Reference : Failing as Doorman and Disc Jockey at the Same Time: Amygdalar Dysfunction in Parkins... |
Scientific journals : Article | |||
Life sciences : Multidisciplinary, general & others | |||
http://hdl.handle.net/10993/26497 | |||
Failing as Doorman and Disc Jockey at the Same Time: Amygdalar Dysfunction in Parkinson’s Disease | |
English | |
Diederich, Nico [University of Luxembourg > Luxembourg Centre for Systems Biomedicine (LCSB) > > ; Centre Hospitalier de Luxembourg > Department of Neurosciences > > ; Rush University Medical Center > Department of Neurological Sciences] | |
Goldman, Jennifer [Rush University Medical Center > Department of Neurological Sciences] | |
Stebbins, Glenn [Rush University Medical Center > Department of Neurological Sciences] | |
Goetz, Christopher [Rush University Mecidal Center > Department of Neurological Sciences] | |
2015 | |
Movement Disorders | |
Wiley Liss, Inc. | |
00 | |
00 | |
Yes (verified by ORBilu) | |
0885-3185 | |
1531-8257 | |
New York | |
NY | |
[en] amygdala ; anxiety ; emotional face recognition ; hallucinations ; impulse control disorders | |
[en] In Braak’s model of ascending degeneration in Parkinson’s disease (PD), involvement of the
amygdala occurs simultaneously with substantia nigra degeneration. However, the clinical manifestations of amygdalar involvement in PD have not been fully delineated. Considered a multitask manager, the amygdala is a densely connected “hub,” coordinating and integrating tasks ranging from prompt, multisensorial emotion recognition to adequate emotional responses and emotional tuning of memories. Although phylogenetically predisposed to handle fear, the amygdala handles both aversive and positive emotional inputs. In PD, neuropathological and in vivo studies suggest primarily amygdalar hypofunction. However, as dopamine acts as an inverted U-shaped amygdalar modulator, medicationinduced hyperactivity of the amygdala can occur.We propose that amygdalar (network) dysfunction contributes to reduced recognition of negative emotional face expressions, impaired theory of mind, reactive hypomimia, and impaired decision making. Similarly, impulse control disorders in predisposed individuals, hallucinations, anxiety, and panic attacks may be related to amygdalar dysfunction. When available, we discuss amygdala-independent trigger mechanisms of these symptoms. Although dopaminergic agents have mostly an activation effect on amygdalar function, adaptive and compensatory network changes may occur as well, but these have not been sufficiently explored. In conclusion, our model of amygdalar involvement brings together several elements of Parkinson’s disease phenomenology heretofore left unexplained and provides a framework for testable hypotheses in patients during life and in autopsy analyses. VC 2015 International Parkinson and Movement Disorder Society | |
Luxembourg Centre for Systems Biomedicine (LCSB): Experimental Neurobiology (Balling Group) | |
http://hdl.handle.net/10993/26497 | |
10.1002/mds.26460 |
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