Objective: To investigate whether the magnitude of presynaptic dopamine depletion is a risk factor for the development of levodopa-induced dyskinesia (LID) in Parkinson disease (PD) by quantitatively analyzing ¹⁸F-FP-CIT PET data. Methods: This retrospective cohort study enrolled a total of 127 drug-naive de novo patients with PD who completed ¹⁸F-FP-CIT PET scanning at their initial evaluation. The patients visited our outpatient clinic every 3–6 months and had been followed for a minimum of 2 years since beginning dopaminergic medication. The predictive power of the quantitatively analyzed ¹⁸F-FP-CIT uptake of striatal subregions and other clinical factors for the development of LID was evaluated using Cox proportional hazard models. Results: During a mean follow-up period of 3.4 years, 35 patients with PD (27.6%) developed LID. Patients with LID showed less dopamine transporter (DAT) activity in the putamen than did those without LID. Multivariate Cox proportional hazard models revealed that the DAT uptakes of the anterior putamen (hazard ratio [HR] 0.530; p = 0.032), posterior putamen (HR 0.302; p = 0.024), and whole putamen (HR 0.386; p = 0.022) were significant predictors of the development of LID, whereas DAT activities in the caudate and ventral striatum were not significantly correlated with the development of LID. In addition, younger age at onset of PD and higher dose of levodopa were also significant predictors of the development of LID. Conclusions: The present results provide convincing evidence that presynaptic dopaminergic denervation in PD plays a crucial role in the development of LID.

Background Visual hallucinations (VH), which are common in patients with Parkinson's disease (PD), lead to increased disability and are a significant predictor of the development of dementia. However, the neuroanatomical basis for VH in non-demented PD patients remains controversial. Methods A total of 110 patients with PD were classified into PD with VH (n=46) and PD without VH (n=64) groups, depending on the presence of VH assessed by the caregiver-based structured interview of the Neuropsychiatric Inventory. We performed voxel-based morphometry (VBM) for grey matter (GM) volume and a region-of-interest-based volumetric analysis of the substantia innominata (SI) between two groups. Results The comprehensive neuropsychological assessment showed that PD patients with VH showed more severe cognitive deficits in delayed visual memory and frontal executive functions compared with those without VH. A VBM analysis revealed that PD patients with VH had significantly lower GM volume in the right orbitofrontal, left temporal and left thalamic areas compared with those without VH. The normalised SI volume was significantly reduced in PD patients with VH compared with those without VH (1.28±0.22 vs 1.41±0.25, p=0.005). Conclusions The present study demonstrates that non-demented PD patients with VH exhibited a smaller volume in the frontal, temporal and thalamic areas as well as the SI, suggesting that PD hallucinators may have distinctive neuroanatomical bases relative to PD non-hallucinators.

To explore whether the Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA) can be used to screen for dementia or mild cognitive impairment (MCI) in less educated patients with Parkinson's disease (PD). We reviewed the medical records of PD patients who had taken the Korean MMSE (K-MMSE), Korean MoCA (K-MoCA), and comprehensive neuropsychological tests. Predictive values of the K-MMSE and K-MoCA for dementia or MCI were analyzed in groups divided by educational level. The discriminative powers of the K-MMSE and K-MoCA were excellent [area under the curve (AUC) 0.86-0.97] for detecting dementia but not for detecting MCI (AUC 0.64-0.85). The optimal screening cutoff values of both tests increased with educational level for dementia (K-MMSE < 15 for illiterate, < 20 for 0.5-3 years of education, < 23 for 4-6 years, < 25 for 7-9 years, and < 26 for 10 years or more; K-MoCA < 7 for illiterate, < 13 for 0.5-3 years, < 16 for 4-6 years, < 19 for 7-9 years, < 20 for 10 years or more) and MCI (K-MMSE < 19 for illiterate, < 26 for 0.5-3 years, < 27 for 4-6 years, < 28 for 7-9 years, and < 29 for 10 years or more; K-MoCA < 13 for illiterate, < 21 for 0.5-3 years, < 23 for 4-6 years, < 25 for 7-9 years, < 26 for 10 years or more). Both MMSE and MoCA can be used to screen for dementia in patients with PD, regardless of educational level; however, neither test is sufficient to discriminate MCI from normal cognition without additional information.