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| 3. |
- Ekbom, K, et al.
(författare)
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Cluster headache and aura
- 2009
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Ingår i: Headache. - : Wiley. - 1526-4610. ; 49:5, s. 786-787
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 4. |
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| 5. |
- Meyer, EL, et al.
(författare)
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beta-Receptor response to noradrenaline in cluster headache. A study of adipose tissue lipolysis
- 2006
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Ingår i: Cephalalgia : an international journal of headache. - : SAGE Publications. - 0333-1024. ; 26:7, s. 831-836
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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.
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| 8. |
- Meyer, EL, et al.
(författare)
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Nocturnal secretion of growth hormone, noradrenaline, cortisol and insulin in cluster headache remission
- 2007
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Ingår i: Cephalalgia : an international journal of headache. - : SAGE Publications. - 0333-1024. ; 27:8, s. 912-919
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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.
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| 10. |
- Sjostrand, C, et al.
(författare)
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Familial cluster headache. Is atypical cluster headache in family members part of the clinical spectrum?
- 2005
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Ingår i: Cephalalgia : an international journal of headache. - : SAGE Publications. - 0333-1024. ; 25:11, s. 1068-1077
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Tidskriftsartikel (refereegranskat)abstract
- Familial cluster headache (CH) was analysed in 21 Swedish families. Diagnosis was made according to The International Classification of Headache Disorders 2004. We identified 55 affected, of whom 42 had episodic or chronic CH, one had probable CH and 12 had atypical symptoms. The atypical cases did not fulfil the diagnostic criteria for CH, but had clinical symptoms with more resemblance to CH than to migraine or other trigeminal autonomic cephalgia syndromes. The overall male : female ratio was 1.8 : 1. The overall mean age at onset was significantly lower in the second/third generation than in the first generation (mean age at onset 22 vs. 31 years, SD ± 7 vs. 13 years; P < 0.01). This may be anticipation or selection bias, since individuals with late age at onset from the second/third generation may not yet have symptoms. The prevalence of migraine was 24% (13/55), i.e. similar to the prevalence in the general population. The high incidence of atypical CH cases in the Swedish families with other members affected with CH may suggest that the spectrum of CH is broader than previously thought. We suggest that atypical CH in CH families may represent an expanded spectrum of the disease with a common aetiology, i.e. a common genetic background.
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