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Ventral striatal dopaminergic defect is associated with hallucinations in Parkinson's disease
Author(s) -
Jaakkola E.,
Joutsa J.,
Mäkinen E.,
Johansson J.,
Kaasinen V.
Publication year - 2017
Publication title -
european journal of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 124
eISSN - 1468-1331
pISSN - 1351-5101
DOI - 10.1111/ene.13390
Subject(s) - dopamine transporter , dopaminergic , medicine , striatum , ropinirole , parkinson's disease , putamen , dopamine , pathogenesis , disease , neuroscience , psychology , dopamine agonist
Background and purpose Visual hallucinations ( VH s) are a common complication of Parkinson's disease ( PD ). The pathogenesis of VH s in PD is still largely unclear. The aim of this study was to investigate the dopaminergic mechanisms of VH s and specifically whether the degree of striatal dopamine transporter ( DAT ) function or extrastriatal serotonin transporter ( SERT ) function can predict the appearance of VH s in patients with PD . Methods Twenty‐two PD patients scanned with [ 123 I] FP ‐ CIT single photon emission computed tomography at an early stage of their disease who later developed VH s were identified and compared with 48 non‐hallucinating PD patients. The groups were matched for age, medication, disease duration and motor symptom severity. Clinical follow‐up after the scan was a median (range) of 6.9 (3.8–9.6) years. Imaging analyses were performed with both regions‐of‐interest‐based and voxel‐based ( Statistical Parametric Mapping ) methods for the striatal and extrastriatal regions. Results The median interval between the scan and the emergence of VH s was 4.8 years. Patients who developed VH s had 18.4% lower DAT binding in the right ventral striatum ( P = 0.009), 16.7% lower binding in the left ventral striatum ( P = 0.02) and 18.8% lower binding in the right putamen ( P = 0.03) compared to patients who did not develop VH s. Conclusions Low striatal DAT function may predispose PD patients to VH s, and the regional distribution of the findings suggests a particular role of the ventral striatum. This is in line with non‐ PD research that has implicated ventral striatal dysfunction in psychosis.