Interictal regional slow activity in temporal lobe epilepsy correlates with lateral temporal hypometabolism as imaged with18FDG PET: neurophysiological and metabolic implications
- Michael Koutroumanidisa,c,
- Colin D Binniea,
- Robert D C Elwesa,
- Charles E Polkeya,
- Paul Seedb,
- Gonzalo Alarcona,
- Tim Coxa,
- Sally Barringtond,
- Paul Marsdend,
- Michael N Maiseyd,
- Chrysostomos P Panayiotopoulosc
- aEpilepsy Surgery Centre, King’s College Hospital, bDepartment of Public Health Medicine, Guy’s and St Thomas’ UMDS, cDepartment of Clinical Neurophysiology and Epilepsies, dClinical PET Centre, St Thomas’ Hospital, London, UK
- Professor C D Binnie, Department of Clinical Neurophysiology, King’s College Hospital, Denmark Hill, London, SE5 9RS, UK. Telephone 0044 171 3465309; fax 0044 171 3463445.
- Received 29 September 1997
- Revised 26 March 1998
- Accepted 31 March 1998
Abstract
OBJECTIVES The phenomenon of interictal regional slow activity (IRSA) in temporal lobe epilepsy and its relation with cerebral glucose metabolism, clinical data, MRI, and histopathological findings was studied.
METHODS Interictal18F-fluorodeoxyglucose positron emission tomography (FDG PET) was performed under continuous scalp EEG monitoring in 28 patients with temporal lobe epilepsy not associated with intracranial foreign tissue lesions, all of whom subsequently underwent resective surgery. Regions of interest (ROIs) were drawn according to a standard template. IRSA was considered lateralised when showing a 4:1 or greater ratio of predominance on one side.
RESULTS Sixteen patients (57%) had lateralised IRSA which was always ipsilateral to the resection and of maximal amplitude over the temporal areas. Its presence was significantly related to the presence of hypometabolism in the lateral temporal neocortex (p=0.0009). Logistic regression of the asymmetry indices for all measured cerebral regions confirmed a strong association between IRSA and decreased metabolism of the posterior lateral temporal neocortex only (p=0.009). No significant relation could be shown between slow activity and age at onset, duration of the epilepsy, seizure frequency, and MRI evidence for hippocampal atrophy. Furthermore, IRSA was not specifically related to mesial temporal sclerosis or any other pathology.
CONCLUSIONS Interictal regional slowing in patients with temporal lobe epilepsy not associated with a mass lesion is topographically related to the epileptogenic area and therefore has a reliable lateralising, and possibly localising, value. Its presence is irrelevant to the severity or chronicity of the epilepsy as well as to lateral deactivation secondary to neuronal loss in the mesial temporal structures. Although slow EEG activity is generally considered as a non-specific sign of functional disturbance, interictal regional slowing in temporal lobe epilepsy should be conceptualised as a distinct electrographic phenomenon which is directly related to the epileptogenic abnormality. The strong correlation between interictal regional slowing and lateral temporal hypometabolism suggests in turn that the second may delineate a field of reduced neuronal inhibition which can receive interictal and ictal propagation.
