Abstracts

Neurologically normal patients with primary depression have hippocampal volumes smaller than controls. Temporal lobe epilepsy (TLE) patients have a wider range of abnormalities in the mesial temporal structures, which allows investigation of the association of hippocampal volume with severity of depressive symptoms. Based on the hyperexcitable hippocampal efferents to limbic structures, we hypothesized that TLE patients will express increased symptoms of depression. In addition, we speculated that severe hippocampal atrophy will not support the hyperexcitable network required to maintain clinical depression., We evaluated 28 consecutive adults with TLE using clinical variables, long-term video/EEG monitoring, high resolution MRI and tests for depression, including the Beck Depression Inventory (BDI). On the MRI we manually delineated regions of interest in the mesial temporal (hippocampus, amygdala) and prefrontal (gyrus rectus, pregenual cortex, subgenual and subcallosal cortex) structures, based on prior human and animal studies of mood dysfunction. Distribution of the data was tested using the Kolmogorov-Smirnov test. Student[apos]s t-test was used to determine group differences, with a significance level set at p[lt] 0.05. Data were analyzed using the SPSS statistical software., Based on a total BDI score greater than 15, 42.8% of the group were experiencing significant symptoms of depression. None of the subjects in the quartile with the smallest left hippocampal volume had a BDI score greater than 15, whereas 57.1% of the subjects in the upper three quartiles had increased symptoms of depression, p[lt] 0.008. No other brain structure volume had an association with depressive symptoms., Patients with hippocampal volume loss that is consistent with severe hippocampal sclerosis had no evidence of significant symptoms of depression. This finding suggests that there is a critical number of hyperexcitable hippocampal neurons required to maintain depression in temporal lobe epilepsy.[figure1], (Supported by NIH grants NS40808 and NS047551 and Epilepsy Foundation fellowship grant.)