{"id":1146,"date":"2012-06-20T13:52:36","date_gmt":"2012-06-20T13:52:36","guid":{"rendered":"https:\/\/touchneurology.com\/2012\/06\/20\/childhood-absence-epilepsy-a-review-of-treatment-strategies-and-perspectives-for-the-future-2\/"},"modified":"2012-06-20T13:52:36","modified_gmt":"2012-06-20T13:52:36","slug":"childhood-absence-epilepsy-a-review-of-treatment-strategies-and-perspectives-for-the-future-2","status":"publish","type":"post","link":"https:\/\/touchneurology.com\/epilepsy\/journal-articles\/childhood-absence-epilepsy-a-review-of-treatment-strategies-and-perspectives-for-the-future-2\/","title":{"rendered":"Childhood Absence Epilepsy\u2014A Review of Treatment Strategies and Perspectives for the Future"},"content":{"rendered":"

Childhood absence epilepsy (CAE) is one of the most common forms of paediatric epilepsy, accounting for between 10 and 17 % of all cases of childhood onset epilepsies.1<\/sup> CAE is defined by age-related onset, clinical and electrographical characteristics, and a presumed genetic aetiology.2<\/sup> The syndrome typically begins at between four and eight years of age in an otherwise healthy child. Typical absence seizures are characterised by brief loss of awareness associated with bilateral, synchronous symmetrical 3 Hz spike-waves on a normal background of electroencephalographic (EEG) activity.2<\/sup> Although CAE is usually considered to be a benign form of epilepsy, the remission rate varies across studies from 21 to 95 %.3,4<\/sup> About 15 % of patients could progress to juvenile myoclonic epilepsy, favoured by risk factors such as absence status before or during anti-epileptic drug (AED) treatment, development of tonic-clonic or myoclonic seizures after onset of treatment, or abnormal background on initial EEG.5<\/sup> In addition, it has been shown that affected children, including those who are seizure free, can develop both psychosocial and educational difficulties.6<\/sup> Neuropsychological deficits include lower scores at measures of general cognitive functioning and memory performances, with selective involvement of nonverbal memory and delayed recall.7<\/sup> These difficulties could reflect the impact of either seizures or of a neurodevelopmental susceptibility, AEDs or a mixture of these factors. In this context, therapeutic decisions should balance the anti-epileptic efficacy and tolerability of AEDs, with a specific attention to their impact on cognition.
\nWhat do Anti-epileptic Drug Trials Show?<\/b>
\nDespite the increasing number of AEDs that have been licensed for the treatment of seizure disorders over the past 20 years, only a few have been evaluated in the treatment of CAE. Consequently, valproic acid (VPA) and ethosuximide (ESM) have been used as first-line agents for the treatment of absence seizures for over 40 years.8<\/sup> Over these four decades, only nine randomised controlled trials (RCTs) have been published in the field,9\u201317<\/sup> with many suffering from major methodological limitations. RCTs are separated into four classes according to the rating scale of their level-of-evidence,18<\/sup> the highest being class I. To be classified as class I or II, monotherapy AED trials should fulfil:<\/p>\n