Interictal regional slow activity in temporal lobe epilepsy correlates with lateral temporal hypometabolism as imaged with 18FDG PET: neurophysiological and metabolic implications
a Epilepsy Surgery
Centre, King's College Hospital, b Department of Public Health
Medicine, Guy's and St Thomas' UMDS, c Department of Clinical Neurophysiology and
Epilepsies, d Clinical
PET Centre, St Thomas' Hospital, London, UK
Correspondence to: 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 and in revised form 26 March 1998;
Accepted 31 March
1998
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
Interictal
18F-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.
© 1998 by Journal of Neurology, Neurosurgery, and Psychiatry
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