Abstracts

To investigate the interiktal and postiktal perfusion changes in patients with focal epilepsies. Six patients with temporal lobe epilepsy (n=5) and parietal lobe epilepsy (n=1) (3 male, 3 female, age range 23 to 47 years) with complex partial seizures (n=6), additional secondary generalyzed seizures (n=4) and simple partial seizures (n=2) participated in this study. Three patients had a hippocampus sclerosis and one patient had a posttraumatic atrophy in the lateral temporal cortex. MR perfusion measurement with bolus application of 0,2 mol/kg Gd-DTPA and echo planar imaging was performed interiktally, and postiktally after 1 to 12 min, 13 to 30 min, 30 to 60 min and 60 to 100 min, respectively, as part of a presurgical evaluation. Bolus-to-peak-ratio was measured in the hippocampus, parahippocampal gyrus, thalamus, cortex and white matter. An asymmetry index (AI) reflecting hyperperfusion (AI[gt]1) and hypoperfusion (AI[lt]1) of the ictogenic vs. the non-ictogenic side was calculated. Interiktally perfusion was increased in the hippocampus of the ictogenic side (AI[gt]1) in 5 patients. In 4 patients the AI decreased in the first half hour postiktally (25-39%) and returned to baseline in the later measurements. In the parahippocampal gyrus the AI was elevated interiktally and showed a further increase in the early postiktal measurements (8-24%). In the late postiktal measurements the AI decreased. The thalamus showed little perfusion change postiktally (8-24%). In the white matter the AI increased in the first half hour in the patients with hippocampal sclerosis and decreased in the late measurements. In the cortex perfusion changes were parallel to the hippocampus showing a decrease in the early (10-26%) and an increase in the late measurements. Our patients with temporal lobe epilepsy showed in initial drop and a delayed increase of perfusion postiktally in the affected hippocampus and a reverse pattern in the adjacent parahippocampal gyrus. The postiktal perfusion changes were minor in the thalamus and non-uniform in the cortex and white matter. This may be due to the spread of the iktal activity from the hippocampus to the adjacent lateral areas while the remote areas are less involved.