Abstracts

Rationale: It has been shown in recent publications that a subset of epilepsies caused by pre-/perinatal hypoxic-ischemic events (HIE) actually follows the path of age-related (benign) focal epilepsies of childhood (Wanigasinghe et al, Dev Med Child Neurol. 2010 Nov;52(11):1021-7; Mukhin et al. , Epilepsia 2015,Vol.56,Issue Suppl.S1, page 173(p0707,abstr.). In a previous retrospective investigation of 131 hemispherectomized/ hemispherotomized children and adolescents we were able to show that there was an impressive overrepresentation of ARED in children with pre-/perinatal insults in comparison to children with developmental lesions (18/49 (36 %) vs. 8/70 (11 %); Tarta-Arsene et al. Epilepsia,2015, Vol. 56,Issue Suppl.S1, page 249 (p1014, abstr.). There was no difference with respect to the percentages of a positive family anamnesis in both groups. Postoperative outcome was not different whether patients had ARED in the EEG or not. In a study of a large cohort of former premature children with epilepsies it was found that the incidence and prevalence of ARED was particularly high in children with periventricular leukomalacia (unpublished data, Epilepsy Center Vogtareuth). We hypothesized that the overrepresentation of ARED in children with congenital hemiparesis and severe drug resistant epilepsies due to pre-/perinatal vascular insults is related to additional white matter damage . Methods: Reevaluation of the pre-operative MRIs of the 49 hemispherectomized/ hemispherotomized children and adolescents with pre-/perinatal vascular insults by 2 investigators (1 pediatric radiologist [PW], 1 pediatric epileptologist [H.H]) with special expertise in the evaluation of MRIs of patients with epilepsy, who were blinded with respect to the EEG findings in these 49 patients. The diagnosis of an additional white matter damage (gliosis in addition to the zone of infarction) was made when the changes were located within the periventricular zone or within deep white matter. Results: White matter damage (gliosis in addition to the zone of infarction)) was diagnosed in 16 of the 18 (89 %) children who had ARED in their EEG and in 16/31 (52 %) patients with no ARED in their EEG (p=0,002). Conclusions: White matter damage (glioses) is a provocative factor for the generation of ARED in children with congenital hemiparesis and severe drug resistant epilepsies due to pre-/perinatal vascular insults. This finding should help to reduce diagnostic and therapeutic uncertainties as (additional) ARED are frequently not recognized as such in patients with focal structural (cortical) epilepsies. The pathophysiological mechanism by which ARED are provoked in white matter changes are not known. Funding: Dr. Tarta-Arsene research while she was at the center in Vogtareuth was supported by a grant from the Michael-Foundation, Germany (Michael Focused Fellowship Programm)