Abstracts

Rationale: Frontal lobe epilepsy due to focal cortical dysplasia generally presents refractory motor seizures associated to cognitive impairment in many patients. We aimed to investigate progression of Gray Matter (GM) and White Matter (WM) atrophy outside the epileptic zone and in the contralateral hemisphere. Methods: We selected 23 patients (15 female, 33.4±11.7 years of age) with refractory frontal lobe epilepsy and probable focal cortical dysplasia. They underwent high resolution MRI (2T) (3D acquisition with 1mm isotropic voxels) in two occasions (interval 4.8±2.4 years). We performed the VBM technique on MATLAB7.5/SPM5 (www.fil.ion.ucl.ac.uk) to extract GM and WM maps from controls and patients and to test for baseline atrophy (T-test with 91 controls [48 women, 30.5± 13.7years]) and progression of atrophy (Paired T-test adjusted for the interval between scans). We preprocessed the scans with MRICRO software (www.mricro.com) and flipped to left images from patients with right side epilepsy in order to investigate all patients simultaneously. To control for multiple comparisons we applied 1% of False Discovery Rate on statistical analyses in SPM. Significance was set at p<0.05 with clusters> 150 voxels and T-statistic >3.5. Results: Patients and controls were balanced for age (p=0.7) and gender (p=0.2). On baseline analysis (T-test with control group) we did not identify areas with GM atrophy, but observed some areas with WM atrophy including bilateral frontal (more widespread within ipsilateral hemisphere) and occipital lobes, ipsilateral cingulate gyrus, cerebellum and parietal lobe. We did not observe progression of WM atrophy, although we detected some areas with GM atrophy compared to the baseline. These encompassed bilateral cingulated gyri, bilateral frontal and occipital lobes (more widespread in contralateral hemisphere), contralateral cerebellum, temporal and parietal lobes. Conclusions: Our preliminary results suggest progression of structural damage in patients with refractory frontal lobe seizures. The progression of GM atrophy may be secondary to persistent and bilateral epileptic discharges in chronic refractory epilepsy. The observation of GM atrophy within contralateral cerebellum may be related to the cerebellar diaschisis detected in PET studies with long-standing partial seizures (mainly frontal epilepsy). These findings support the idea of progression of cognitive impairment in patients with chronic, intractable epilepsy. Although the mechanisms underlying the development of structural damage outside the epileptogenic area are not well understood, our results provide support in favor of early surgical intervention, as the plastic changes to recover function are greater at younger age.