Complete remission in nonsyndromic childhood-onset epilepsy
Article first published online: 27 JUN 2011
Copyright © 2011 American Neurological Association
Annals of Neurology
Volume 70, Issue 4, pages 566–573, October 2011
How to Cite
Berg, A. T., Testa, F. M. and Levy, S. R. (2011), Complete remission in nonsyndromic childhood-onset epilepsy. Ann Neurol., 70: 566–573. doi: 10.1002/ana.22461
- Issue published online: 25 OCT 2011
- Article first published online: 27 JUN 2011
- Accepted manuscript online: 29 APR 2011 12:51PM EST
- Manuscript Accepted: 22 APR 2011
- Manuscript Revised: 10 APR 2011
- Manuscript Received: 22 JAN 2011
Determine the probability of attaining complete remission in children with nonsyndromic epilepsy (NSE) over the course of ≥10 years from initial diagnosis; identify early predictors of complete remission; and assess the risk of relapse after achieving complete remission.
In a prospective community-based cohort, complete remission was defined as 5 years seizure-free and medication-free. Any subsequent seizure for any reason was a relapse. Univariate and bivariate analyses were conducted with standard methods including the Kaplan-Meier approach. Proportional hazards modeling was used for multivariable analysis.
Of 613 cohort members, 347 had NSEs, of whom 294 (85%) were followed ≥10 years (maximum = 17.9). A total of 170 in 294 (58%) achieved complete remission, 10 of whom (6%) relapsed. Seizure outcome at 2 years (remission, pharmacoresistant, unclear) (p < 0.0001) and underlying cause (p < 0.0001) distinguished groups with complete remission ranging from ∼20% to ∼75%. Older age at onset was independently associated with a poorer chance of complete remission. Relapses occurred up to 7.5 years after attaining complete remission and were marginally associated with underlying cause (p = 0.06).
Complete remission occurs in over one-half of young people with NSE and generally persists. Meaningful but imperfect predication is possible based on underlying cause and early seizure control. The finding of age effects may play a role in meaningful identification of phenotypes, which could become fruitful targets for genetic and imaging investigations in these otherwise poorly differentiated epilepsies. ANN NEUROL 2011;