Reproduction and genetic causal attribution of epilepsy.
Reproduction and genetic causal attribution of epilepsy.
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This study addresses the contribution of genetics-related concerns to reduced childbearing among people with epilepsy. Surveys were completed by 606 adult patients with epilepsy of unknown cause at our medical center. Poisson regression analysis was used to assess the relations of number of offspring to: (1) genetic attribution (GA: participants’ belief that genetics was a cause of their epilepsy), assessed via a novel scale developed from four survey items (Cronbach’s alpha = .89), (2) participants’ estimates of epilepsy risk in the child of a parent with epilepsy (1%, 5%–10%, 25%, and 50%–100%), and (3) participants’ reports of the influence on their reproductive decisions of “the chance of having a child with epilepsy” (none/weak/moderate, strong/very strong). Analyses were adjusted for age, education, race/ethnicity, religion, type of epilepsy (generalized, focal, and both/unclassifiable), and age at epilepsy onset (<10, 10–19, and ≥20 years). Among participants 18–45 years of age, the number of offspring decreased significantly with increasing GA (highest vs lowest GA quartile rate ratio [RR] = .5, p < .001), and increasing estimated epilepsy risk in offspring (with 5%–10% as referent because it is closest to the true value, RR for 25%: .7, p = .05; RR for 50%–100%: .6, p = .03). Number of offspring was not related to the reported influence of “the chance of having a child with epilepsy” on reproductive decisions. Among participants >45 years of age, the number of offspring did not differ significantly according to GA quartile or estimated offspring epilepsy risk. However, those reporting a strong/very strong influence on their reproductive decisions of “the chance of having a child with epilepsy” had only 60% as many offspring as others. These findings suggest that overestimating the risk of epilepsy in offspring can have important consequences for people with epilepsy. Patient and provider education about recurrence risks and genetic testing options to clarify risks are critical, given their potential influence on reproductive decisions.
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影响因子:
5.6
作者:
Sorge ST;Hesdorffer DC;Phelan JC;Winawer MR;Shostak S;Goldsmith J;Chung WK;Ottman R
通讯作者:
Ottman R
影响因子:
4.8
作者:
通讯作者:
--
影响因子:
5
作者:
Artama, M;Isojärvi, JIT;Auvinen, A
通讯作者:
Auvinen, A
影响因子:
2.6
作者:
Vazquez, Blanca;Gibson, Patricia;Kustra, Robert
通讯作者:
Kustra, Robert
影响因子:
5.6
作者:
Hesdorffer DC;Caplan R;Berg AT
通讯作者:
Berg AT