Failing as doorman and disc jockey at the same time: Amygdalar dysfunction in Parkinson's disease.

摘要: Abstract In Braak's model of ascending degeneration in Parkinson's disease (PD), involvement the amygdala occurs simultaneously with substantia nigra degeneration. However, clinical manifestations amygdalar PD have not been fully delineated. Considered a multitask manager, is densely connected "hub," coordinating and integrating tasks ranging from prompt, multisensorial emotion recognition to adequate emotional responses tuning memories. Although phylogenetically predisposed handle fear, handles both aversive positive inputs. PD, neuropathological vivo studies suggest primarily hypofunction. as dopamine acts an inverted U-shaped modulator, medication-induced hyperactivity can occur. We propose that (network) dysfunction contributes reduced negative face expressions, impaired theory mind, reactive hypomimia, decision making. Similarly, impulse control disorders individuals, hallucinations, anxiety, panic attacks may be related dysfunction. When available, we discuss amygdala-independent trigger mechanisms these symptoms. dopaminergic agents mostly activation effect on function, adaptive compensatory network changes occur well, but sufficiently explored. conclusion, our brings together several elements phenomenology heretofore left unexplained provides framework for testable hypotheses patients during life autopsy analyses. © 2015 International Parkinson Movement Disorder Society.