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Evolution of lobar abnormalities of cerebral glucose metabolism in 41 children with drug-resistant epilepsy
Journal article   Open access   Peer reviewed

Evolution of lobar abnormalities of cerebral glucose metabolism in 41 children with drug-resistant epilepsy

Tuhina Govil-Dalela, Ajay Kumar, Michael E Behen, Harry T Chugani and Csaba Juhász
Epilepsia (Copenhagen), Vol.59(7), pp.1307-1315
07/2018
DOI: 10.1111/epi.14404
PMCID: PMC6031462
PMID: 29786852
url
https://doi.org/10.1111/epi.14404View
Published (Version of record) Open Access

Abstract

We analyzed long-term changes of lobar glucose metabolic abnormalities in relation to clinical seizure variables and development in a large group of children with medically refractory epilepsy. Forty-one children (25 males) with drug-resistant epilepsy had a baseline positron emission tomography (PET) scan at a median age of 4.7 years; the scans were repeated after a median of 4.3 years. Children with progressive neurological disorders or space-occupying lesion-related epilepsy and those who had undergone epilepsy surgery were excluded. The number of affected lobes on 2-deoxy-2( F)-fluoro-D-glucose-PET at baseline and follow-up was correlated with epilepsy variables and developmental outcome. On the initial PET scan, 24 children had unilateral and 13 had bilateral glucose hypometabolism, whereas 4 children had normal scans. On the follow-up scan, 63% of the children showed an interval expansion of the hypometabolic region, and this progression was associated with persistent seizures. In contrast, 27% showed less extensive glucose hypometabolism at follow-up; most of these subjects manifested a major interval decrease in seizure frequency. Delayed development was observed in 21 children (51%) at baseline and 28 (68%) at follow-up. The extent of glucose hypometabolism at baseline correlated with developmental levels at the time of both baseline (r = .31, P = .05) and follow-up scans (r = .27, P = .09). In this PET study of unoperated children with focal epilepsy, the lobar pattern of glucose hypometabolism changed over time in 90% of the cases. The results support the notion of an expansion of metabolic dysfunction in children with persistent frequent seizures and its association with developmental delay, and support that optimized medical treatment to control seizures may contribute to better neurocognitive outcome if no surgery can be offered.
 Adolescent Anticonvulsants - therapeutic use Blood Glucose - metabolism Brain - diagnostic imaging Brain - drug effects Brain - physiopathology Child Child, Preschool Developmental Disabilities - diagnostic imaging Developmental Disabilities - drug therapy Developmental Disabilities - physiopathology Disease Progression Dominance, Cerebral - drug effects Dominance, Cerebral - physiology Drug Resistant Epilepsy - diagnostic imaging Drug Resistant Epilepsy - drug therapy Drug Resistant Epilepsy - physiopathology Electroencephalography - drug effects Energy Metabolism - drug effects Energy Metabolism - physiology Female Fluorodeoxyglucose F18 Follow-Up Studies Humans Infant Magnetic Resonance Imaging Male Positron-Emission Tomography Retrospective Studies

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