Evidence map›Paper›PMID 27558297›Full record

ArticleEpilepsia2016

Depression and genetic causal attribution of epilepsy in multiplex epilepsy families.

Shawn T Sorge, Dale C Hesdorffer, Jo C Phelan, Melodie R Winawer, Sara Shostak, Jeff Goldsmith, Wendy K Chung, Ruth Ottman

Open access · bronzeAbstract read
In one paragraph

Article in Epilepsia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.9field-weighted citation impact, top 24% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 9 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Shawn T SorgeGH Sergievsky Center, Columbia University, New York, New York, U.S.A.
Dale C HesdorfferGH Sergievsky Center, Columbia University, New York, New York, U.S.A.
Jo C PhelanDepartment of Sociomedical Sciences, Columbia University, New York, New York, U.S.A.
Melodie R WinawerGH Sergievsky Center, Columbia University, New York, New York, U.S.A.
Sara ShostakDepartment of Sociology, Brandeis University, Waltham, Massachusetts, U.S.A.
Jeff GoldsmithDepartment of Biostatistics, Mailman School of Public Health, Columbia University, New York, New York, U.S.A.
Wendy K ChungDepartment of Pediatrics, Columbia University, New York, New York, U.S.A.
Ruth OttmanGH Sergievsky Center, Columbia University, New York, New York, U.S.A.. ro6@columbia.edu.
Columbia University · USBrandeis University · US

Funding

Center for Research on the Ethical, Legal and Social Implications of Psychiatric, Neurologic and Behavioral GeneticsP50HG007257 · NHGRI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI APPELBAUM, PAUL STUART · 2013 to 2017
$5.4M
Psychosocial Impact of Genetics in EpilepsyR01NS078419 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI OTTMAN, RUTH · 2012 to 2015
$2.3M
NHGRI NIH HHS P50 HG007257NINDS NIH HHS R01 NS078419
6 · The paper itself

Abstract

objectivesRapid advances in genetic research and increased use of genetic testing have increased the emphasis on genetic causes of epilepsy in patient encounters. Research in other disorders suggests that genetic causal attributions can influence patients' psychological responses and coping strategies, but little is known about how epilepsy patients and their relatives will respond to genetic attributions of epilepsy. We investigated the possibility that among members of families containing multiple individuals with epilepsy, depression, the most frequent psychiatric comorbidity in the epilepsies, might be related to the perception that epilepsy has a genetic cause.

methodsA self-administered survey was completed by 417 individuals in 104 families averaging 4 individuals with epilepsy per family. Current depression was measured with the Patient Health Questionnaire. Genetic causal attribution was assessed by three questions addressing the following: perceived likelihood of having an epilepsy-related mutation, perceived role of genetics in causing epilepsy in the family, and (in individuals with epilepsy) perceived influence of genetics in causing the individual's epilepsy. Relatives without epilepsy were asked about their perceived chance of developing epilepsy in the future, compared with the average person.

resultsPrevalence of current depression was 14.8% in 182 individuals with epilepsy, 6.5% in 184 biologic relatives without epilepsy, and 3.9% in 51 individuals married into the families. Among individuals with epilepsy, depression was unrelated to genetic attribution. Among biologic relatives without epilepsy, however, prevalence of depression increased with increasing perceived chance of having an epilepsy-related mutation (p = 0.02). This association was not mediated by perceived future epilepsy risk among relatives without epilepsy. SIGNIFICANCE: Depression is associated with perceived likelihood of carrying an epilepsy-related mutation among individuals without epilepsy in families containing multiple affected individuals. This association should be considered when addressing mental health issues in such families.

Indexed as

Family HealthAdolescentAdultAgedDepressionEpilepsyFemaleHumansMaleMiddle AgedPredictive Value of TestsPsychometricsRetrospective StudiesSurveys and QuestionnairesYoung AdultDepressionEpidemiologyEpilepsyGenetic attributionGenetics

Identifiers

PMID27558297
PMCPMC5056147
OpenAlexW2516920097

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.