Abstracts

Hippocampal sclerosis in temporal lobe epilepsy (TLE) is often associated with a T2 hyperintensity. In this study we used voxel-wise analysis of regional T2 relaxation rate (T2rr) to test the following hypotheses: 1. TLE with hippocampal sclerosis (TLE-MTS) have decreased T2rr in the ipsilateral hippocampus but also in extratemporal regions. 2. TLE with normal MRI (TLE-no) have no or only mild hippocampal T2rr decreases not detectable by a voxel-based analysis but similar extrahippocampal abnormalities as TLE-MTS., The study included 42 patients (mean age 35.3 (10.6) suffering from temporal lobe epilepsy (24 TLE-MTS, 18 TLE-no) and 30 healthy volunteers (mean age 30.3 (7.9)). All subjects were studied on a 1.5 T system with a double spin echo (DSE) with either TR/TE1/TE2 2575/20/80 msec (19 controls, 13 TLE-MTS, 7 TLE-no) or with TR/TE1/TE2 5000/20/80 msec (11 controls, 11 TLE-MTS, 11 TLE-no). T2rr maps were calculated from the DSE according to T2 rate = ln (S1/S2) where S1 represents the signal for the early and S2 the signal for the late echo. The analysis was done in SPM2 using an ANCOVA with age and TR as nuisance variables., In comparison with controls, TLE-MTS had large regions of decreased T2rr in the ipsilateral hippocampus, parahippocampal gyrus, temporal, frontal and fronto-orbital regions and several smaller clusters occipito-parietal and insular and in contralateral orbito-frontal and frontal regions. TLE-no had small regions of decreased T2rr in the ipsilateral inferior temporal gyrus and the parahippocampal gyrus. When compared with TLE-no, TLE-MTS had clusters of decreased T2rr in the ipsilateral hippocampal head and white matter of the temporal pole and temporal stem; there were no regions of decreased T2rr when TLE-no were compared to TLE-MTS., TLE-MTS had the most prominent T2rr decreases in the hippocampus consistent with the hippocampus being the epileptogenic focus. In addition TLE-MTS had also widespread ipsi- and contralateral extrahippocampal T2rr decreases. The aetiology of these extrahippocampal abnormalities is not clear. Their distribution is consistent with excitotoxic effects due to seizure spread but also with developmental abnormalities facilitating seizure generation/propagation. In TLE-no the region of T2rr decreases was restricted to a small area in the ipsilateral inferior and medial temporal lobe but spared the hippocampus suggesting that the hippocampus is not consistently involved in seizure generation/propagation in TLE-no. The absence of extratemporal abnormalities might indicate that TLE-no are protected against whatever factors cause the extratemporal abnormalities in TLE-MTS. This further supports the notion that TLE-no are a different clinico-pathological entity than TLE-MTS and maybe even heterogeneous in themselves., (Supported by RO1-NS31966 to KDL.)