Abstracts

The childhood absence epilepsy (CAE) is usually well controlled epilepsy by drug therapy. Between 5% and 10% of CAE are refractory to a combination of valproate, ethosuccimide and lamotrigine, especially if there is a beginning before 3 years of age. In refractory CAE, there are often learning disorders and the absence seizures persist usually after 20 years of age. The aim of this study is to evaluate the efficacy of vagus nerve stimulation (VNS) on refractory CAE.
We retrospectively analysed the data of 5 patients with refractory CAE but without other type of seizure. VNS started after at least 2 years of failure of anti-absence drug therapy. The age at the beginning of CAE ranged from 2 to 6 years and the age at the implantation between 4 and 12 years (mean: 7 years of age). Each patient has had a counting of seizures by 24 hours EEG video recording before VNS implantation and each 6 months after VNS implantation, without any change in drug therapy. The effect of VNS on alertness was assessed subjectively by the parents.
After 6 months of VNS, there was no significant decrease in seizure frequency in all the patients but alertness improved after 3months in 3 patients. After 6 months, the stimuli duration parameters were 1mn [quot]on[quot] and 1.1mn [quot]off[quot], with a good tolerance. One child has 18 months follow-up with disappearance of absence seizures and two other children have 12 months follow-up with respectively 70% and 85% decrease in seizure frequency.
The data about the efficacy of VNS in CAE are very few in literature. It is the first study with an implantation at a so young age, with only one type of seizures and with an evaluation by a 24 hours EEG recording before and every 6 months after VNS. So, we can determine the timing of the effect. The improvement of alertness appears in the first 3 months and the decreases in seizure frequency begin from 6 months. Thalamus is involved by neuronal network of absence seizures and by VNS according to the data of PET and FMRI studies. The efficacy of VNS on absence seizures of CAE does not seem secondary to the increase of alertness and is possibly due to a long term mechanism of action on thalamus.