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Behavioral and Psychological Symptoms that Predict Cognitive Decline or Impairment in Cognitively Normal Middle-Aged or Older Adults: a Meta-Analysis.

Author(s): Hudon C, Escudier F, De Roy J, Croteau J, Cross N, Dang-Vu TT, Zomahoun HTV, Grenier S, Gagnon JF, Parent A, Bruneau MA, Belleville S, Conso...

Neuropsychol Rev. 2020 May 11;: Authors: Hudon C, Escudier F, De Roy J, Croteau J, Cross N, Dang-Vu TT, Zomahoun HTV, Grenier S, Gagnon JF, Parent A, Bruneau MA, Belleville S, Consortium for the E...

Article GUID: 32394109
Chronic Neuroleptic-Induced Parkinsonism Examined with Positron Emission Tomography.

Author(s): Galoppin M, Berroir P, Soucy JP, Suzuki Y, Lavigne GJ, Gagnon JF, Montplaisir JY, Stip E, Blanchet PJ

Mov Disord. 2020 Apr 30;: Authors: Galoppin M, Berroir P, Soucy JP, Suzuki Y, Lavigne GJ, Gagnon JF, Montplaisir JY, Stip E, Blanchet PJ

Article GUID: 32353194
Brain perfusion during rapid-eye-movement sleep successfully identifies amnestic mild cognitive impairment.

Author(s): Brayet P, Petit D, Baril AA, Gosselin N, Gagnon JF, Soucy JP, Gauthier S, Kergoat MJ, Carrier J, Rouleau I, Montplaisir J

Sleep Med. 2017 Jun;34:134-140 Authors: Brayet P, Petit D, Baril AA, Gosselin N, Gagnon JF, Soucy JP, Gauthier S, Kergoat MJ, Carrier J, Rouleau I, Montplaisir J

Article GUID: 28522082
Brain cholinergic alterations in idiopathic REM sleep behaviour disorder: a PET imaging study with 18F-FEOBV.

Author(s): Bedard MA, Aghourian M, Legault-Denis C, Postuma RB, Soucy JP, Gagnon JF, Pelletier A, Montplaisir J

Sleep Med. 2019 Jan 06;58:35-41 Authors: Bedard MA, Aghourian M, Legault-Denis C, Postuma RB, Soucy JP, Gagnon JF, Pelletier A, Montplaisir J

Article GUID: 31078078
Effects of exercise training on cognition in chronic obstructive pulmonary disease: A systematic review.

Author(s): Desveaux L, Harrison SL, Gagnon JF, Goldstein RS, Brooks D, Pepin V

Respir Med. 2018 06;139:110-116 Authors: Desveaux L, Harrison SL, Gagnon JF, Goldstein RS, Brooks D, Pepin V

Article GUID: 29857994
Title:Chronic Neuroleptic-Induced Parkinsonism Examined with Positron Emission Tomography.
Authors:Galoppin M,  Berroir P,  Soucy JP,  Suzuki Y,  Lavigne GJ,  Gagnon JF,  Montplaisir JY,  Stip E,  Blanchet PJ
Link:https://www.ncbi.nlm.nih.gov/pubmed/32353194?dopt=Abstract
DOI:10.1002/mds.28046
Category:Mov Disord
PMID:32353194
Dept Affiliation: PERFORM
1 Department of Medicine, University of Montreal Hospital Center, Montreal, Canada.
2 PERFORM Centre, Concordia University, Montreal, Canada.
3 McConnell Brain Imaging Centre, Montreal Neurological Institute, McGill University, Montreal, Canada.
4 Department of Stomatognathic Function and Occlusal Reconstruction, Graduate School of Biomedical Sciences, Tokushima University, Tokushima, Japan.
5 Centre for Advanced Research in Sleep Medicine, Hopital du Sacre-Coeur de Montreal, Montreal, Canada.
6 Faculty of Dental Medicine, University of Montreal, Montreal, Canada.
7 Department of Psychiatry, United Arab Emirates University, Al Ain, United Arab Emirates.
8 Montreal Mental Health University Institute, Montreal, Canada.

Description:

Chronic Neuroleptic-Induced Parkinsonism Examined with Positron Emission Tomography.

Mov Disord. 2020 Apr 30;:

Authors: Galoppin M, Berroir P, Soucy JP, Suzuki Y, Lavigne GJ, Gagnon JF, Montplaisir JY, Stip E, Blanchet PJ

Abstract

BACKGROUND: Neuroleptic drug-induced parkinsonism (NIP) is a leading cause of parkinsonism, particularly in aging. Based on abnormal dopamine transporter scan results, individuals displaying chronic NIP are often diagnosed with Lewy-body Parkinson's disease (PD), but this assumption needs further substantiation.

OBJECTIVE: To quantitate the profile of striatal dopaminergic nerve terminal density in NIP relative to PD.

METHODS: We used the positron emission tomography ligand [11 C](+)-dihydrotetrabenazine targeting vesicular monoamine transporter type 2 (VMAT2) binding sites and collected various clinical parameters (motor ratings, olfaction, polysomnography to document rapid eye movement sleep muscle activity, quantitative sensory testing for pain thresholds) possibly predicting binding results in patients older than age 50 living with schizophrenia spectrum disorders under long-term stable antipsychotic drug treatment, with (N = 11) or without (N = 11) chart documention of chronic NIP, and compared them to healthy volunteers (N = 11) and others medicated for PD (N = 12).

RESULTS: Striatal VMAT2 binding was dichotomous in the NIP group between those with spared (N = 5) or low (N = 6) PD-like values. Striatal binding reduction in the low VMAT2-NIP group was asymmetric without the gradient of maximal involvement in the posterior putamen typical of PD. Anosmia was the only nonmotor parameter measured matching the abnormal striatal VMAT2 binding status.

CONCLUSION: These preliminary observations suggest that striatal VMAT2 binding is abnormal in a fraction of chronic NIP cases and differs in spatial distribution from PD. The possibility of a drug-induced axonopathy and resultant synaptopathy, as well as the evolution of the binding deficit, warrant further longitudinal studies in a large cohort. © 2020 International Parkinson and Movement Disorder Society.

PMID: 32353194 [PubMed - as supplied by publisher]