Cortical and subcortical glucose metabolism in childhood epileptic encephalopathies
- aDepartment of Paediatric Neurology, The General Infirmary at Leeds, UK, bClinical PET Centre, Department of Radiological Sciences, UMDS, London, UK, cDepartment of Paediatric Neurology, Guy’s Hospital, London, UK
- Dr C D Ferrie, Department of Paediatric Neurology, Clarendon Wing, The General Infirmary at Leeds, Belmont Grove, Leeds, LS2 9NS.
- Received 22 October 1996
- Revised 9 April 1997
- Accepted 21 April 1997
Abstract
OBJECTIVES Nearly one third of children with cryptogenic epileptic encephalopathies have been reported to have focal cortical defects on 18fluorodeoxyglucose (FDG) PET. As diffuse cortical dysfunction and involvement of subcortical structures, particularly the thalami, is postulated to underlie the propensity to seizures in these conditions, the aim was to determine the frequency of bilateral and diffuse cortical metabolic defects and of subcortical metabolic abnormalities in the same patients.
METHODS The interictal uptake of FDG was studied in 32 children with epileptic encephalopathies. Using a semiquantitative technique, the ratio of uptake in cortical regions and subcortical structures to that in the cerebellum was compared with that of age matched historical controls. Uptake more than 2 SD above (“hypermetabolic”) or below (“hypometabolic”) that of age matched controls was considered abnormal.
RESULTS Diffusely abnormal cortical uptake (nearly always hypometabolic) occurred in almost two thirds of patients; in all but two of the remaining patients at least one cortical region showed significantly decreased uptake bilaterally. When analysed as age cohorts, the mean cortical:cerebellar FDG uptake was significantly lower than that of controls in all cortical regions (P<0.005). Ninety per cent of patients had evidence of relative thalamic hypometabolism and in each age group there was a significant reduction in relative thalamic FDG uptake compared with that of controls (P<0.005). In nine out of 11 patients with unilateral cortical hypometabolic defects thalamic FDG uptake was lower ipsilateral to the cortical abnormality.
CONCLUSIONS Diffuse cortical dysfunction is common in the epileptic encephalopathies and may reflect the underlying cause of the condition or arise as a consequence of uncontrolled seizures. Altered thalamic glucose metabolism is further evidence of subcortical involvement in these conditions.
- positron emission tomography
- Lennox-Gastaut syndrome, infantile spasms, severe myoclonic epilepsy in infancy
