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Interictal metabolism and blood flow are uncoupled in temporal lobe cortex of patients with complex partial epilepsy

From the Epilepsy Research Branch (Drs. Gaillard, White, Malow, Sato, and Theodore, and S. Fazilat and P. Reeves), National Institute of Neurological Disorders and Stroke, and the PET Imaging Section (Dr. Herscovitch), PET Department, Clinical Center, National Institutes of Health, Bethesda, MD.
Received August 18, 1994. Accepted in final form March 6, 1995.
Address correspondence and reprint requests to Dr Gaillard, Department of Neurology, Children's National Medical Center, The George Washington University, 111 Michigan Avenue, NW, Washington, DC 20010.

We used positron emission tomography (PET) with¹⁸ F-2-deoxyglucose (FDG) and¹⁵ O water in 20 patients with complex partial seizures to compare glucose metabolism and blood flow in temporal lobe epileptic foci identified by ictal scalp-sphenoidal video-EEG telemetry. Glucose metabolism was measured 20 minutes after blood flow without moving the patient from the scanner. We also studied 11 patients with^99m Tc-HMPAO single-photon emission computed tomography (SPECT). Both local cerebral metabolic rate of glucose (LCMRGlc) and regional cerebral blood flow (rCBF) were significantly decreased in temporal cortex ipsilateral to the EEG focus. However, LCMRGlc was reduced by 11.2% in inferior lateral and 11.1% in inferior mesial temporal cortex and rCBF by only 3.2% and 6.1%. The ratio of LCMRGlc to rCBF was significantly reduced in inferior lateral temporal cortex ipsilateral to the ictal focus (p less than 0.009). Moreover, using standardized criteria, blinded raters found that 16 of 20 patients had focal FDG-PET hypometabolism, all in the epileptogenic region; 10 of 20 had focal¹⁵ O water PET hypoperfusion, but it was falsely lateralized in two of these 10; and five of 11 had focal^99m Tc-HMPAO SPECT hypoperfusion, but it was falsely lateralized in two of these five. Our data suggest that interictal glucose metabolism and blood flow may be uncoupled in epileptogenic cortex.

NEUROLOGY 1995;45: 1841-1847

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