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Abstract
Objective: To assess whether a functional dysregulation of the habenula and amygdala, as modulators of the reward brain circuit, contributes to Parkinson disease (PD) punding.
Methods: Structural and resting-state functional MRI were obtained from 22 patients with PD punding, 30 patients with PD without any impulsive-compulsive behavior (ICB) matched for disease stage and duration, motor impairment, and cognitive status, and 30 healthy controls. Resting-state functional connectivity of the habenula and amygdala bilaterally was assessed using a seed-based approach. Habenula and amygdala volumes and cortical thickness measures were obtained.
Results: Compared to both healthy controls and PD cases without any ICB (PD–no ICB), PD-punding patients showed higher functional connectivity of habenula and amygdala with thalamus and striatum bilaterally, and lower connectivity between bilateral habenula and left frontal and precentral cortices. In PD-punding relative to PD–no ICB patients, a lower functional connectivity between right amygdala and hippocampus was also observed. Habenula and amygdala volumes were not different among groups. PD-punding patients showed a cortical thinning of the left superior frontal and precentral gyri and right middle temporal gyrus and isthmus cingulate compared to healthy controls, and of the right inferior frontal gyrus compared to both controls and PD–no ICB patients.
Conclusions: A breakdown of the connectivity among the crucial nodes of the reward circuit (i.e., habenula, amygdala, basal ganglia, frontal cortex) might be a contributory factor to punding in PD. This study provides potential instruments to detect and monitor punding in patients with PD.
GLOSSARY
- DDS=
- dopamine dysregulation syndrome;
- GM=
- gray matter;
- ICB=
- impulsive-compulsive behavior;
- LEDD=
- levodopa equivalent daily dose;
- PD=
- Parkinson disease;
- PRS=
- Punding Rating Scale;
- TFE=
- turbo field echo;
- UPDRS=
- Unified Parkinson's Disease Rating Scale;
- VTA=
- ventral tegmental area
Footnotes
↵* These authors contributed equally to this work.
Go to Neurology.org for full disclosures. Funding information and disclosures deemed relevant by the authors, if any, are provided at the end of the article.
Supplemental data at Neurology.org
- Received November 30, 2016.
- Accepted in final form March 15, 2017.
- © 2017 American Academy of Neurology
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