Vladana Markovic1, Federica Agosta1, Elisa Canu1, Alberto Inuggi1, Igor Petrovic1, Iva Stankovic1, Francesca Imperiale1, Tanja Stojkovic1, Vladimir S Kostic1, Massimo Filippi2. 1. From the Neuroimaging Research Unit (V.M., F.A., E.C., F.I., M.F.) and Department of Neurology, Institute of Experimental Neurology, Division of Neuroscience (M.F.), San Raffaele Scientific Institute, Vita-Salute San Raffaele University, Milan, Italy; Clinic of Neurology, School of Medicine (V.M., I.P., I.S., T.S., V.S.K.), University of Belgrade, Serbia; and Unit of Robotics, Brain and Cognitive Sciences (A.I.), Istituto Italiano di Tecnologia, Genoa, Italy. 2. From the Neuroimaging Research Unit (V.M., F.A., E.C., F.I., M.F.) and Department of Neurology, Institute of Experimental Neurology, Division of Neuroscience (M.F.), San Raffaele Scientific Institute, Vita-Salute San Raffaele University, Milan, Italy; Clinic of Neurology, School of Medicine (V.M., I.P., I.S., T.S., V.S.K.), University of Belgrade, Serbia; and Unit of Robotics, Brain and Cognitive Sciences (A.I.), Istituto Italiano di Tecnologia, Genoa, Italy. filippi.massimo@hsr.it.
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.
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 ICBpatients, 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 ICBpatients. 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.
Authors: Pedro Barbosa; Sean S O'Sullivan; Eileen Joyce; Andrew J Lees; Thomas T Warner; Atbin Djamshidian Journal: Mov Disord Clin Pract Date: 2021-11-11
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