Abstracts

Rationale: Depression is one of the most problematic co-morbidities in temporal lobe epilepsy (TLE). Although the neurobiological underpinnings of depression in TLE are not well understood, previous research has implicated atrophy to medial temporal structures (i.e., hippocampus) and disruptions in fronto-limbic connectivity. This study sought to investigate the relationship among depressive symptoms, hippocampal atrophy (HA), and functional connectivity (FC) in TLE. Methods: Volumetric MRI and functional connectivity MRI (fcMRI) were performed on nineteen patients with TLE (11 left TLEs and 8 right TLEs) and 20 healthy controls. For the fcMRI analysis, the hippocampi and amygdalae were selected as seed regions, and five prefrontal and five cingulate regions of interest (ROIs) were selected as targets. FC strengths were calculated by isolating the low-frequency blood-oxygen-level-dependent signals from fMRI data and then correlating the signal time course of the seed regions with the signals within ROIs. Depression was measured by the Beck Depression Inventory-II. Correlation coefficients were calculated to evaluate relationships among variables.Results: Reduced FC was found between the ipsilateral hippocampus and ventral posterior cingulate cortex (vPCC) relative to the contralateral side, F = 9.864, p = .006, coupled with greater ipsilateral HA, in patients with TLE. Neither HA nor hippocampal-vPCC FC asymmetry were robust predictors of depression. Rather, depressive symptoms were positively correlated with hippocampal-anterior prefrontal FC (p < .001) of the left hemisphere in left TLE. FC of the right amygdala to the bilateral superor frontal ROIs were also positively correlated with depression symptoms in left TLE (p < .01). For right TLE, amygdala-anterior prefrontal FC was negatively correlated with depressive symptoms (p = .043). Conclusions: These results indicate that fronto-limbic dysfunction is a core contributor to depression in TLE. However, the nature of this network dysfunction differs between patients with left and right TLE. In addition, the right amygdala may play a role in depression symptomatology regardless of side of the epileptogenic focus. These findings may inspire differential treatment for depression in these two patient groups.