| 1. |
|
|
| 2. |
|
|
| 3. |
|
|
| 4. |
|
|
| 5. |
|
|
| 6. |
|
|
| 7. |
|
|
| 8. |
- Sjostrand, C, et al.
(författare)
-
Migraine and olfactory stimuli
- 2010
-
Ingår i: Current pain and headache reports. - : Springer Science and Business Media LLC. - 1534-3081 .- 1531-3433. ; 14:3, s. 244-251
-
Tidskriftsartikel (refereegranskat)
|
|
| 9. |
- Ekbom, K, et al.
(författare)
-
Age at onset and sex ratio in cluster headache: observations over three decades
- 2002
-
Ingår i: Cephalalgia : an international journal of headache. - : SAGE Publications. - 0333-1024. ; 22:2, s. 94-100
-
Tidskriftsartikel (refereegranskat)abstract
- Five hundred and fifty-four patients with episodic cluster headache (ECH) and chronic cluster headache (CCH) were examined between 1963 and 1997. Mean age at onset was significantly higher in women with CCH compared with women with ECH and in men with ECH or CCH. In women with CCH age at onset was evenly distributed from 10 to 69 years, whereas in men with CCH and in both sexes with ECH, there was a peak when they were in their 20s. In women with ECH a second peak of onset occurred in their 50s. Although not statistically significant, primary CCH started later in women (mean 50.8 years) than secondary CCH (mean 35.5 years). There was a significant variation in the male : female ratio with respect to age at onset, being largest between 30 and 49 years of age (ECH 7.2 : 1; CCH 11.0 : 1) and lowest after 50 (ECH 2.3 : 1; CCH 0.6 : 1). During the observation period of more than 30 years there was a trend towards a decreasing male preponderance; the male: female ratio was significantly higher among patients with onset before rather than after 1970. The proportion of episodic vs. chronic CH did not change during the study period. The nature of the sex- and age-related pattern of cluster headache onset remains to be elucidated but mechanisms associated with sex hormone regulation, perhaps of hypothalamic origin, may be involved, as well as environmental factors related to lifestyle.
|
|
| 10. |
- Ekbom, K, et al.
(författare)
-
Cluster headache and aura
- 2009
-
Ingår i: Headache. - : Wiley. - 1526-4610. ; 49:5, s. 786-787
-
Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
|
|
| 11. |
|
|
| 12. |
|
|
| 13. |
|
|
| 14. |
- Ekbom, K, et al.
(författare)
-
Periods of cluster headache induced by nitrate therapy and spontaneous remission of angina pectoris during active clusters
- 2004
-
Ingår i: Cephalalgia : an international journal of headache. - : SAGE Publications. - 0333-1024. ; 24:2, s. 92-98
-
Tidskriftsartikel (refereegranskat)abstract
- Glyceryl trinitrate (GTN) is known to induce single extra attacks of cluster headache (CH) during active cluster periods, most probably via actions of nitric oxide (NO). Induction of whole periods of CH by organic nitrates has, however, attracted little attention in the literature. We report on eight patients with episodic CH and coexistent effort-induced angina pectoris. Cases 1-6 had been free of their headaches for many years but got recurrence of CH within a few weeks after the administration of long-acting organic nitrates (isosorbide-dinitrate, isosorbide-5-mononitrate or slow-release GTN) aimed at treating their chest pains. These nitrate-induced headache periods were more severe and had a longer duration than the previous spontaneous ones. Furthermore, one of the subjects and two additional cases experienced a marked reduction of their anginal attacks during successive CH periods. Exercise time to effort-induced angina was increased in all three patients and one of them revealed a markedly elevated threshold for eliciting ischaemic cardiac symptoms by standardized physical exercise on a cycle ergometer. We hypothesize whether extra CH periods elicited by sustained nitrate therapy and remission of angina pectoris during active clusters are caused by central mechanisms involving inhibition of sympathetic tone and effects on both cranial vessels and cardiac functions.
|
|
| 15. |
- Fourier, C, et al.
(författare)
-
A genetic CLOCK variant associated with cluster headache causing increased mRNA levels
- 2018
-
Ingår i: Cephalalgia : an international journal of headache. - : SAGE Publications. - 1468-2982. ; 38:3, s. 496-502
-
Tidskriftsartikel (refereegranskat)abstract
- Cluster headache is characterized by recurrent unilateral headache attacks of severe intensity. One of the main features in a majority of patients is a striking rhythmicity of attacks. The CLOCK ( Circadian Locomotor Output Cycles Kaput) gene encodes a transcription factor that serves as a basic driving force for circadian rhythm in humans and is therefore particularly interesting as a candidate gene for cluster headache. Methods We performed an association study on a large Swedish cluster headache case-control sample (449 patients and 677 controls) screening for three single nucleotide polymorphisms (SNPs) in the CLOCK gene implicated in diurnal preference (rs1801260) or sleep duration (rs11932595 and rs12649507), respectively. We further wanted to investigate the effect of identified associated SNPs on CLOCK gene expression. Results We found a significant association with rs12649507 and cluster headache ( p = 0.0069) and this data was strengthened when stratifying for reported diurnal rhythmicity of attacks ( p = 0.0009). We investigated the effect of rs12649507 on CLOCK gene expression in human primary fibroblast cultures and identified a significant increase in CLOCK mRNA expression ( p = 0.0232). Conclusions Our results strengthen the hypothesis of the involvement of circadian rhythm in cluster headache.
|
|
| 16. |
|
|
| 17. |
|
|
| 18. |
|
|
| 19. |
|
|
| 20. |
|
|
| 21. |
|
|
| 22. |
|
|
| 23. |
- Fourier, C, et al.
(författare)
-
The molecular clock gene cryptochrome 1 (CRY1) and its role in cluster headache
- 2021
-
Ingår i: Cephalalgia : an international journal of headache. - : SAGE Publications. - 1468-2982. ; 41:13, s. 1374-1381
-
Tidskriftsartikel (refereegranskat)abstract
- Cluster headache is a severe primary headache disorder commonly featuring a strikingly distinct circadian attack pattern. Therefore, the circadian system has been suggested to play a crucial role in the pathophysiology of cluster headache. Cryptochromes are key components of the molecular clock generating circadian rhythms and have previously been shown to be associated with several psychiatric disorders, including seasonal affective disorder, bipolar disorder, and depression. Methods In this case-control study, we investigated the role of cryptochrome ( CRY) genes in cluster headache by screening 628 cluster headache patients and 681 controls from Sweden for four known genetic variants in the CRY1 (rs2287161 and rs8192440) and CRY2 (rs10838524 and rs1554338) genes. In addition, we analyzed CRY1 gene expression in primary fibroblast cell lines from eleven patients and ten controls. Results The exonic CRY1 variant rs8192440 was associated with cluster headache on allelic level ( p=0.02) and this association was even more pronounced in a subgroup of patients with reported diurnal rhythmicity of attacks ( p=0.002). We found a small significant difference in CRY1 gene expression between cluster headache patients and control individuals ( p=0.04), but we could not identify an effect of the associated variant rs8192440 on CRY1 expression. Conclusions We discovered a disease-associated variant in the CRY1 gene and slightly increased CRY1 gene expression in tissue from cluster headache patients, strengthening the hypothesis of circadian dysregulation in cluster headache. How this gene variant may contribute to the pathophysiology of the disease remains subject to further studies.
|
|
| 24. |
|
|
| 25. |
|
|
| 26. |
|
|
| 27. |
|
|
| 28. |
- Meyer, EL, et al.
(författare)
-
beta-Receptor response to noradrenaline in cluster headache. A study of adipose tissue lipolysis
- 2006
-
Ingår i: Cephalalgia : an international journal of headache. - : SAGE Publications. - 0333-1024. ; 26:7, s. 831-836
-
Tidskriftsartikel (refereegranskat)abstract
- We have previously shown decreased lipolysis in both phases of cluster headache (CH), as an indication of a sympathetic dysregulation. Reduced lipolysis could be a result of diminished β-receptor sensitivity in adipose tissue. The aim of this study was to measure the lipolytic response to noradrenaline in 10 CH patients in remission and in 10 healthy subjects, to estimate β-receptor function. Microdialysis technique was used to measure the increase of glycerol, the end-product of lipolysis, during infusion of noradrenaline into the adipose tissue. Noradrenaline infusion resulted in a distinct elevation of glycerol. The average glycerol increase was significantly higher in CH patients (121± ± 48) than in healthy subjects (77± ± 41) ( P < 0.05), which indicates increased β-receptor response to noradrenaline in CH patients in remission. This may be due to up-regulated β-receptor sensitivity, secondary to reduced sympathetic outflow and a primary autonomic disturbance in CH.
|
|
| 29. |
|
|
| 30. |
|
|
| 31. |
|
|
| 32. |
|
|
| 33. |
- Meyer, EL, et al.
(författare)
-
Nocturnal secretion of growth hormone, noradrenaline, cortisol and insulin in cluster headache remission
- 2007
-
Ingår i: Cephalalgia : an international journal of headache. - : SAGE Publications. - 0333-1024. ; 27:8, s. 912-919
-
Tidskriftsartikel (refereegranskat)abstract
- We have previously shown decreased, nocturnal lipolysis in both phases of cluster headache (CH). Lipolysis is stimulated by noradrenaline (NA), growth hormone (GH) and cortisol, and inhibited by insulin, hormones which are directly or indirectly regulated by the hypothalamus. Our aim was to investigate the nocturnal secretion of NA, GH, cortisol and insulin in nine CH patients in remission and 10 healthy controls. Nocturnal venous blood samples were collected in hourly intervals for analysis of NA, cortisol and insulin and in 30-min intervals for GH. We found a reduced increase in GH between 24.00 h and 01.00 h (ANOVA, P < 0.05) in CH patients. Nocturnal secretion of NA, cortisol and insulin did not differ significantly between the groups. The altered nocturnal GH pattern that was seen in CH patients in remission might in part explain the altered nocturnal lipolysis previously found and further indicate a permanent hypothalamic disturbance in CH.
|
|
| 34. |
|
|
| 35. |
|
|
| 36. |
|
|
| 37. |
|
|
| 38. |
|
|
| 39. |
|
|
| 40. |
|
|
| 41. |
- Olofsgard, FJ, et al.
(författare)
-
Investigating Vitamin D Receptor Genetic Markers in a Cluster Headache Meta-Analysis
- 2023
-
Ingår i: International journal of molecular sciences. - : MDPI AG. - 1422-0067. ; 24:6
-
Tidskriftsartikel (refereegranskat)abstract
- Patients diagnosed with the primary headache disorder known as cluster headache (CH) commonly report that their headache attacks occur in patterns of both circadian and seasonal rhythmicity. Vitamin D is essential for a variety of bodily functions and vitamin D levels are largely regulated by daylight exposure in connection with seasonal variation. For this Sweden-based study, the association between CH and three single-nucleotide polymorphisms in the vitamin D receptor gene, rs2228570, rs1544410, and rs731236, were investigated, as well as CH bouts and trigger factors in relation to seasonal and weather changes. Over 600 study participants with CH and 600 controls were genotyped for rs2228570, and genotyping results for rs1544410 and rs731236 were obtained from a previous genome-wide association study. The genotyping results were combined in a meta-analysis, with data from a Greek study. No significant association was found between rs2228570 and CH or the CH subtype in Sweden, nor did the meta-analysis show significant results for any of the three markers. The most common period of the year to experience CH bouts in Sweden was autumn, and conditions linked to weather or weather changes were also identified as potential triggers for CH bouts for a quarter of the responders who reported bout triggers. Though we cannot rule out vitamin D involvement in CH, this study does not indicate any connection between CH and the three vitamin D receptor gene markers.
|
|
| 42. |
- Olofsgard, FJ, et al.
(författare)
-
PER Gene Family Polymorphisms in Relation to Cluster Headache and Circadian Rhythm in Sweden
- 2021
-
Ingår i: Brain sciences. - : MDPI AG. - 2076-3425. ; 11:8
-
Tidskriftsartikel (refereegranskat)abstract
- The trigeminal autonomic cephalalgia, cluster headache (CH), is one of the most painful disorders known to man. One of the disorder’s most striking features is the reported diurnal rhythmicity of the attacks. For a majority of patients, the headache attacks occur at approximately the same time every day. Genetic variants of genes involved in the circadian rhythm such as Period Circadian Regulator 1, 2, and 3 (PER1, 2 and 3) are hypothesized to have an effect on the rhythmicity of the attacks. Six PER1, 2 and 3 genetic markers; the indel rs57875989 and five single nucleotide polymorphisms (SNPs), rs2735611, rs2304672, rs934945, rs10462020, and rs228697, were genotyped, using TaqMan® or regular polymerase chain reaction (PCR), in a Swedish CH case control material. Logistic regression showed no association between CH and any of the six genetic variants; rs57875989, p = 0.523; rs2735611, p = 0.416; rs2304672, p = 0.732; rs934945, p = 0.907; rs10462020, p = 0.726; and rs228697, p = 0.717. Furthermore, no difference in allele frequency was found for patients reporting diurnal rhythmicity of attacks, nor were any of the variants linked to diurnal preference. The results of this study indicate no involvement of these PER genetic variants in CH or diurnal phenotype in Sweden.
|
|
| 43. |
|
|
| 44. |
|
|
| 45. |
|
|
| 46. |
- Ran, CE, et al.
(författare)
-
Analysis of NOS Gene Polymorphisms in Relation to Cluster Headache and Predisposing Factors in Sweden
- 2021
-
Ingår i: Brain sciences. - : MDPI AG. - 2076-3425. ; 11:1
-
Tidskriftsartikel (refereegranskat)abstract
- Cluster headache is characterized by activation of the autonomic-trigeminal reflex. Nitric oxide can trigger headaches in patients, and nitric oxide signaling is known to be affected in cluster headache. Based on the hypothesis of nitric oxide being involved in cluster headache pathophysiology we investigated nitric oxide synthases as potential candidate genes for cluster headache. We analyzed eight variants in the three forms of nitric oxide synthase (NOS) genes, inducible NOS (iNOS), endothelial NOS (eNOS) and neuronal NOS (nNOS), and tested for association with cluster headache. Swedish cluster headache patients (n = 542) and controls (n = 581) were genotyped using TaqMan® assays on an Applied Biosystems 7500 qPCR cycler. This is the largest performed genetic study on NOS involvement in cluster headache so far. We found an association between cluster headache and one iNOS haplotype consisting of the minor alleles of rs2297518 and rs2779249 (p = 0.022). In addition, one of the analyzed nNOS variants, rs2682826, was associated with reported triptan use (p = 0.039). Our data suggest that genetic variants in NOS genes do not have a strong influence on cluster headache pathophysiology, but that certain combinations of genetic variants in NOS genes may influence the risk of developing the disorder or triptan use.
|
|
| 47. |
- Ran, C, et al.
(författare)
-
Anoctamin 3: A Possible Link between Cluster Headache and Ca2+ Signaling
- 2019
-
Ingår i: Brain sciences. - : MDPI AG. - 2076-3425. ; 9:8
-
Tidskriftsartikel (refereegranskat)abstract
- Cluster headache is a severe primary headache characterized by extremely painful attacks of unilateral headache. Verapamil is commonly used as a prophylactic treatment with good effect. In order to search for new pathways involved in the pathophysiology of cluster headache, we analyzed genetic variants that were previously linked to verapamil response in migraine in a Swedish cluster headache case-control sample. We used TaqMan qPCR for genetic screening and performed a gene expression analysis on associated genes in patient-derived fibroblasts, and further investigated which reference genes were suitable for analysis in fibroblasts from cluster headache patients. We discovered a significant association between anoctamin 3, a gene encoding a calcium-activated ion channel, and cluster headache. The association was not dependent on verapamil treatment since the associated variant, rs1531394, was also overrepresented in patients not using verapamil. No difference was found in the anoctamin 3 gene expression between controls and patients. Also, we determined that TBP, IPO8 and PDHB were suitable reference genes in cluster headache fibroblasts. This finding is the first report of an association between a variant in a gene encoding an ion-channel and cluster headache, and the first significant genetic evidence of calcium involvement in cluster headache pathophysiology.
|
|
| 48. |
|
|
| 49. |
|
|
| 50. |
|
|
