VIP-induced attacks. Conclusion: Cluster headache attacks induced by PACAP38 or VIP infusion are not associated with changes in plasma levels of VIP. Further studies are needed to investigate the role of VIP and the parasympathetic system in cluster headache. Clinical trial registration: The parent study is registered at ClinicalTrials.gov (NCT03814226).
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- 2023
6. The influence of lifestyle and gender on cluster headache
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Lund, Nunu L.T., Snoer, Agneta H., and Jensen, Rigmor H.
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- 2019
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7. Guidelines of the International Headache Society for controlled clinical trials in cluster headache
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Schoenen, Jean, Snoer, Agneta Henriette, Brandt, Roemer B, Fronczek, Rolf, Wei, Diana Y, Chung, Chin-Sang, Diener, Hans Christoph, Dodick, David W, Fontaine, Denys, Goadsby, Peter J, Matharu, Manjit Singh, May, Arne, McGinley, James S, Tepper, Stewart J, Jensen, Rigmor Højland, Ferrari, Michel D, Terwindt, Gisela, Tassorelli, Cristina, Ashina, Messoud, Leroux, Elizabeth, Lipton, Richard B, Pozo-Rosich, Patricia, Wang, Shuu-Jiun, Christensen, Marie Deen, Martini, Daniela, and van den Hoek, Thomas
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Medizin ,Headache ,cluster headache ,Humans ,classifications ,Neurology (clinical) ,General Medicine ,Controlled Clinical Trials as Topic ,Guidelines ,ICHD-3 - Abstract
In 1995, a committee of the International Headache Society developed and published the first edition of the Guidelines for Controlled Trials of Drugs in Cluster Headache. These have not been revised. With the emergence of new medications, neuromodulation devices and trial designs, an updated version of the International Headache Society Guidelines for Controlled Clinical Trials in Cluster Headache is warranted. Given the scarcity of evidence-based data for cluster headache therapies, the update is largely consensus-based, but takes into account lessons learned from recent trials and demands by patients. It is intended to apply to both drug and neuromodulation treatments, with specific proposals for the latter when needed. The primary objective is to propose a template for designing high quality, state-of-the-art, controlled clinical trials of acute and preventive treatments in episodic and chronic cluster headache. The recommendations should not be regarded as dogma and alternative solutions to particular methodological problems should be explored in the future and scientifically validated.
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- 2022
8. Cluster headache beyond the pain phase: A prospective study of 500 attacks
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Snoer, Agneta, Lund, Nunu, Beske, Rasmus, Hagedorn, Andreas, Jensen, Rigmor Højland, and Barloese, Mads
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- 2018
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9. Corrigendum to: PACAP38- and VIP-induced cluster headache attacks are not associated with changes of plasma CGRP or markers of mast cell activation
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Pellesi, Lanfranco, primary, Chaudhry, Basit Ali, additional, Vollesen, Anne Luise Haulund, additional, Snoer, Agneta Henriette, additional, Baumann, Katrine, additional, Skov, Per Stahl, additional, Jensen, Rigmor Højland, additional, and Ashina, Messoud, additional
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- 2022
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10. Intranasal treatment of cluster headache:A response
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Petersen, Anja S., Barloese, Mads C.J., Holm, Per, Jensen, Rigmor H., Snoer, Agneta H., Petersen, Anja S., Barloese, Mads C.J., Holm, Per, Jensen, Rigmor H., and Snoer, Agneta H.
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- 2022
11. Intranasal ketamine for acute cluster headache attacks—Results from a proof-of-concept open-label trial
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Petersen, Anja S., Pedersen, Adam S., Barloese, Mads C.J., Holm, Per, Pedersen, Ole, Jensen, Rigmor H., Snoer, Agneta H., Petersen, Anja S., Pedersen, Adam S., Barloese, Mads C.J., Holm, Per, Pedersen, Ole, Jensen, Rigmor H., and Snoer, Agneta H.
- Abstract
Objective: To investigate the safety and efficacy of intranasal ketamine for the treatment of a single cluster headache (CH) attack. Background: Acute treatment options for patients with CH who have an insufficient response to oxygen and triptans are limited. Intranasal ketamine has anecdotally been successful in treating a CH attack. Methods: We conducted an open-label pilot study enrolling 23 patients with chronic CH (International Classification of Headache Disorders, 3rd edition), and of these, 20 patients treated a single CH attack with intranasal ketamine. Under in-hospital observation, patients received 15 mg of intranasal ketamine every 6 min a maximum of five times. The primary endpoint was a 50% reduction in pain intensity within 15 min after initiating treatment. Results: The primary endpoint was not met; 15 min after the first ketamine administration, the mean reduction in pain intensity was 1.1 (95% confidence interval [CI]: −0.6 to 2.7, p = 0.188) on the numeric rating scale (NRS), equivalent to a 15% reduction in pain intensity. However, 30 min after the first application, the pain intensity was reduced by 59% on an 11-point NRS (mean difference: 4.3, 95% CI: 2.4–6.2, p < 0.001, N = 16) and 11 out of 16 (69%) scored 4 or below on the NRS. Four patients received rescue medication 15 min after the first ketamine application and were therefore excluded from the analysis at 30 min. Half of the patients preferred ketamine to oxygen and/or sumatriptan injection. No serious adverse events were identified during the trial. Conclusion: Intranasal ketamine may be an effective acute treatment for CH at 30 min but should be tested in a larger controlled design. Patients and physicians should be conscious of the abuse potential of ketamine.
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- 2022
12. The economic and personal burden of cluster headache:a controlled cross-sectional study
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Petersen, Anja Sofie, Lund, Nunu, Snoer, Agneta, Jensen, Rigmor Højland, Barloese, Mads, Petersen, Anja Sofie, Lund, Nunu, Snoer, Agneta, Jensen, Rigmor Højland, and Barloese, Mads
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Background: Cluster headache is a less-prevalent primary headache disorder but is overrepresented with regards to use of health care and social services. More insight into the socioeconomic impact is required. Methods: We investigated both the personal and societal disease burden and cost in 400 patients with well-classified cluster headache according to the ICHD-criteria and 200 sex- and age matched controls. All participants completed a cross sectional questionnaire and semi-structured interview. Results: Patients with chronic cluster headache constituted 146 out of 400 (37%). Overall, restriction in personal and/or professional life was reported by 94% of patients during attack periods. Even in remission, nine times as many episodic patients rated their health as poor/very poor compared to controls (9% vs 1%, p = 0.002). For chronic patients, the odds of rating health as good/very good were ten times lower compared to controls (OR:10.10, 95%CI:5.29–18.79. p < 0.001) and three times lower compared to episodic patients in remission (OR:3.22, 95%CI:1.90–5.47, p < 0.001). Additionally, chronic cluster headache patients were 5 times more likely to receive disability pension compared to episodic (OR:5.0, 95%CI:2.3–10.9, p < 0.001). The mean direct annual costs amounted to 9,158€ and 2,763€ for chronic and episodic patients, respectively (p < 0.001). We identified a substantial loss of productivity due to absence from work resulting in a higher indirect cost of 11,809 €/year/patient in the chronic population and 3,558 €/year/patient in the episodic population. Presenteeism could not be quantified but productivity was reduced in patients by 65% in periods with attacks compared to controls. Conclusion: Cluster headache has a major negative impact on personal life, self-perceived health, and societal cost. Patients with the chronic variant are vastly more burdened. Patients with the episodic form were still markedly affected during the remission period. This
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- 2022
13. PACAP38- and VIP-induced cluster headache attacks are not associated with changes of plasma CGRP or markers of mast cell activation
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Pellesi, Lanfranco, Chaudhry, Basit Ali, Vollesen, Anne Luise Haulund, Snoer, Agneta Henriette, Baumann, Katrine, Skov, Per Stahl, Jensen, Rigmor Højland, Ashina, Messoud, Pellesi, Lanfranco, Chaudhry, Basit Ali, Vollesen, Anne Luise Haulund, Snoer, Agneta Henriette, Baumann, Katrine, Skov, Per Stahl, Jensen, Rigmor Højland, and Ashina, Messoud
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Background Pituitary adenylate cyclase-activating polypeptide-38 (PACAP38) and vasoactive intestinal polypeptide can provoke cluster headache attacks in up to half of cluster headache patients in their active phase. At present, it is unknown whether provoked attacks are mediated via calcitonin gene-related peptide or mast cell activation. Methods All enrolled patients with cluster headache were randomly allocated to receive a continuous infusion of either PACAP38 (10 pmol/kg/min) or vasoactive intestinal polypeptide (8 pmol/kg/min) over 20 min. We collected clinical data and measured plasma levels of calcitonin gene-related peptide and markers of mast cell activation (tryptase and histamine) at fixed time points: at baseline (T0), at the end of the infusion (T20), 10 min after the infusion (T30), and 70 min after the infusion (T90). Results Blood was collected from episodic cluster headache patients in active phase (n = 14), episodic cluster headache patients in remission (n = 15), and chronic cluster headache patients (n = 15). At baseline, plasma levels of calcitonin gene-related peptide, tryptase, and histamine were not different among the three study groups. Plasma levels of calcitonin gene-related peptide (p = 0.7074), tryptase (p = 0.6673), or histamine (p = 0.4792) remained unchanged during provoked attacks compared to attack-free patients. Conclusion Cluster headache attacks provoked by either PACAP38 or vasoactive intestinal polypeptide were not accompanied by alterations of plasma calcitonin gene-related peptide, tryptase or histamine. The provoked attacks may not be mediated by calcitonin gene-related peptide or mast cell activation.
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- 2022
14. Intranasal treatment of cluster headache: A response
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Petersen, Anja S., primary, Barloese, Mads C. J., additional, Holm, Per, additional, Jensen, Rigmor H., additional, and Snoer, Agneta H., additional
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- 2022
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15. PACAP38- and VIP-induced cluster headache attacks are not associated with changes of plasma CGRP or markers of mast cell activation
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Pellesi, Lanfranco, primary, Chaudhry, Basit Ali, additional, Vollesen, Anne Luise Haulund, additional, Snoer, Agneta Henriette, additional, Baumann, Katrine, additional, Skov, Per Stahl, additional, Jensen, Rigmor Højland, additional, and Ashina, Messoud, additional
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- 2021
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16. Intranasal ketamine for acute cluster headache attacks—Results from a proof‐of‐concept open‐label trial
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Petersen, Anja S., primary, Pedersen, Adam S., additional, Barloese, Mads C. J., additional, Holm, Per, additional, Pedersen, Ole, additional, Jensen, Rigmor H., additional, and Snoer, Agneta H., additional
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- 2021
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17. sj-pdf-1-cep-10.1177_0333102421989255 - Supplemental material for Prevalence of pre-cluster symptoms in episodic cluster headache: Is it possible to predict an upcoming bout?
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Pedersen, Adam Sebastian, Snoer, Agneta, Barloese, Mads, Petersen, Anja, and Jensen, Rigmor Højland
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FOS: Psychology ,FOS: Clinical medicine ,170199 Psychology not elsewhere classified ,110319 Psychiatry (incl. Psychotherapy) ,110306 Endocrinology ,111599 Pharmacology and Pharmaceutical Sciences not elsewhere classified ,110904 Neurology and Neuromuscular Diseases ,Neuroscience - Abstract
Supplemental material, sj-pdf-1-cep-10.1177_0333102421989255 for Prevalence of pre-cluster symptoms in episodic cluster headache: Is it possible to predict an upcoming bout? by Adam Sebastian Pedersen, Agneta Snoer, Mads Barloese, Anja Petersen and Rigmor Højland Jensen in Cephalalgia
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- 2021
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18. Prevalence of pre-cluster symptoms in episodic cluster headache:Is it possible to predict an upcoming bout?
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Pedersen, Adam Sebastian, Snoer, Agneta, Barloese, Mads, Petersen, Anja, Jensen, Rigmor Højland, Pedersen, Adam Sebastian, Snoer, Agneta, Barloese, Mads, Petersen, Anja, and Jensen, Rigmor Højland
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Background: Early symptoms prior to a cluster headache bout have been reported to occur days or weeks before the actual beginning of the cluster headache bouts. This study aimed to describe the prevalence of pre-cluster (premonitory) symptoms and examine the predictability of an upcoming cluster headache bout. Methods: 100 patients with episodic cluster headache were included in this retrospective cross-sectional study. All patients underwent a semi-structured interview including 25 questions concerning pre-cluster symptoms. Results: Pre-cluster symptoms were reported by 86% of patients with a mean of 6.8 days (interquartile range 3–14) preceding the bout. An ability to predict an upcoming bout was reported by 57% with a mean 4.6 days (interquartile range 2–7) before the bout. Occurrence of shadow attacks was associated with increased predictability (odds ratio: 3.06, confidence interval: 1.19–7.88, p-value = 0.020). In remission periods, 58% of patients reported mild cluster headache symptoms and 53% reported occurrence of single shadow attacks. Conclusions: The majority of episodic cluster headache patients experienced pre-cluster symptoms, and more than half could predict an upcoming bout, suggesting the significant potential of early intervention. Furthermore, the experience of mild cluster headache symptoms and infrequent shadow attacks in remission periods is common and suggest an underlying pathophysiology extending beyond the cluster headache bouts.
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- 2021
19. The effect of pituitary adenylate cyclase-activating peptide-38 and vasoactive intestinal peptide in cluster headache
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Vollesen, Anne Luise H., Snoer, Agneta, Chaudhry, Basit, Petersen, Anja Sofie, Hagedorn, Andreas, Hoffmann, Jan, Jensen, Rigmor H., Ashina, Messoud, Vollesen, Anne Luise H., Snoer, Agneta, Chaudhry, Basit, Petersen, Anja Sofie, Hagedorn, Andreas, Hoffmann, Jan, Jensen, Rigmor H., and Ashina, Messoud
- Abstract
Background: Previously reported increases in serum levels of vasodilating neuropeptides pituitary adenylate cyclase-activating peptide-38 (PACAP38) and vasoactive intestinal peptide (VIP) during attacks of cluster headache could indicate their involvement in cluster headache attack initiation. We investigated the attack-inducing effects of PACAP38 and vasoactive intestinal peptide in cluster headache, hypothesising that PACAP38, but not vasoactive intestinal peptide, would induce cluster-like attacks in episodic active phase and chronic cluster headache patients. Methods: In a double-blind crossover study, 14 episodic cluster headache patients in active phase, 15 episodic cluster headache patients in remission phase and 15 chronic cluster headache patients were randomly allocated to receive intravenous infusion of PACAP38 (10 pmol/kg/min) or vasoactive intestinal peptide (8 pmol/kg/min) over 20 min on two study days separated by at least 7 days. We recorded headache intensity, incidence of cluster-like attacks, cranial autonomic symptoms and vital signs using a questionnaire (0–90 min). Results: In episodic cluster headache active phase, PACAP38 induced cluster-like attacks in 6/14 patients and vasoactive intestinal peptide induced cluster-like attacks in 5/14 patients (p = 1.000). In chronic cluster headache, PACAP38 and vasoactive intestinal peptide both induced cluster-like attacks in 7/15 patients (p = 0.765). In episodic cluster headache remission phase, neither PACAP38 nor vasoactive intestinal peptide induced cluster-like attacks. Conclusions: Contrary to our hypothesis, attack induction was lower than expected and roughly equal by PACAP38 and vasoactive intestinal peptide in episodic active phase and chronic cluster headache patients, which contradicts the PAC1-receptor as being solely responsible for attack induction. Trial registration: clinicaltrials.gov (identifier NCT03814226).
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- 2020
20. S100B and NSE in Cluster Headache – Evidence for Glial Cell Activation?
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Snoer, Agneta H., Vollesen, Anne Luise H., Beske, Rasmus Paulin, Guo, Song, Hoffmann, Jan, Jørgensen, Niklas R., Martinussen, Torben, Ashina, Messoud, Jensen, Rigmor H., Snoer, Agneta H., Vollesen, Anne Luise H., Beske, Rasmus Paulin, Guo, Song, Hoffmann, Jan, Jørgensen, Niklas R., Martinussen, Torben, Ashina, Messoud, and Jensen, Rigmor H.
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Objective: Neuronal-specific enolase (NSE) and protein S100B have gained considerable interest as the markers of CNS injury, glial cell activation, and/or blood-brain barrier (BBB) disruption. No studies have investigated NSE and S100B in cluster headache (CH), but these biomarkers could contribute to the understanding of CH. Methods: Patients with episodic CH in bout (eCHa), in remission (eCHr), and chronic CH (cCH) were included in this randomized, double-blind, placebo-controlled, 2-way cross-over provocation study carried out at the Danish Headache Center. The primary endpoints included (1) differences of NSE and S100B in between groups (eCHa, eCHr, and cCH) at baseline; (2) differences over time in plasma concentrations of NSE and S100B between patient developing an attack and those who did not; (3) differences in plasma concentrations over time of NSE and S100B between active day and placebo day. Baseline findings were compared to the historical data on migraine patients and healthy controls and presented with means ± SD. Results: Nine eCHa, 9 eCHr, and 13 cCH patients completed the study and blood samples from 11 CGRP-induced CH attacks were obtained. There were no differences in NSE levels between CH groups at baseline, but CH patients in active disease phase had higher levels compared with 32 migraine patients (9.1 ± 2.2 µg/L vs 6.0 ± 2.2 µg/L, P <.0001) and 6 healthy controls (9.1 ± 2.2 µg/L vs 7.3 ± 2.0 µg/L, P =.007). CGRP-infusion caused no NSE changes and, but a slight, non-significant, increase in NSE was seen in patients who reported a CGRP-induced CH attack (2.39 µg/L, 95% Cl [−0.26, 3.85], P =.061). At baseline S100B levels in eCHa patients were higher compared to cCH patients (0.06 ± 0.02 µg/L vs 0.04 ± 0.02 µg/L, P =.018). Infusion of CGRP and CGRP-induced attacks did not change S100B levels. Apart from induced CH-attacks no other adverse events were noted. Conclusions: At baseline eCHa patients had higher S100B plasma levels than cCH patie
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- 2020
21. Serotonin and Neuropeptides in Blood From Episodic and Chronic Migraine and Cluster Headache Patients in Case-Control and Case-Crossover Settings:A Systematic Review and Meta-Analysis
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Frederiksen, Simona D., Bekker-Nielsen Dunbar, Maria, Snoer, Agneta H., Deen, Marie, Edvinsson, Lars, Frederiksen, Simona D., Bekker-Nielsen Dunbar, Maria, Snoer, Agneta H., Deen, Marie, and Edvinsson, Lars
- Abstract
Objective: The aim of this systematic review and meta-analysis (SR-MA) was to identify signaling molecule profiles and blood-derived biomarkers in migraine and cluster headache (CH) patients. Background: Currently no migraine and CH valid biomarkers are available. Blood tests based on biomarker profiles have been used to gather information about the nervous system. Such tests have not yet been established within the primary headache field. Methods: Case-control and case-crossover studies investigating whole blood, plasma, and serum were identified worldwide. The qualitative synthesis focused on 9 signaling molecules (serotonin [5-HT], calcitonin gene-related peptide [CGRP], endothelin-1 [ET-1], neurokinin A, neurokinin B, neuropeptide Y, pituitary adenylate cyclase-activating peptide 38 [PACAP-38], substance P (SP), and vasoactive intestinal peptide) and the quantitative synthesis on 5-HT and CGRP (≥5 comparisons available). The meta-analysis was conducted using standard and 3-level random effect models. Results: Fifty-four eligible studies were identified (87.0% migraine, 9.3% CH, 3.7% migraine, and CH), and 2768 headache patients and 1165 controls included. Comparable fluctuations of 5-HT, CGRP, ET-1, PACAP-38, and SP in blood were generally observed between migraine and CH. Significant findings were observed for some subgroups and strata, for example, higher interictal and ictal 5-HT venous blood levels (ratio of means = 1.32, 95% CI: 1.08; 1.61; ratio of means = 1.23, 95% CI: 1.01; 1.49) in episodic migraine with aura with a female-dominated case group, higher interictal CGRP blood levels in episodic migraine (ratio of means = 1.63, 95% CI: 1.18; 2.26), and chronic migraine (ratio of means = 1.89, 95% CI: 1.33; 2.68), and higher ictal CGRP blood levels (ratio of means = 1.35, 95% CI: 1.09; 1.68) in episodic migraine were observed. In most subgroups, the quantitative synthesis revealed a high degree of heterogeneity between studies in part explained by the blo
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- 2020
22. Prevalence of pre-cluster symptoms in episodic cluster headache: Is it possible to predict an upcoming bout?
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Pedersen, Adam Sebastian, primary, Snoer, Agneta, additional, Barloese, Mads, additional, Petersen, Anja, additional, and Jensen, Rigmor Højland, additional
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- 2021
- Full Text
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23. The effect of pituitary adenylate cyclase-activating peptide-38 and vasoactive intestinal peptide in cluster headache
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Vollesen, Anne Luise H, primary, Snoer, Agneta, additional, Chaudhry, Basit, additional, Petersen, Anja Sofie, additional, Hagedorn, Andreas, additional, Hoffmann, Jan, additional, Jensen, Rigmor H, additional, and Ashina, Messoud, additional
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- 2020
- Full Text
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24. S100B and NSE in Cluster Headache – Evidence for Glial Cell Activation?
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Snoer, Agneta H., primary, Vollesen, Anne Luise H., additional, Beske, Rasmus Paulin, additional, Guo, Song, additional, Hoffmann, Jan, additional, Jørgensen, Niklas R., additional, Martinussen, Torben, additional, Ashina, Messoud, additional, and Jensen, Rigmor H., additional
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- 2020
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25. Serotonin and Neuropeptides in Blood From Episodic and Chronic Migraine and Cluster Headache Patients in Case‐Control and Case‐Crossover Settings: A Systematic Review and Meta‐Analysis
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Frederiksen, Simona D., primary, Bekker‐Nielsen Dunbar, Maria, additional, Snoer, Agneta H., additional, Deen, Marie, additional, and Edvinsson, Lars, additional
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- 2020
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26. Cluster headache is associated with unhealthy lifestyle and lifestyle-related comorbid diseases:Results from the Danish Cluster Headache Survey
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Lund, Nunu, Petersen, Anja, Snoer, Agneta, Jensen, Rigmor H., Barloese, Mads, Lund, Nunu, Petersen, Anja, Snoer, Agneta, Jensen, Rigmor H., and Barloese, Mads
- Abstract
Aim: To compare the prevalence of unhealthy lifestyle factors and comorbid disorders in cluster headache patients with headache-free controls, in order to discuss pathophysiology and possible consequences. Methods: Cluster headache patients from the Danish cluster headache survey aged 18–65 years, diagnosed according to ICHD-II, were compared to sex- and age-matched headache-free controls. Participants completed questionnaires and structured interviews. Results: A total of 400 cluster headache patients and 200 controls participated. Patients had a more unhealthy lifestyle compared with controls in the form of current and current/former smoking (48.3% vs. 9.0%, p < 0.001 and 74.5% vs. 30.0%, p < 0.001, respectively), higher average alcohol intake per week (98.2 grams vs. 77.9 grams, p = 0.033) and BMI (26.1 vs. 24.2 kg/m 2 , p < 0.001), whereas coffee and energy drink consumption was equally distributed. Further, lifestyle-related, psychiatric and pain-related diseases were much more prevalent in patients compared with controls, except for diabetes. Sub-group analyses revealed that current/former smokers had a worse clinical presentation than never smokers. Conclusion: Unhealthy lifestyle factors and lifestyle-related diseases were more prevalent in cluster headache patients compared to controls. As lifestyle-related diseases might have serious consequences in the management of cluster headache, it is key to inform patients at an early time point about the possible risks of their lifestyle choices.
- Published
- 2019
27. S100B and NSE in cluster headache -evidence for glial cell activation?
- Author
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Snoer, Agneta, Vollesen, Anne Luise H., Beske, Rasmus P., Guo, Song, Hoffmann, Jan, Fahrenkrug, Jan, Joergesen, Niklas R., Martinussen, Torben, Jensen, Rigmor H., Ashina, Messoud, Snoer, Agneta, Vollesen, Anne Luise H., Beske, Rasmus P., Guo, Song, Hoffmann, Jan, Fahrenkrug, Jan, Joergesen, Niklas R., Martinussen, Torben, Jensen, Rigmor H., and Ashina, Messoud
- Published
- 2019
28. Verapamil and Cluster Headache:Still a Mystery. A Narrative Review of Efficacy, Mechanisms and Perspectives
- Author
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Petersen, Anja S., Barloese, Mads C.J., Snoer, Agneta, Soerensen, Anne Mette S., Jensen, Rigmor H., Petersen, Anja S., Barloese, Mads C.J., Snoer, Agneta, Soerensen, Anne Mette S., and Jensen, Rigmor H.
- Abstract
Objective: A evaluation of the effect of verapamil and other calcium channel blockers in cluster headache (CH) treatment and an investigation of possible effect mechanisms. Background: Verapamil has been used in the prevention of CH for almost 3 decades, however, the mode of action and therapeutic target is still unknown. Methods: A Pubmed search was conducted: “Verapamil”[Mesh] and “Cluster Headache”[Mesh]. We identified 5 relevant studies for CH. Publications were included if they made a substantial contribution within 3 prespecified areas: Efficacy (randomized controlled-trials or open labels studies), safety, and mechanism of effect. Results: Clinical effect: Clinical preventive treatment of CH with verapamil is based on 2 randomized controlled studies and 3 open-label studies. In total, 183 CH patients participated. Verapamil 360 mg/day was used in both controlled studies. Half of the chronic patients experienced benefit from verapamil treatment and the attack burden of episodic patients was, on average, reduced by 1 attack/day. Open-label studies support a dose-dependent level of efficacy. Mechanism of effect: Human and animal studies indicate that verapamil may exert its effect by modulating circadian rhythms, perhaps in central pacemakers, and/or by affecting release of calcitonin gene-related peptide. Conclusion: Verapamil appears to be an effective prophylactic drug in the treatment of CH and despite the scarcity of controlled trials, it is still the drug of choice. A chronotherapeutic approach might increase the effect. More basic and pharmacokinetic research is needed before the mechanism can be fully understood.
- Published
- 2019
29. The spectrum of cluster headache:A case report of 4600 attacks
- Author
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Hagedorn, Andreas, Snoer, Agneta, Jensen, Rigmor, Haddock, Bryan, Barloese, Mads, Hagedorn, Andreas, Snoer, Agneta, Jensen, Rigmor, Haddock, Bryan, and Barloese, Mads
- Abstract
Introduction: Knowledge of the clinical features of cluster headache is mainly based on retrospective and cross-sectional studies. Here, we present a case of a chronic cluster headache patient who prospectively recorded timing and clinical features of all attacks for 6 years, aiming to describe the clinical spectrum and timing of cluster headache symptoms experienced and to identify daily and/or seasonal rhythmicity. Methods: Registration of attack timing, duration, associated symptoms and severity was done prospectively on a smartphone application. Pain severity was recorded on a 0–10 scale. Attacks were divided into mild, moderate, severe, and very severe. We analysed diurnal rhythmicity by multimodal Gaussian analysis and spectral analysis. Results: In total, 4600 attacks were registered (mean duration 39.3 (SD 18.5) min. Mean severity 3.6 (SD 1.28)). Mild attacks accounted for 14.2%, moderate 65.7%, severe 16.9% and very severe 3.2% of all attacks. Nocturnal attacks were more severe than daytime attacks. The number of autonomic symptoms and duration of attacks increased with pain severity. Peak chronorisk (risk of attacks occurring according to hour of day) was at 12.48 in the registration period. Over time, circadian rhythmicity and attack frequency varied. Conclusion: Clinical characteristics of cluster headache attacks can vary greatly within the individual patient. Clinicians attempting to personalise the administration of preventive treatment should pay notice to the variation over time in diurnal rhythmicity. The recorded self-limiting mild attacks that do not fulfill the ICHD-3 criteria for a cluster headache attack warrant further investigation, as they could hold important information about disease activity.
- Published
- 2019
30. Sleep in cluster headache revisited: Results from a controlled actigraphic study
- Author
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Lund, Nunu LT, Snoer, Agneta Henriette, Jennum, Poul Jørgen, Jensen, Rigmor Højland, Barloese, Mads Christian J, Lund, Nunu LT, Snoer, Agneta Henriette, Jennum, Poul Jørgen, Jensen, Rigmor Højland, and Barloese, Mads Christian J
- Published
- 2019
31. Calcitonin-gene related peptide and disease activity in cluster headache
- Author
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Snoer, Agneta, Vollesen, Anne Luise H., Beske, Rasmus P., Guo, Song, Hoffmann, Jan, Fahrenkrug, Jan, Jørgensen, Niklas Rye, Martinussen, Torben, Jensen, Rigmor H., Ashina, Messoud, Snoer, Agneta, Vollesen, Anne Luise H., Beske, Rasmus P., Guo, Song, Hoffmann, Jan, Fahrenkrug, Jan, Jørgensen, Niklas Rye, Martinussen, Torben, Jensen, Rigmor H., and Ashina, Messoud
- Published
- 2019
32. Verapamil and Cluster Headache: Still a Mystery. A Narrative Review of Efficacy, Mechanisms and Perspectives
- Author
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Petersen, Anja S., primary, Barloese, Mads C. J., additional, Snoer, Agneta, additional, Soerensen, Anne Mette S., additional, and Jensen, Rigmor H., additional
- Published
- 2019
- Full Text
- View/download PDF
33. The spectrum of cluster headache: A case report of 4600 attacks
- Author
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Hagedorn, Andreas, primary, Snoer, Agneta, additional, Jensen, Rigmor, additional, Haddock, Bryan, additional, and Barloese, Mads, additional
- Published
- 2019
- Full Text
- View/download PDF
34. Calcitonin gene-related peptide and disease activity in cluster headache
- Author
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Snoer, Agneta, primary, Vollesen, Anne Luise H, additional, Beske, Rasmus P, additional, Guo, Song, additional, Hoffmann, Jan, additional, Fahrenkrug, Jan, additional, Jørgensen, Niklas Rye, additional, Martinussen, Torben, additional, Jensen, Rigmor H, additional, and Ashina, Messoud, additional
- Published
- 2019
- Full Text
- View/download PDF
35. Sleep in cluster headache revisited: Results from a controlled actigraphic study
- Author
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Lund, Nunu LT, primary, Snoer, Agneta Henriette, additional, Jennum, Poul Jørgen, additional, Jensen, Rigmor Højland, additional, and Barloese, Mads Christian J, additional
- Published
- 2018
- Full Text
- View/download PDF
36. Alterations in CGRP and PACAP38 levels in cluster headache
- Author
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Snoer, Agneta, Vollesen, Anne Luise Haulund, Beske, Rasmus Paulin, Guo, Song, Hoffmann, Jan, Fahrenkrug, Jan, Jorgesen, Niklas Rye, Martinussen, Torben, Jensen, Rigmor Hojland, Ashina, Messoud, Snoer, Agneta, Vollesen, Anne Luise Haulund, Beske, Rasmus Paulin, Guo, Song, Hoffmann, Jan, Fahrenkrug, Jan, Jorgesen, Niklas Rye, Martinussen, Torben, Jensen, Rigmor Hojland, and Ashina, Messoud
- Published
- 2018
37. Cluster headache beyond the pain phase:A prospective study of 500 attacks
- Author
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Snoer, Agneta, Lund, Nunu, Beske, Rasmus, Hagedorn, Andreas, Jensen, Rigmor Højland, Barloese, Mads, Snoer, Agneta, Lund, Nunu, Beske, Rasmus, Hagedorn, Andreas, Jensen, Rigmor Højland, and Barloese, Mads
- Abstract
OBJECTIVE: To describe the nature, prevalence, and duration of symptoms in the preictal, ictal, and postictal phases of cluster headache (CH) attacks.METHODS: Fifty-seven patients with episodic or chronic CH participated in this prospective, observational study. In a questionnaire concerning 33 CH and migraine-related symptoms, patients reported the clinical features of up to 10 CH attacks/patient. The questionnaire was divided into 3 sections: a preictal phase, ictal phase, and postictal phase. For each phase, patients documented whether the given symptom was present, and if possible estimated the duration of the symptom.RESULTS: In total, 500 CH attack descriptions were obtained. In the preictal phase, general symptoms (most frequently concentration difficulties, restlessness, and mood changes) occurred 20 minutes prior to 46.0% of attacks. Local painful and autonomic symptoms were observed 10 minutes prior to 54.6% and 35% of attacks, respectively. Postictally, pain and autonomic symptoms resolved over 20 minutes, leaving patients with fatigue (36.2%), decreased energy (39.0%), and concentration difficulties (27.6%), lasting a median of 60 minutes.CONCLUSIONS: Preictal and postictal symptoms are very frequent in CH, demonstrating that CH attacks are not composed of a pain phase alone. Since the origin of CH attacks is unresolved, studies of preictal and postictal symptoms could contribute to the understanding of CH pathophysiology and, potentially, early, abortive treatment strategies.
- Published
- 2018
38. Pre-attack signs and symptoms in cluster headache:Characteristics and time profile
- Author
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Snoer, Agneta, Lund, Nunu, Beske, Rasmus, Jensen, Rigmor, Barloese, Mads, Snoer, Agneta, Lund, Nunu, Beske, Rasmus, Jensen, Rigmor, and Barloese, Mads
- Abstract
Introduction In contrast to the premonitory phase of migraine, little is known about the pre-attack (prodromal) phase of a cluster headache. We aimed to describe the nature, prevalence, and duration of pre-attack symptoms in cluster headache. Methods Eighty patients with episodic cluster headache or chronic cluster headache, according to ICHD-3 beta criteria, were invited to participate. In this observational study, patients underwent a semi-structured interview where they were asked about the presence of 31 symptoms/signs in relation to a typical cluster headache attack. Symptoms included previously reported cluster headache pre-attack symptoms, premonitory migraine symptoms and accompanying symptoms of migraine and cluster headache. Results Pre-attack symptoms were reported by 83.3% of patients, with an average of 4.25 (SD 3.9) per patient. Local and painful symptoms, occurring with a median of 10 minutes before attack, were reported by 70%. Local and painless symptoms and signs, occurring with a median of 10 minutes before attack, were reported by 43.8% and general symptoms, occurring with a median of 20 minutes before attack, were reported by 62.5% of patients. Apart from a dull/aching sensation in the attack area being significantly ( p < 0.05) more frequent among men and episodic patients, compared with women and chronic patients respectively, no other differences in the prevalence of pre-attack symptoms were identified between groups. Conclusion Pre-attack symptoms are frequent in cluster headache. Since the origin of cluster headache attacks is still unresolved, studies of pre-attack symptoms could contribute to the understanding of cluster headache pathophysiology. Furthermore, identification and recognition of pre-attack symptoms could potentially allow earlier abortive treatment.
- Published
- 2018
39. Effect of Infusion of Calcitonin Gene-Related Peptide on Cluster Headache Attacks
- Author
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Vollesen, Anne Luise H., primary, Snoer, Agneta, additional, Beske, Rasmus P., additional, Guo, Song, additional, Hoffmann, Jan, additional, Jensen, Rigmor H., additional, and Ashina, Messoud, additional
- Published
- 2018
- Full Text
- View/download PDF
40. Cluster headache is associated with unhealthy lifestyle and lifestyle-related comorbid diseases: Results from the Danish Cluster Headache Survey
- Author
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Lund, Nunu, primary, Petersen, Anja, additional, Snoer, Agneta, additional, Jensen, Rigmor H, additional, and Barloese, Mads, additional
- Published
- 2018
- Full Text
- View/download PDF
41. Pre-attack signs and symptoms in cluster headache: Characteristics and time profile
- Author
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Snoer, Agneta, primary, Lund, Nunu, additional, Beske, Rasmus, additional, Jensen, Rigmor, additional, and Barloese, Mads, additional
- Published
- 2017
- Full Text
- View/download PDF
42. Pre-attack signs and symptoms in cluster headache: Characteristics and time profile.
- Author
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Snoer, Agneta, Lund, Nunu, Beske, Rasmus, Jensen, Rigmor, and Barloese, Mads
- Subjects
- *
HEADACHE , *DISEASE duration , *EPISODIC memory , *DISEASE prevalence , *PATHOLOGICAL physiology , *SCIENTIFIC observation - Abstract
Introduction In contrast to the premonitory phase of migraine, little is known about the pre-attack (prodromal) phase of a cluster headache. We aimed to describe the nature, prevalence, and duration of pre-attack symptoms in cluster headache. Methods Eighty patients with episodic cluster headache or chronic cluster headache, according to ICHD-3 beta criteria, were invited to participate. In this observational study, patients underwent a semi-structured interview where they were asked about the presence of 31 symptoms/signs in relation to a typical cluster headache attack. Symptoms included previously reported cluster headache pre-attack symptoms, premonitory migraine symptoms and accompanying symptoms of migraine and cluster headache. Results Pre-attack symptoms were reported by 83.3% of patients, with an average of 4.25 (SD 3.9) per patient. Local and painful symptoms, occurring with a median of 10 minutes before attack, were reported by 70%. Local and painless symptoms and signs, occurring with a median of 10 minutes before attack, were reported by 43.8% and general symptoms, occurring with a median of 20 minutes before attack, were reported by 62.5% of patients. Apart from a dull/aching sensation in the attack area being significantly ( p < 0.05) more frequent among men and episodic patients, compared with women and chronic patients respectively, no other differences in the prevalence of pre-attack symptoms were identified between groups. Conclusion Pre-attack symptoms are frequent in cluster headache. Since the origin of cluster headache attacks is still unresolved, studies of pre-attack symptoms could contribute to the understanding of cluster headache pathophysiology. Furthermore, identification and recognition of pre-attack symptoms could potentially allow earlier abortive treatment. [ABSTRACT FROM AUTHOR]
- Published
- 2018
- Full Text
- View/download PDF
43. Transient global amnesia after cerebral angiography still occurs: Case report and literature review
- Author
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Foss-Skiftesvik, Jon, primary, Snoer, Agneta Henriette, additional, Wagner, Aase, additional, and Hauerberg, John, additional
- Published
- 2014
- Full Text
- View/download PDF
44. Cluster headache is associated with unhealthy lifestyle and lifestyle-related comorbid diseases: Results from the Danish Cluster Headache Survey.
- Author
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Lund, Nunu, Petersen, Anja, Snoer, Agneta, Jensen, Rigmor H., and Barloese, Mads
- Subjects
- *
CLUSTER headache , *UNHEALTHY lifestyles , *DISEASES - Abstract
Aim: To compare the prevalence of unhealthy lifestyle factors and comorbid disorders in cluster headache patients with headache-free controls, in order to discuss pathophysiology and possible consequences.Methods: Cluster headache patients from the Danish cluster headache survey aged 18-65 years, diagnosed according to ICHD-II, were compared to sex- and age-matched headache-free controls. Participants completed questionnaires and structured interviews.Results: A total of 400 cluster headache patients and 200 controls participated. Patients had a more unhealthy lifestyle compared with controls in the form of current and current/former smoking (48.3% vs. 9.0%, p < 0.001 and 74.5% vs. 30.0%, p < 0.001, respectively), higher average alcohol intake per week (98.2 grams vs. 77.9 grams, p = 0.033) and BMI (26.1 vs. 24.2 kg/m2, p < 0.001), whereas coffee and energy drink consumption was equally distributed. Further, lifestyle-related, psychiatric and pain-related diseases were much more prevalent in patients compared with controls, except for diabetes. Sub-group analyses revealed that current/former smokers had a worse clinical presentation than never smokers.Conclusion: Unhealthy lifestyle factors and lifestyle-related diseases were more prevalent in cluster headache patients compared to controls. As lifestyle-related diseases might have serious consequences in the management of cluster headache, it is key to inform patients at an early time point about the possible risks of their lifestyle choices. [ABSTRACT FROM AUTHOR]- Published
- 2019
- Full Text
- View/download PDF
45. Guidelines of the International Headache Society for Controlled Clinical Trials in Cluster Headache.
- Author
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Schoenen J, Snoer AH, Brandt RB, Fronczek R, Wei DY, Chung CS, Diener HC, Dodick DW, Fontaine D, Goadsby PJ, Matharu MS, May A, McGinley JS, Tepper SJ, Jensen RH, and Ferrari MD
- Subjects
- Humans, Headache therapy, Controlled Clinical Trials as Topic, Cluster Headache drug therapy
- Abstract
In 1995, a committee of the International Headache Society developed and published the first edition of the Guidelines for Controlled Trials of Drugs in Cluster Headache. These have not been revised. With the emergence of new medications, neuromodulation devices and trial designs, an updated version of the International Headache Society Guidelines for Controlled Clinical Trials in Cluster Headache is warranted. Given the scarcity of evidence-based data for cluster headache therapies, the update is largely consensus-based, but takes into account lessons learned from recent trials and demands by patients. It is intended to apply to both drug and neuromodulation treatments, with specific proposals for the latter when needed. The primary objective is to propose a template for designing high quality, state-of-the-art, controlled clinical trials of acute and preventive treatments in episodic and chronic cluster headache. The recommendations should not be regarded as dogma and alternative solutions to particular methodological problems should be explored in the future and scientifically validated.
- Published
- 2022
- Full Text
- View/download PDF
46. PACAP38- and VIP-induced cluster headache attacks are not associated with changes of plasma CGRP or markers of mast cell activation.
- Author
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Pellesi L, Chaudhry BA, Vollesen ALH, Snoer AH, Baumann K, Skov PS, Jensen RH, and Ashina M
- Subjects
- Histamine, Humans, Pituitary Adenylate Cyclase-Activating Polypeptide, Tryptases, Vasoactive Intestinal Peptide, Calcitonin Gene-Related Peptide blood, Cluster Headache, Mast Cells
- Abstract
Background: Pituitary adenylate cyclase-activating polypeptide-38 (PACAP38) and vasoactive intestinal polypeptide can provoke cluster headache attacks in up to half of cluster headache patients in their active phase. At present, it is unknown whether provoked attacks are mediated via calcitonin gene-related peptide or mast cell activation., Methods: All enrolled patients with cluster headache were randomly allocated to receive a continuous infusion of either PACAP38 (10 pmol/kg/min) or vasoactive intestinal polypeptide (8 pmol/kg/min) over 20 min. We collected clinical data and measured plasma levels of calcitonin gene-related peptide and markers of mast cell activation (tryptase and histamine) at fixed time points: at baseline (T
0 ), at the end of the infusion (T20 ), 10 min after the infusion (T30 ), and 70 min after the infusion (T90 )., Results: Blood was collected from episodic cluster headache patients in active phase (n = 14), episodic cluster headache patients in remission (n = 15), and chronic cluster headache patients (n = 15). At baseline, plasma levels of calcitonin gene-related peptide, tryptase, and histamine were not different among the three study groups. Plasma levels of calcitonin gene-related peptide ( p = 0.7074), tryptase ( p = 0.6673), or histamine ( p = 0.4792) remained unchanged during provoked attacks compared to attack-free patients., Conclusion: Cluster headache attacks provoked by either PACAP38 or vasoactive intestinal polypeptide were not accompanied by alterations of plasma calcitonin gene-related peptide, tryptase or histamine. The provoked attacks may not be mediated by calcitonin gene-related peptide or mast cell activation. Trial Registration : The study is registered at ClinicalTrials.gov (NCT03814226).- Published
- 2022
- Full Text
- View/download PDF
47. Intranasal ketamine for acute cluster headache attacks-Results from a proof-of-concept open-label trial.
- Author
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Petersen AS, Pedersen AS, Barloese MCJ, Holm P, Pedersen O, Jensen RH, and Snoer AH
- Subjects
- Administration, Intranasal, Adult, Analgesics administration & dosage, Analgesics adverse effects, Chronic Disease, Female, Humans, Ketamine administration & dosage, Ketamine adverse effects, Male, Middle Aged, Pilot Projects, Proof of Concept Study, Treatment Outcome, Analgesics pharmacology, Cluster Headache drug therapy, Ketamine pharmacology
- Abstract
Objective: To investigate the safety and efficacy of intranasal ketamine for the treatment of a single cluster headache (CH) attack., Background: Acute treatment options for patients with CH who have an insufficient response to oxygen and triptans are limited. Intranasal ketamine has anecdotally been successful in treating a CH attack., Methods: We conducted an open-label pilot study enrolling 23 patients with chronic CH (International Classification of Headache Disorders, 3rd edition), and of these, 20 patients treated a single CH attack with intranasal ketamine. Under in-hospital observation, patients received 15 mg of intranasal ketamine every 6 min a maximum of five times. The primary endpoint was a 50% reduction in pain intensity within 15 min after initiating treatment., Results: The primary endpoint was not met; 15 min after the first ketamine administration, the mean reduction in pain intensity was 1.1 (95% confidence interval [CI]: -0.6 to 2.7, p = 0.188) on the numeric rating scale (NRS), equivalent to a 15% reduction in pain intensity. However, 30 min after the first application, the pain intensity was reduced by 59% on an 11-point NRS (mean difference: 4.3, 95% CI: 2.4-6.2, p < 0.001, N = 16) and 11 out of 16 (69%) scored 4 or below on the NRS. Four patients received rescue medication 15 min after the first ketamine application and were therefore excluded from the analysis at 30 min. Half of the patients preferred ketamine to oxygen and/or sumatriptan injection. No serious adverse events were identified during the trial., Conclusion: Intranasal ketamine may be an effective acute treatment for CH at 30 min but should be tested in a larger controlled design. Patients and physicians should be conscious of the abuse potential of ketamine., (© 2021 American Headache Society.)
- Published
- 2022
- Full Text
- View/download PDF
48. Frequent or chronic migraine negatively impacts personal, social and professional life.
- Author
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Snoer AH, Høst C, Dømgaard M, and Hansen JM
- Subjects
- Adult, Cohort Studies, Cross-Sectional Studies, Humans, Disabled Persons, Migraine Disorders
- Abstract
INTRODUCTION Migraine affects 16% of the population and is a leading cause of disability. We aimed to describe the treatment status and impact of migraine in a selected cohort of patients with ≥ 4 migraine days per month. METHODS The study was conducted as a large, cross-sectional, multi-country online survey of adults (≥ 18 years) with migraine. Data presented here stem from 306 Danish respondents. Pre-specified quotas were applied so that 90% of respondents had used preventive migraine treatment and 80% had one or more treatment failures. RESULTS The median number of headache days per months was 11.3 (8-17.8) and 89 (29%) of patients met the criteria for chronic migraine. Most patients (n = 213; 70%) had taken preventive treatment (PT) for their migraines and among these 170 (80%) had experienced at least one treatment failure. Ninety-four (44.1%) patients reported being dissatisfied or mostly dissatisfied with their PTs. A negative impact of migraine on either private, social or professional life was reported by 303 (99.0%) patients; and among these, 195 (64.4%) reported an impact in all three domains. CONCLUSIONS Frequent or chronic migraine is associated with a considerable negative impact on personal, social and professional life. Treatment failure is frequent in this patient group, highlighting the need for continuous research and awareness of new treatment possibilities. FUNDING Novartis Pharmaceutical Corporation. TRIAL REGISTRATION not relevant., (Articles published in the DMJ are “open access”. This means that the articles are distributed under the terms of the Creative Commons Attribution Non-commercial License, which permits any non-commercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited.)
- Published
- 2021
49. Sleep in cluster headache revisited: Results from a controlled actigraphic study.
- Author
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Lund NL, Snoer AH, Jennum PJ, Jensen RH, and Barloese MCJ
- Subjects
- Actigraphy methods, Adult, Female, Humans, Male, Middle Aged, Circadian Rhythm physiology, Cluster Headache physiopathology, Sleep physiology
- Abstract
Background and Aim: Cluster headache attacks exhibit a nocturnal predilection, but little is known of long-term sleep and circadian rhythm. The aim was to compare actigraphy measures, firstly in episodic cluster headache patients in bout and in remission and, secondly, to compare each disease phase with controls., Methods: Episodic cluster headache patients (ICHD III-beta), from the Danish Headache Center and healthy, age- and sex-matched controls participated. Sleep and activity were measured using actigraphy continuously for 2 weeks, along with sleep diaries and, for patients, also attack registration., Results: Patients in bout (n = 17, 2.3 attacks/day) spent more time in bed (8.4 vs. 7.7 hours, p = 0.021) and slept more (7.2 vs. 6.6 hours, p = 0.036) than controls (n = 15). In remission (n = 11), there were no differences compared with controls. Neither were there differences between patients in the two disease phases. In five patients, attacks/awakenings occurred at the same hour several nights in a row., Conclusion: Actigraphy offers the possibility of a continuous and long study period in a natural (non-hospital) environment. The study indicates that sleep does not differ between the bout and remission phase of episodic cluster headache. The repeated attacks/awakenings substantiate that circadian or homeostatic mechanisms are involved in the pathophysiology. The protocol was made available at ClinicalTrials.gov (NCT02853487).
- Published
- 2019
- Full Text
- View/download PDF
50. Transient global amnesia after cerebral angiography still occurs: Case report and literature review.
- Author
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Foss-Skiftesvik J, Snoer AH, Wagner A, and Hauerberg J
- Abstract
Transient global amnesia is considered a very rare complication of diagnostic cerebral angiography, and has been reported only in a limited number of case reports more than 15 years ago. We describe a patient experiencing transient global amnesia following cerebral digital subtraction angiography. While the condition by definition is self-limiting, its differential diagnoses may cause severe morbidity and/or mortality if left untreated. It is therefore important to build and maintain awareness of transient global amnesia as a possible complication of cerebral angiography.
- Published
- 2015
- Full Text
- View/download PDF
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