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Familial risks for epilepsy among siblings based on hospitalizations in Sweden

Hemminki, K (author)
Li, XJ (author)
Johansson, SE (author)
Karolinska Institutet
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Sundquist, K (author)
Karolinska Institutet
Sundquist, J (author)
Karolinska Institutet
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 (creator_code:org_t)
2006-09-15
2006
English.
In: Neuroepidemiology. - : S. Karger AG. - 0251-5350 .- 1423-0208. ; 27:2, s. 67-73
  • Journal article (peer-reviewed)
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  • <i>Purpose:</i> Epilepsy is a common disabling condition, with high heritability according to twin studies. Characterization of familial risks for common subtypes of epilepsy will advance the search for the heritable causes of these conditions and their underlying mechanisms. We aim at defining familial risks for siblings to be hospitalized because of epilepsy. <i>Methods:</i> A nationwide ad hoc epilepsy database was constructed by linking the Multigeneration Register on 0- to 69-year-old siblings to the Hospital Discharge Register for data on epilepsies covering the years 1987–2001. Standardized risk ratios (SIRs) were calculated for affected sibling pairs by comparing them to those whose siblings had no epilepsy. <i>Results:</i> Among a total of 26,799 hospitalized cases, 598 affected siblings were identified with a familial SIR of 2.35; the SIR was highest at ages 0–4 years (6.82). Infantile spasms showed the highest risk for any subtype (10.45), when a co-sibling was diagnosed with any epilepsy. When both siblings were diagnosed with a concordant (same) subtype of epilepsy, the SIRs were high, i.e. 8.43 for generalized idiopathic epilepsy, 2.56 for partial epilepsy, 24.72 for status epilepticus and 24.39 for other epilepsies. Generalized idiopathic epilepsy was also associated with grand mal (4.06) and other epilepsies (7.61). The numbers of cases were small but concordant diagnoses always showing higher SIRs compared with discordant diagnoses. <i>Conclusions:</i> Within the limits of the present sample size, our results suggest high familial aggregation for certain subtypes of epilepsy for which distinct genetic mechanisms may underlie.

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Hemminki, K
Li, XJ
Johansson, SE
Sundquist, K
Sundquist, J
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Neuroepidemiolog ...
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Karolinska Institutet

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