Abstracts

Rationale: T2 relaxometry can assist the diagnosis of hippocampal sclerosis (HS). However, the ability of detecting epileptic pathology other than HS remains unclear. We hypothesized that T2 relaxometry increase diagnostic power to detect non-sclerotic epileptogenic abnormality of the hippocampus in presurgical evaluation of temporal lobe epilepsy (TLE).Methods: This study prospectively included 23 patients who underwent hippocampectomy as a part of surgical treatment of refractory TLE. Eight patients had structural epileptogenic lesions in extra-hippocampal temporal lobe. Eleven patients underwent intracranial EEG study before resective surgery. Visual assessment of hippocampal atrophy and increased T2 signal, manual volumetry and T2 relaxometry of hippocampus were performed pre-operatively using 3T MRI, and compared with neuropathological findings and intracranial EEG findings. MRI of 30 age-matched healthy controls was used to establish normal values.Results: Visual assessment, volumetry, and T2 relaxometry detected hippocampal abnormalities of surgical side in 12 (52%) and 13 (57%), 19 (83%) patients respectively. Hippocampal volume loss was always associated with prolonged T2 relaxation time, and supported by histopathological diagnosis of HS in all except one case. Hippocampal abnormality was detected only by T2 relaxometry in six patients. Pathological diagnosis of these cases included mild HS in one, microdysgenesis in one, granule cell pathology (GCP) in two, and gliosis in two. Four patients with normal hippocampal volume and T2 relaxation time had no HS or GCP. Various degrees of gliosis were found in all cases. Prolonged T2 relaxation time was associated with medial temporal seizure onset in intracranial EEG (p = 0.02).Conclusions: Volumetry and T2 relaxometry were equally powerful in detecting hippocampal sclerosis. However, T2 relaxometry is superior to MRI volumetry in detecting non-atrophic hippocampal abnormalities in patients with TLE.T2 relaxometry enhances the detection of non-sclerotic epileptogenic abnormality of the hippocampus.