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Michael Bjørn Russell

Publications and source records attributed to Michael Bjørn Russell.

8 recordsLinked to original sources
PubMed2006

Are infrequent episodic, frequent episodic and chronic tension-type headache inherited? A population-based study of 11 199 twin pairs.

The objective was to investigate the importance of genetic and environmental factors for infrequent episodic, frequent episodic and chronic tension-type headache. Twin pairs recruited from the population-based Danish Twin Registry received a posted questionnaire. Only twin pairs where both twins replied were included. A total of 3523 monozygotic (MZ), 4150 dizygotic (DZ) same-gender and 3526 DZ opposite-gender twin pairs were included. The prevalence of frequent episodic and chronic tension-type headache was significantly more frequent in women than men, and significantly higher in those with co-occurrence of migraine. The concordance rates were significantly higher in MZ than same-gender DZ twin pairs with no or frequent episodic tension-type headache, while the difference was not significant in chronic tension-type headache. The concordance rates of infrequent episodic tension-type headache in MZ and same-gender DZ twin pairs was significantly different in women but not in men, although the difference was small in both genders. We conclude that genetic factors play a role in no and frequent episodic tension-type headache, while infrequent episodic tension-type headache is caused primarily by environmental factors. The data regarding chronic tension-type headache were limited, so no firm conclusion could be drawn.

Adult↗
PubMed2006

Tension-type headache in adolescents and adults: a population based study of 33,764 twins.

The aim of this study was to evaluate the 1-year-period prevalence of tension-type headache in a large population based sample. The study population included 33,764 twins aged 12-41 years old from the population based new Danish Twin Registry. They received a posted headache questionnaire and the response rate was 83.5%. The self-reported 1-year-period prevalence of tension-type headache was 86.0%; 78.9% among men and 92.5% among women. The 1-year-period prevalence of infrequent episodic, frequent episodic and chronic tension-type headache was 63.5, 21.6 and 0.9%, respectively. Frequent episodic and chronic tension-type headache was significantly more frequent in women than men. The prevalence of frequent episodic tension-type headache increased slightly in men until age 39 then it declined, while it increased about 20% point in women from age 12 years to age 20-39 years old and then it declined. Congruently, the prevalence of chronic tension-type headache increased until age 39 and declined thereafter in both sexes. Chronic tension-type headache is rare in persons 12-14 years old. These effects were confirmed by age trends of the different subtypes of tension-type headache using a regression model. The prevalence of migraine varied from 7.0 to 16.8% in men and from 8.2 to 31.0% in women. It increased from age 12 to 34 years and then declined. The risk and frequency of tension-type headache was significantly higher in those with migraine than those who had never had migraine. Future large longitudinal follow-up studies are required.

Adolescent↗
PubMed2005

Tension-type headache in 40-year-olds: a Danish population-based sample of 4000.

The aim of this study was to evaluate the one-year prevalence of tension-type headache in the general population. Three thousand men and one thousand women aged 40 years from the Danish population were included. They received a mailed questionnaire and the response rate was 87%. The self-reported one-year prevalence of tension-type headache was 84.7%. The one-year prevalence of infrequent episodic, frequent episodic and chronic tension-type headache was 48.2%, 33.8% and 2.3%, respectively. No tension-type headache and infrequent episodic tension-type headache was significantly more frequent in men than women (p<0.0005 and p=0.004), while frequent and chronic tension-type headache was significantly more frequent in women than men (p<0.0005 and p<0.0005). No tension-type headache and infrequent tension-type headache was significantly more frequent among those without than with self-reported migraine (no headache, men, p<0.0005 and women, p=0.002 and infrequent, men, p<0.0005 and women, p<0.0005), while episodic frequent and chronic tension-type headache was significantly more frequent among those with than those without self-reported migraine, with the exception of chronic tension-type in women (frequent episodic, men, p<0.0005 and women, p<0.0005 and chronic, men, p<0.0005 and women, p=0.08). Women are more prone to tension-type headache than men and they have it more frequently than men. Self-reported migraine increases the risk for frequent episodic and chronic tension-type headache.

Adult↗
PubMed2005

[Episodic ataxias].

BACKGROUND: Episodic ataxias (EAs) exist in sporadic and familial forms. They have considerable genetic and clinical heterogeneity. Better understanding of the disorders will hopefully improve management. MATERIAL AND METHODS: This review is based on personal experience and recent literature. RESULTS: EAs are rare autosomal dominant paroxysmic disorders. At present, five forms have been identified. EA 1 is caused by mutations in the potassium channel gene KCNA1 on chromosome 12p13, EA 2 by mutations in the calcium channel gene CACNA1A gene on chromosome 19p13, and EA 5 by mutations in the calcium channel gene CACNB4&beta on chromosome 2q22-q23. Neither gene nor linkage has been identified for EA 3 and 4. As the name indicates, EAs are characterized by paroxystic ataxia. Patients with EA 1 also have interictal myokymia. EAs are characterized by both locus and allelic heterogeneity, since different genes can cause an almost similar phenotype and different mutations in a gene can cause different disorders. Beside EA, mutations in the KCNA1 gene can cause partial epilepsy and myokymia alone, mutations in the CACNA1A gene can cause familial hemiplegic migraine 1 and spinocerebellar ataxia 6, while mutations in the CACNB4&beta4 gene can cause generalized epilepsy and juvenile myoclonic epilepsy. EA can often be efficiently treated with acetazolamide. INTERPRETATION: EAs are rare autosomal dominant disorders caused by mutations in ion-channel genes. The disorders are not life threatening but disabling without treatment or when medical treatment is ineffective or not tolerated.

Adolescent↗
PubMed2005

[Cerebral cavernous malformations].

BACKGROUND: Cerebral cavernous malformations exist in sporadic and familial forms. They have considerable genetic and clinical heterogeneity. Better understanding of these disorders may improve management. MATERIAL AND METHODS: This review is based on personal experience and recent literature. RESULTS: Cerebral cavernous malformations are venous malformations that can be detected with gradient echo MRI of the brain. Approximately 0.5% of the general population have the sporadic form with a single or a few cerebral cavernous malformations which mostly are asymptomatic. Those with the familial form usually have several cavernous malformations caused by an autosomal dominant condition. So far, 3 loci have been identified: CCM1 on chromosome 7q, CCM2 on chromosome 7p, and CCM3 on chromosome 3q, occurring in, respectively, approximately 40%, 20% and 40% of the families. CCM1 is caused by a mutation in the KRIT1 gene and CCM2 is caused by a mutation in the MGC4607 gene, while the gene for CCM3 is not yet identified. Mean age at onset is 20-40, but onset can occur at all ages. The most frequent symptoms are seizures, cerebral haemorrhage, chronic headache and focal neurological deficits. Many carriers are, however, asymptomatic. INTERPRETATION: Sporadic cerebral cavernous malformation is often asymptomatic, while the familial form shows phenotypic and genetic heterogeneity. The symptoms are depending on the location of the malformations as well as whether haemorrhage does occur.

Cavernous Sinus↗
PubMed2004

Epidemiology and genetics of cluster headache.

Cluster headache, the most severe primary headache, is characterised by unilateral pain, ipsilateral autonomic features, and, in many cases, restlessness. Recent epidemiological studies indicate that the prevalence of cluster headache is about one person per 500. Genetic epidemiological surveys indicate that first-degree relatives are five to 18 times-and second-degree relatives, one to three times-more likely to have cluster headache than the general population. Inheritance is likely to be autosomal dominant with low penetrance in some families, although there may also be autosomal recessive or multifactorial inheritance in others. To date, no molecular genetic clues have been identified for cluster headache. Identification of genes for cluster headache is likely to be difficult because most families reported have few affected members and genetic heterogeneity is likely. Future focus should be on ion channel genes and clock genes. This review summarises the epidemiology and genetics of cluster headache.

Age Factors↗
PubMed2002

Migraine without aura and migraine with aura are distinct disorders. A population-based twin survey.

OBJECTIVE: To investigate the co-occurrence of migraine without aura (MWOA) and migraine with aura (MWA) in a population-based twin survey. BACKGROUND: Migraine without aura and MWA are multifactorial disorders. If MWOA and MWA share common genes, co-occurrence should be observed more frequently than expected, ie, the product of the prevalence in the general population. MATERIAL AND METHODS: The study population included all living Danish monozygotic (MZ) and same-gender dizygotic (DZ) twin pairs born between 1953 and 1960: 5360 twins (2026 MZ, 3334 DZ). The sample included 2840 men and 2520 women. All received a posted questionnaire, and those with possible migraine were interviewed via telephone by trained physicians (V.U. or M.G.). Twins who did not respond to the questionnaire and who had a co-twin with possible migraine were contacted by telephone. The questionnaire response rate was 87% (4660 of 5360), and the telephone interview was participated in by 90% (2035 of 2272). The physician interviewers were unaware of questionnaire answers, zygosity, and the clinical diagnosis of the co-twin. The criteria of the International Headache Society were used to establish a diagnosis of migraine. RESULTS: Lifetime prevalence in the twin sample: 7% of men and 19% of women had MWOA, while 7% of men and 8% of women had MWA. Lifetime prevalence of MWA in twin pairs with MWOA: MZ men, 2% (1 of 47); MZ women, 6% (5 of 90); DZ men, 9% (7 of 75); and DZ women, 10% (19 of 182). Lifetime prevalence of MWOA in twin pairs with MWA: MZ men, 3% (1 of 33); MZ women, 5% (3 of 58); DZ men, 9% (4 of 44); and DZ women, 13% (10 of 76). The observed and the expected numbers of twins with co-occurrence of MWOA and MWA based on the prevalence in the general population were not significantly different in either men or women (men, P=.1 and women, P=.5). CONCLUSION: The results strongly suggest that MWOA and MWA are distinct disorders, and identification of common genes for MWOA and MWA, thus, should not be expected to result from future genetic research.

Adult↗