Abstracts

Rationale: Imaging studies of newly diagnosed epilepsy may provide important information about epilepsy diagnosis and prognosis. However, patients are rarely studied from the point of diagnosis using quantitative MRI, despite this being a crucial time point in understanding the underlying neurobiology of epilepsy [Pitkänen et al., Lancet Neurol, 2002;1;173]. Approximately 40% of patients never achieve seizure freedom [Brodie et al., Neurology, 2012;78;1548]. However, there are no current imaging biomarkers of treatment outcome. The purpose of this study was to determine whether volumes of subcortical structures that have been demonstrated to be important in refractory epilepsy are atrophied in patients with newly diagnosed focal epilepsy (NDfE), and whether volume alterations are related to clinical aspects of the disorder. Methods: A total of 82 patients with NDfE and 40 healthy controls received a T1-coronal FLAIR MRI scan. Volume estimation of the left and right hippocampus, thalamus, putamen, caudate nucleus and temporal lobe were performed using stereology in conjunction with point counting (Fig.1) on MRIs for all participants. To control for individual differences subcortical volumes were normalised using whole brain volume and Mann-Whitney U tests were performed. Clinical data was obtained for patients, including age of first seizure, duration of epilepsy, seizure remission at six and twelve months, seizure type (complex partial and secondary generalised tonic-clonic), therapy type (monotherapy or polytherapy) and EEG finding. Results: Normalized volume of the left (U = 878, p<0.001) and right (U = 1127, p = 0.005) thalamus, left (U = 1068, p = 0.002) and right (U = 1208, p = 0.018) hippocampus, and left temporal lobe (U = 1057, p = 0.001) were significantly smaller in patients relative to controls. Only the findings in the left hemisphere survived Bonferroni correction. A decrease in volume of 7.5% in the left thalamus, 5.0% in the right thalamus, 9.3% in the left hippocampus, 8.2% in the right hippocampus and 5.5% in the left temporal lobe was observed in patients relative to controls. Individual volumetric analysis revealed abnormal volume (defined as volumes lower than two standard deviations below the control mean) in the left thalamus of fourteen (17.1%) patients, the right thalamus of four (4.9%) patients, the left hippocampus of nine (11.0%) patients, and the right hippocampus of three (3.7%) patients, only two (2.4%) patients had abnormal left temporal lobe volume. Furthermore, smaller right putamen volumes were observed in patients who experienced CPS relative to those who did not (U = 604, p = 0.041) and in those who had abnormal EEG findings (U = 143, p = 0.043). Putamen results did not survive Bonferroni correction. Conclusions: This study reports the first evidence for thalamic atrophy in NDfE, the results also support previous findings of hippocampal atrophy [Van Paesschen et al., Neurology, 1997;49;753]. The cause of volume loss in brain structures in NDfE is unclear but likely not due to the chronicity of the disorder. Greater effects were observed in the left hemisphere, which may indicate a greater proportion of patients with a left hemispheric onset in this study. Funding: No funding