Abstracts

Visual inspection of MRI reveals increased T2 signal abnormalities in the temporopolar region ipsilateral to the seizure focus in 30-60% of temporal lobe epilepsy (TLE). T2 signal changes posterior to the temporal pole, as well as bilateral T2 signal changes, are difficult to appreciate visually and have not been explored quantitatively. In addition, the relationship of these abnormalities to hippocampal changes found in TLE has not been adequately investigated.
The purpose of this study was to assess temporal lobe white matter (WM) T2-signal changes quantitatively using T2 relaxometry, and to examine the relationship of these changes to hippocampal volume and hippocampal T2 signal abnormalities in patients with medically intractable TLE.
We studied 56 consecutive TLE patients (mean age = 35 years) and 30 neurologically normal controls. For computation of T2 values, images were acquired using a conventional dual-echo spin-echo pulse sequence (TE 20, 120 ms; TR 3240 ms, slice thickness 5 mm with 0.5 mm inter-slice gap) on a 1.5 T scanner. Twenty-three contiguous oblique coronal slices covering the whole brain with a voxel size of 0.94 x 0.94 mm2 were acquired. Slices were oriented orthogonal to the axis of the hippocampal body. For each individual, single-exponential-decay equations were fit to the T2 imaging data obtained in each pixel and then T2 relaxation times were calculated for each pixel. For each slice a map was then constructed in which pixel-intensity corresponded to the calculated T2 relaxation time. Averages of 6 slices were used to calculate left and right hippocampal T2 relaxation times (Hippo-T2) and left and right temporal lobe WM T2 relaxation times (WM-T2). Mean T2 relaxation time was calculated in each ROI. Finally, a total mean WM-T2 and Hippo-T2 was calculated by averaging the values of all ROIs in all slices. Volumetric MRI of the hippocampus showed unilateral hippocampal atrophy (HA) in 27 patients, while 29 patients had normal hippocampal volumes (NV).
WM-T2 was increased ipsilateral to the seizure focus in TLE patients with HA and those with NV ([italic]p[/italic] [lt] 0.001). Contralateral WM-T2 was increased in left and right TLE with HA ([italic]p[/italic] [lt] 0.001) and in right TLE with NV ([italic]p[/italic] = 0.002). There was no difference in the mean ipsilateral WM-T2 between patients with HA and those with NV. We found a positive correlation between Hippo-T2 and WM-T2 ipsilateral ([italic]p[/italic] [lt] 0.001) and contralateral ([italic]p[/italic] = 0.01) to the seizure focus. There was no correlation between WM-T2 and duration of epilepsy. There was no difference in mean WM-T2 between patients with a history of febrile convulsions and those without, and patients with frequent or rare/no secondary generalized seizures.
T2 relaxometry demonstrates a bilateral increase in T2 relaxation time throughout the temporal lobe white matter in patients with intractable TLE. These abnormalities may occur regardless of the presence of hippocampal atrophy.