Intact limbic-prefrontal connections and reduced amygdala volumes in Parkinson's disease with mild depressive symptoms

Abstract

BackgroundDepression is very common in Parkinson's disease (PD). The neuropathological basis for this remains unclear; however, dysfunction in prefrontal and limbic regions may play a role. MethodsWe examined non-demented PD patients with and without depression and healthy controls (n = 6 per group) for differences in limbic structures and connections between these structures and the prefrontal cortex. Depressed individuals were selected from a representative sample of 33 PD patients using scores from the 15 question Geriatric Depression Scale (GDS). Magnetic Resonance Diffusion Tensor Imaging (DTI) tractography was used to examine the structural integrity of the uncinate fasciculus (UF), a white matter tract that projects from the hippocampus, amygdala and temporal pole to the orbitofrontal cortex, and the corpus callosum. Integrity of the UF and corpus callosum was established through measures of mean diffusivity (MD), fractional anisotropy (FA) and tract length. A volumetric analysis of the hippocampal head, body and tail, as well as the amygdala was performed to determine whether volume differences in these structures in PD relate to depression. ResultsThe depressed PD group showed smaller amygdala volumes compared to healthy controls, but the groups did not differ on any other measure. ConclusionsThe present study found intact limbic connectivity but suggests that amygdala atrophy may be present in Parkinson's disease with depression. Further work is needed to replicate these findings.