Demonstration of thalarnic activation during typical absence seizures using H215O and PET
- M. C. Prevett, MRCP,
- J. S. Duncan, DM,
- T. Jones, DSc,
- D. R. Fish, MD and
- D. J. Brooks, MD
- From the MRC Cyclotron Unit (Drs. Prevett, Duncan, Jones, and Brooks), Hammersmith Hospital, London, and the Epilepsy Research Group (Drs. Prevett, Duncan, and Fish), University Department of Clinical Neurology, Institute of Neurology, Queen Square, London, UK.
- Address correspondence and reprint requests to Dr Duncan, Epilepsy Research Group, University Department of Clinical Neurology, Institute of Neurology, National Hospital for Neurology and Neurosurgery, Queen Square, London, WClN 3BG, UK.
Abstract
Background The EEG correlate of absence seizures is 3-Hz, generalized spike-wave activity. Depth electrode recordings in animal models suggest that spike-wave activity oscillates within thalamocortical circuits, but the site of the primary abnormality is uncertain. The aim of the present study was to determine whether there is a selective increase in blood flow in the thalamus during absence seizures and, if so, whether it precedes the appearance of spike-wave activity on scalp EEG.
Methods Using PET, regional cerebral blood flow (rCBF) was measured in eight patients with idiopathic generalized epilepsy in whom typical absence seizures were induced by voluntary hyperventilation. Each patient was studied up to 12 times, with an intravenous bolus injection of H215O followed by a 90-second scan. The distribution of rCBF during absence seizures and in the 30 seconds before an absence seizure were compared with the distribution of rCBF when absence seizures did not occur.
Results There was a mean global 14.9% increase in blood flow in association with typical absence seizures and, on top of the global increase, a focal increase in thalamic blood flow of 3.9 to 7.8%. There were no significant focal changes in rCBF in the 30 seconds before the onset of spike-wave activity on the EEG.
Conclusion This study provides evidence for the key role of the thalamus in the pathogene-sis of absence seizures but was unable to show that it is the site of initiation of the seizures.
- Copyright 1995 by the American Academy of Neurology
