Cluster headache is an autosomal dominantly inherited disorder in some families: a complex segregation analysis.

Russell, Michael Bjørn; Andersson, Poul Gertz; Thomsen, Laura H.; Iselius, L

doi:10.1136/jmg.32.12.954

Cited by 92 publications

(57 citation statements)

References 5 publications

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“…A number of recent observations supported a significant genetic component to CH predisposition: compared with the general population, the first-degree relatives of CH patients had a 14-39-fold increase in the disease risk [3][4][5]. Genetic epidemiological studies, however, suggested that CH is a complex disease, with several genetic factors interacting with the environment [6][7][8]. At present, however, no molecular genetic clues have been identified for the disease [8].…”

Section: Introductionmentioning

confidence: 90%

Association between the G1246A polymorphism of the hypocretin receptor 2 gene and cluster headache: a meta-analysis

et al. 2007

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The objective of this study was to investigate the association between polymorphisms of the hypocretin receptor 2 gene (HCRTR2) and the risk of cluster headache (CH). The study is a meta-analysis of published case-control studies investigating the association between polymorphisms of the HCRTR2 gene and CH. Pooled odds ratios (OR) were estimated using both random (RE) and fixed effects (FE) models. Three studies, performed in five different European countries, with 593 cases and 599 controls, were included in the study. Allele G of the G1246A HCRTR2 polymorphism was significantly associated with CH (FE OR 1.58, CI 95% 1.27–1.95; RE OR 1.55 (1.14–2.12)). Carriers of the GG genotype showed a higher disease risk compared to the remaining genotypes (FE OR 1.75, CI 95% 1.37–2.25; RE OR 1.69, CI 95% 1.11–2.58). Our data confirm that the G1246A polymorphism of the HCRTR2 gene may modulate the genetic risk for CH.

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Section: Introductionmentioning

confidence: 90%

Association between the G1246A polymorphism of the hypocretin receptor 2 gene and cluster headache: a meta-analysis

et al. 2007

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“…However, the observation of cluster headache in monozygotic twins [30] and a report on three families in which cluster headache is present in more than one member [31] underscores the importance of considering genetic factors in the etiology. Russell et al [32] investigated the familial occurrence of cluster headache in 370 probands with cluster headache and found a positive family history of cluster headache in 7% of the families. Compared with the general population, this study described a 14-fold increased risk of cluster headache in first-degree relatives and a twofold increased risk for second-degree relatives.…”

Section: The Pathophysiologic Puzzlementioning

confidence: 99%

Hypothalamic involvement and activation in cluster headache

May

Goadsby

2001

Current Science Inc

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Cluster headache is an episodic form of primary neurovascular headache that is both severe and relatively rare. It is characterized by episodes of headache with cranial parasympathetic activation and sympathetic impairment that come in bouts, or clusters. Its pathophysiology can be divided into understanding the attack phenotype and the biotype of the periodicity. Acute attacks of cluster headache are marked by trigeminal nerve-mediated pain and with cranial autonomic activation, trigeminal-autonomic cephalalgia; an activation that characterizes the phenotype of a group of headaches. The signature feature of cluster headache is its periodicity, the daily cycle of attacks when the patient is in an active bout, or the circumannual, or other period, cycling that distinguishes the on period from the off period. Functional brain imaging with positron emission tomography and structural imaging with voxel-based morphometry have identified an area in the posterior hypothalamic gray as key in understanding cluster headache. This area is subtly enlarged in its gray matter volume, active during an acute cluster headache but inactive when patients are challenged between bouts. Cluster headache is likely to be a form of primary neurovascular pain whose phenotypic expression relies on the trigeminal-autonomic reflex, with a biotype determined by the brain area, the posterior hypothalamus, in which the lesion seems to be located. Understanding both the phenotypic expression and the biotype will, respectively, enable better acute attack treatments and better preventative management of this horrible form of headache.

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“…Additional evidence suggesting a genetic or hereditary predisposition comes from several twins studies demonstrating 100% concordance in monozygotic twins [26][27][28]. More recently, Russell et al [29,30] have demonstrated a 14-fold increase in the risk of cluster headache in first-degree relatives. Their findings suggest that in some families, cluster headache may have an autosomal-dominant inheritance pattern.…”

Section: Geneticsmentioning

confidence: 94%

Treatment and management of cluster headache

Dodick

Capobianco

2001

Current Science Inc

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Cluster headache is an uncommon yet well-defined neurovascular syndrome occurring in both episodic and chronic varieties. The most striking feature of cluster headache is the unmistakable circadian and circannual periodicity. Inheritance may play a role in some families. The attacks are of extreme intensity, of short duration, occur unilaterally, and are accompanied by signs and symptoms of autonomic dysfunction. In contrast to migraine, during an attack the cluster patient prefers to pace about. Attacks frequently occur at night. Although the pathophysiology of cluster headache remains to be fully elucidated, several seminal observations have recently been made. The medical treatment of cluster headache includes both acute therapy aimed at aborting individual attacks and prophylactic therapy aimed at preventing recurrent attacks during the cluster period. Agents used for acute therapy include inhalation of oxygen, sumatriptan, and dihydroergotamine. Transitional prophylaxis involves the short-term use of either corticosteroids or ergotamine derivatives. The cornerstone of maintenance prophylaxis is verapamil, yet methysergide, lithium, and divalproex sodium may also be employed. In some patients, melatonin or topiramate may be useful adjunctive therapies.

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Cluster headache is an autosomal dominantly inherited disorder in some families: a complex segregation analysis.

Cited by 92 publications

References 5 publications

Association between the G1246A polymorphism of the hypocretin receptor 2 gene and cluster headache: a meta-analysis

Association between the G1246A polymorphism of the hypocretin receptor 2 gene and cluster headache: a meta-analysis

Hypothalamic involvement and activation in cluster headache

Treatment and management of cluster headache

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