Brain structural and functional signatures of impulsive–compulsive behaviours in Parkinson’s disease

• Published in: Molecular psychiatry Vol. 23; no. 2; pp. 459 - 466
• Main Authors: Imperiale, F, Agosta, F, Canu, E, Markovic, V, Inuggi, A, Jecmenica-Lukic, M, Tomic, A, Copetti, M, Basaia, S, Kostic, V S, Filippi, M
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 01.02.2018; Nature Publishing Group
• Subjects: 631/378; 631/477; Adult; Aged; Basal ganglia; Basal Ganglia - pathology; Behavioral Sciences; Biological Psychology; Brain - physiopathology; Brain mapping; Brain research; Care and treatment; Cognitive ability; Comparative analysis; Compulsive behavior; Compulsive Behavior - diagnostic imaging; Compulsive Behavior - physiopathology; Development and progression; Diffusion Magnetic Resonance Imaging - methods; Female; Functional magnetic resonance imaging; Humans; Image processing; Image Processing, Computer-Assisted; Impulsive Behavior - physiology; Impulsivity; Magnetic Resonance Imaging - methods; Male; Medicine; Medicine & Public Health; Middle Aged; Morphometry; Movement disorders; Neural networks; Neural Pathways - physiopathology; Neurodegenerative diseases; Neuroimaging; Neurosciences; NMR; Nuclear magnetic resonance; original-article; Parkinson disease; Parkinson Disease - diagnostic imaging; Parkinson Disease - physiopathology; Parkinson's disease; Pharmacotherapy; Psychiatry; Sensorimotor system; Structure-function relationships; Substantia alba; Visual pathways; White Matter - pathology
• ISSN: 1359-4184; 1476-5578; 1476-5578
• DOI: 10.1038/mp.2017.18

This study assessed brain structural and functional alterations in patients with Parkinson’s disease and impulsive–compulsive behaviours (PD-ICB) compared with controls and PD no-ICB cases. Eighty-five PD patients (35 PD-ICB) and 50 controls were recruited. All subjects underwent three-dimensional T1-weighted, diffusion tensor (DT), and resting state functional magnetic resonance imaging (RS fMRI). We assessed cortical thickness with surface-based morphometry, subcortical volumes using FIRST, DT MRI metrics using region of interest and tractography approaches, and RS fMRI using a model free approach. Compared with controls, both PD groups showed a pattern of brain structural alterations in the basal ganglia (more evident in PD no-ICB patients), sensorimotor and associative systems. Compared with PD no-ICB, PD-ICB cases showed left precentral and superior frontal cortical thinning, and motor and extramotor white matter tract damage. Compared with controls, all patients had an increased functional connectivity within the visual network. Additionally, PD no-ICB showed increased functional connectivity of bilateral precentral and postcentral gyri within the sensorimotor network compared with controls and PD-ICB. Severity and duration of PD-ICB modulated the functional connectivity between sensorimotor, visual and cognitive networks. Relative to PD no-ICB, PD-ICB patients were characterised by a more severe involvement of frontal, meso-limbic and motor circuits. These data suggest ICB in PD as the result of a disconnection between sensorimotor, associative and cognitive networks with increasing motor impairment, psychiatric symptoms, and ICB duration. These findings may have important implications in understanding the neural substrates underlying ICB in PD.