Abstracts

Rationale: Mesial Temporal Sclerosis (MTS) is the most common cause of temporal lobe epilepsy (TLE), characterized by gliosis and atrophy of the hippocampus and related structures, such as the temporal pole, mamilar body and fornix. However, the brain damage is not limited to these structures. There are metabolic changes detected by proton spectroscopy described in posterior temporal lobe and whole brain atrophy measured by automatic segmentation methods. Therefore, the purpose of this study is to test the hypothesis that there is extra temporal brain damage related to MTS. Methods: We studied 20 normal controls (10 men) and 24 TLE patients (14 men) with age, respectively 36.7 ± 11.9 (mean ± SD), and 39.5 ± 9.24 years. All patients and normals had a full clinical follow-up and MRI obtained in 1.5T equipment. The MRI protocol included high resolution whole brain T1-weighted MPRAGE sequence and one pair of identical 3D-GRE sequences except for the presence of one extra pulse of magnetization transfer in the second. The ROI binary maps of whole white matter (WM), gray matter (GM), and cerebrospinal fluid (CSF) were segmented and used for value extraction from magnetization transfer ratio (MTR) maps. Results: The TLE patient group was different from normal in WM-MTR (decrease of 3.84%, p=0.005), GM-MTR (decrease of 6.12%, p=0.002) and percentage of GM (decrease of 21.54%, p=0.0016). The whole brain volume, measured by brain parenchyma fraction (BPF), was 1.32% smaller in TLE patients. The Mean MTR map showed significant signal loss in patients (p≤0.05) in corpus callosum, pons, temporal and frontal lobes. Conclusions: Our results support the hypothesis that there is diffuse brain lesion in MTS, not only in grey but also in white matter, what was detect in patients with repeated seizures, free from status epilepticus. The MTR reduction suggests that demyelination, axonal and cellular loss might be the pathophysiology involved.