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Migraine Disorders: HELP
Articles by Anne Luise Haulund Vollesen
Based on 9 articles published since 2010
(Why 9 articles?)
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Between 2010 and 2020, Anne L. Vollesen wrote the following 9 articles about Migraine Disorders.
 
+ Citations + Abstracts
1 Review Migraine and cluster headache - the common link. 2018

Vollesen, Anne Luise / Benemei, Silvia / Cortese, Francesca / Labastida-Ramírez, Alejandro / Marchese, Francesca / Pellesi, Lanfranco / Romoli, Michele / Ashina, Messoud / Lampl, Christian / Anonymous6920962. ·Danish Headache Center and Department of Neurology, Rigshospitalet Glostrup, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. · Health Sciences Department, University of Florence and Headache Centre, Careggi University Hospital, Florence, Italy. · Department of Medico-Surgical Sciences and Biotechnologies, Sapienza, University of Rome, Polo Pontino, Latina, Italy. · Dep Internal Medicine, Division of Vascular Pharmacology, Erasmus Medical Center, Rotterdam, The Netherlands. · Child Neuropsichiatry Unit, University of Palermo, Palermo, Italy. · Medical Toxicology, Headache and Drug Abuse Center, University of Modena and Reggio Emilia, Modena, Italy. · Neurology Clinic, University of Perugia - S.M. Misericordiae Hospital, Perugia, Italy. · Department of Neurogeriatric Medicine, Headache Medical Center Linz, Ordensklinikum Linz Barmherzige Schwestern, Seilerstaette 4, 4010, Linz, Austria. christian.lampl@ordensklinikum.at. ·J Headache Pain · Pubmed #30242519.

ABSTRACT: Although clinically distinguishable, migraine and cluster headache share prominent features such as unilateral pain, common pharmacological triggers such glyceryl trinitrate, histamine, calcitonin gene-related peptide (CGRP) and response to triptans and neuromodulation. Recent data also suggest efficacy of anti CGRP monoclonal antibodies in both migraine and cluster headache. While exact mechanisms behind both disorders remain to be fully understood, the trigeminovascular system represents one possible common pathophysiological pathway and network of both disorders. Here, we review past and current literature shedding light on similarities and differences in phenotype, heritability, pathophysiology, imaging findings and treatment options of migraine and cluster headache. A continued focus on their shared pathophysiological pathways may be important in paving future treatment avenues that could benefit both migraine and cluster headache patients.

2 Review Targeted Pituitary Adenylate Cyclase-Activating Peptide Therapies for Migraine. 2018

Vollesen, Anne Luise Haulund / Amin, Faisal Mohammad / Ashina, Messoud. ·Danish Headache Center and Department of Neurology, Rigshospitalet Glostrup, Faculty of Health and Medical Sciences, University of Copenhagen, DK-2600, Glostrup, Copenhagen, Denmark. · Danish Headache Center and Department of Neurology, Rigshospitalet Glostrup, Faculty of Health and Medical Sciences, University of Copenhagen, DK-2600, Glostrup, Copenhagen, Denmark. ashina@dadlnet.dk. ·Neurotherapeutics · Pubmed #29464574.

ABSTRACT: Here, we review the role of pituitary adenylate cyclase-activating peptide-38 (PACAP38) in migraine pathophysiology and data implicating PAC

3 Review PACAP38 in human models of primary headaches. 2017

Ashina, Håkan / Guo, Song / Vollesen, Anne L H / Ashina, Messoud. ·Department of Neurology, Danish Headache Center, Rigshospitalet Glostrup, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. · Department of Neurology, Danish Headache Center, Rigshospitalet Glostrup, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. ashina@dadlnet.dk. ·J Headache Pain · Pubmed #29453754.

ABSTRACT: BACKGROUND: To review the role of PACAP38 in human models of primary headaches, discuss possible mechanisms of PACAP38-induced migraine, and outline future directions. DISCUSSION: Experimental studies have established PACAP38 as a potent pharmacological "trigger" molecule of migraine-like attacks. These studies have also revealed a heterogeneous PACAP38 migraine response in migraine without aura patients. In addition, findings from brain imaging studies have demonstrated neuronal and vascular changes in migraine patients both ictally and interictally after PACAP38 infusion. CONCLUSION: Human migraine models have shed light on the importance of PACAP38 in the pathophysiology of primary headaches. These studies have also pointed to the PAC

4 Review Triptans and CGRP blockade - impact on the cranial vasculature. 2017

Benemei, Silvia / Cortese, Francesca / Labastida-Ramírez, Alejandro / Marchese, Francesca / Pellesi, Lanfranco / Romoli, Michele / Vollesen, Anne Luise / Lampl, Christian / Ashina, Messoud / Anonymous70923. ·Health Sciences Department, University of Florence, and Headache Centre, Careggi University Hospital, Viale Pieraccini 6, 50134, Florence, Italy. silvia.benemei@unifi.it. · Department of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Polo Pontino, Latina, Italy. · Dept Internal Medicine, Division of Vascular Pharmacology, Erasmus Medical Center, Rotterdam, The Netherlands. · Child Neuropsichiatry Unit, University of Palermo, Palermo, Italy. · Medical Toxicology Headache and Drug Abuse Center, University of Modena and Reggio Emilia, Modena, Italy. · Neurology Clinic, University Hospital of Perugia, Perugia, Italy. · Danish Headache Center and Department of Neurology, Rigshospitalet Glostrup, Faculty of Health and Medicl Sciences, University of Copenhagen, Copenhagen, Denmark. · Department of Neurogeriatric Medicine, Headache Medical Center Linz, Linz, Austria. · Danish Headache Center and Department of Neurology, Rigshospitalet Glostrup, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. ·J Headache Pain · Pubmed #29019093.

ABSTRACT: The trigeminovascular system plays a key role in the pathophysiology of migraine. The activation of the trigeminovascular system causes release of various neurotransmitters and neuropeptides, including serotonin and calcitonin gene-related peptide (CGRP), which modulate pain transmission and vascular tone. Thirty years after discovery of agonists for serotonin 5-HT

5 Review PACAP38: Emerging Drug Target in Migraine and Cluster Headache. 2017

Vollesen, Anne Luise Haulund / Ashina, Messoud. ·Danish Headache Center and Department of Neurology, Rigshospitalet Glostrup, Faculty of Health and Medical Sciences, University of Copenhagen, Glostrup, Copenhagen, 2600, Denmark. ·Headache · Pubmed #28485845.

ABSTRACT: Here, we review the role of pituitary adenylate cyclase-activating peptide-38 (PACAP38) in migraine and cluster headache (CH). Mounting evidence implicates signaling molecule PACAP38 in the pathophysiology of migraine. Human provocation studies show PACAP38 induces migraine attacks in migraine patients without aura and marked and sustained dilation of extracerebral arteries. PACAP38 selectively targets the PAC

6 Article PACAP38 dose-response pilot study in migraine patients. 2017

Vollesen, Anne Luise Haulund / Guo, Song / Ashina, Messoud. ·Danish Headache Center and Department of Neurology, Rigshospitalet, Faculty of Health and Medical Sciences, University of Copenhagen, Denmark. ·Cephalalgia · Pubmed #27084887.

ABSTRACT: Background Intravenous infusion of 10 pmol/kg/min pituitary adenylate cyclase-activating polypeptide-38 (PACAP38) induces migraine-like attacks in migraine patients without aura (MO). Here, we conducted a pilot study and investigated if lower doses of PACAP38 exert similar migraine-inducing abilities. Methods We randomly allocated six MO patients to receive intravenous infusion of 4, 6, and 8 pmol/kg/min of PACAP38 over 20 minutes in a double-blind, three-way cross-over study. Headache and migraine characteristics were recorded during hospital (0-2 hours) and post-hospital (2-13 hours) phases. Results PACAP38 induced migraine-like attacks in one out of six patients with 4 pmol, two out of six patients with 6 pmol and three out of six patients with 8 pmol ( p = 0.368). All patients reported head pain after 8 pmol/kg/min, whereas five of six participants reported head pain after both 4 and 6 pmol/kg/min. We found no difference between the three doses in the AUC for headache intensity over the 12-hour observation period ( p = 0.142). An exploratory analysis showed a significant difference between 4 pmol and 8 pmol ( p = 0.031). Conclusion A trend of a dose-response relationship between dose of PACAP38 and incidence of migraine was observed. We suggest that 10 pmol/kg/min PACAP38 is the most optimal dose to induce migraine-like attacks.

7 Article Part I: Pituitary adenylate cyclase-activating polypeptide-38 induced migraine-like attacks in patients with and without familial aggregation of migraine. 2017

Guo, Song / Vollesen, Anne Luise Haulund / Hansen, Rikke Dyhr / Esserlind, Ann-Louise / Amin, Faisal Mohammed / Christensen, Anne Francke / Olesen, Jes / Ashina, Messoud. ·The Danish Headache Center and Department of Neurology, Rigshospitalet, Faculty of Health and Medical Sciences, University of Copenhagen, Denmark. ·Cephalalgia · Pubmed #26994299.

ABSTRACT: Background Intravenous infusion of adenylate cyclase-activating polypeptide-38 (PACAP38) provokes migraine-like attacks in 65-70% of migraine sufferers. Whether aggregation of migraine in first-degree relatives contributes to this discrepancy in PACAP38-induced response is unknown. We hypothesized that genetic enrichment plays a role in triggering of migraine and that migraine without aura patients with a high family load ( ≥ 2 first-degree relatives with migraine) would report more migraine-like attacks after intravenous infusion of human PACAP38. Methods In this study, we allocated 32 previously genotyped migraine without aura patients to receive intravenous infusion of 10 pmol/kg/min PACAP38 and recorded migraine-like attacks including headache characteristics and associated symptoms. Information of familial aggregation was obtained by telephone interview of first-degree relatives using a validated semi-structured questionnaire. Results PACAP38 infusion induced a migraine-like attack in 75% (nine out of 12) of patients with high family load compared to 70% (14 out of 20) with low family load ( P = 0.761). In an explorative investigation, we found that the migraine response after PACAP38 was not associated with the risk allele of rs2274316 ( MEF2D), which confers increased risk of migraine without aura and may regulate PACAP38 expression. Conclusion Migraine response to PACAP38 infusion in migraine without aura patients is not associated with high family load or the risk allele of rs2274316 ( MEF2D).

8 Article Part II: Biochemical changes after pituitary adenylate cyclase-activating polypeptide-38 infusion in migraine patients. 2017

Guo, Song / Vollesen, Anne Luise Haulund / Hansen, Young Bae Lee / Frandsen, Erik / Andersen, Malene Rohr / Amin, Faisal Mohammad / Fahrenkrug, Jan / Olesen, Jes / Ashina, Messoud. ·1 Danish Headache Center and Department of Neurology, Rigshospitalet, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. · 2 Department of Clinical Biochemistry, Rigshospitalet, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. · 3 Department of Diagnostics, Rigshospitalet, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. · 4 Department of Clinical Biochemistry, Herlev and Gentofte Hospital, Gentofte, Denmark. · 5 Department of Clinical Biochemistry, Bispebjerg Hospital, University of Copenhagen, Copenhagen, Denmark. ·Cephalalgia · Pubmed #26994298.

ABSTRACT: Background Intravenous infusion of pituitary adenylate cyclase-activating polypeptide-38 (PACAP38) provokes migraine attacks in 65-70% of migraine without aura (MO) patients. We investigated whether PACAP38 infusion causes changes in the endogenous production of PACAP38, vasoactive intestinal polypeptide (VIP), calcitonin gene-related peptide (CGRP), tumour necrosis factor alpha (TNFα), S100 calcium binding protein B (S100B), neuron-specific enolase and pituitary hormones in migraine patients. Methods We allocated 32 previously genotyped MO patients to receive intravenous infusion PACAP38 (10 pmol/kg/minute) for 20 minutes and recorded migraine-like attacks. Sixteen of the patients were carriers of the risk allele rs2274316 ( MEF2D), which confers increased risk of MO and may regulate PACAP38 expression, and 16 were non-carriers. We collected blood samples at baseline and 20, 30, 40, 60 and 90 minutes after the start of the infusion. A control group of six healthy volunteers received intravenous saline. Results PACAP38 infusion caused significant changes in plasma concentrations of VIP ( p = 0.026), prolactin ( p = 0.011), S100B ( p < 0.001) and thyroid-stimulating hormone (TSH; p = 0.015), but not CGRP ( p = 0.642) and TNFα ( p = 0.535). We found no difference in measured biochemical variables after PACAP38 infusion in patients who later developed migraine-like attacks compared to those who did not ( p > 0.05). There was no difference in the changes of biochemical variables between patients with and without the MEF2D-associated gene variant ( p > 0.05). Conclusion PACAP38 infusion elevated the plasma levels of VIP, prolactin, S100B and TSH, but not CGRP and TNFα. Development of delayed migraine-like attacks or the presence of the MEF2D gene variant was not associated with pre-ictal changes in plasma levels of neuropeptides, TNFα and pituitary hormones.

9 Article Premonitory and nonheadache symptoms induced by CGRP and PACAP38 in patients with migraine. 2016

Guo, Song / Vollesen, Anne L H / Olesen, Jes / Ashina, Messoud. ·Danish Headache Center, Department of Neurology, Rigshospitalet, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. ·Pain · Pubmed #27842045.

ABSTRACT: Migraine attacks are often preceded by premonitory symptoms (PS) that may be triggered pharmacologically. We investigated the incidence of PS after administration of calcitonin gene-related peptide (CGRP) or pituitary adenylate cyclase-activating peptide-38 (PACAP38) in patients with migraine without aura (MO) who reported and did not report migraine-like attacks induced by these pharmacological triggers. In addition, we investigated the association between PS and familial predisposition for migraine. In our study, MO patients received continuous intravenous infusion of α-CGRP (n = 40) and PACAP38 (n = 32) for 20 minutes. Premonitory and nonheadache symptoms were recorded by a self-administered questionnaire. Information on familial predisposition was obtained by telephone interview of first-degree relatives using a validated semistructured questionnaire. Twenty-five of 40 patients (63%) developed a migraine-like attack after CGRP infusion and 23 of 32 patients (72%) developed an attack after PACAP38 infusion. Only 2 patients (9%) with a CGRP-induced migraine-like attack reported PS, whereas 11 patients (48%) reported PS after PACAP38. Patients who developed a migraine-like attack did not report more PS than did patients with no attack after CGRP (P = 0.519) or PACAP38 (P = 0.103). Additionally, we found no difference in PS between patients with familial predisposition of migraine (75%) and patients with no family predisposition (56%) (P = 0.101). In conclusion, CGRP did not induce PS, whereas PACAP38 induced PS in 48% of patients. However, CGRP and PACAP38 did not induce more PS in patients who developed an attack compared with those who did not develop an attack.