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Dopamine and eye movement control in Parkinson’s disease: deficits in corollary discharge signals?

Henry Railo, Henri Olkoniemi, Enni Eeronheimo, Oona Pääkkonen, Juho Joutsa, Valtteri Kaasinen
doi: https://doi.org/10.1101/245381
Henry Railo
1Department of Clinical Neurophysiology, University of Turku and Turku University Hospital, FI-20521, Turku, Finland
2Department of Psychology, University of Turku, FI-20014, Turku, Finland
3Brain and Mind Centre, University of Turku, FI-20014, Turku, Finland
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  • For correspondence: hmrail@utu.fi
Henri Olkoniemi
2Department of Psychology, University of Turku, FI-20014, Turku, Finland
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Enni Eeronheimo
2Department of Psychology, University of Turku, FI-20014, Turku, Finland
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Oona Pääkkonen
2Department of Psychology, University of Turku, FI-20014, Turku, Finland
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Juho Joutsa
4Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129
5Berenson-Allen Center for Noninvasive Brain Stimulation, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215
6Department of Neurology, University of Turku, FI-20521, Turku, Finland
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Valtteri Kaasinen
7Division of Clinical Neurosciences, University of Turku and Turku University Hospital, FI-20521 Turku, Finland
8Turku PET Centre, University of Turku and Turku University Hospital, FI-20521 Turku, Finland
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Abstract

Movement in Parkinson’s disease (PD) is fragmented, and the patients depend on visual information in their behavior. This suggests that the patients may have deficits in internally monitoring their own movements. Internal monitoring of movements is assumed to rely on corollary discharge signals that enable the brain to predict the sensory consequences of actions. We studied early-stage PD patients (N=14), and age-matched healthy control participants (N=14) to examine whether PD patients reveal deficits in updating their sensory representations after eye movements. The participants performed a double-saccade task where, in order to accurately fixate a second target, the participant must correct for the displacement caused by the first saccade. In line with previous reports, the patients had difficulties in fixating the second target when the eye movement was performed without visual guidance. Furthermore, the patients had difficulties in taking into account the error in the first saccade when making a saccade towards the second target, especially when eye movements were made towards the side with dominant motor symptoms. Across PD patients, the impairments in saccadic eye movements correlated with the integrity of the dopaminergic system as measured with [123I]FP-CIT SPECT: Patients with lower striatal (caudate, anterior putamen and posterior putamen) dopamine transporter binding made larger errors in saccades. This effect was strongest when patients made memory-guided saccades towards the second target. Our results provide tentative evidence that the motor deficits in PD may be partly accounted by deficits in internal monitoring of movements.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.
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Posted May 14, 2018.
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Dopamine and eye movement control in Parkinson’s disease: deficits in corollary discharge signals?
Henry Railo, Henri Olkoniemi, Enni Eeronheimo, Oona Pääkkonen, Juho Joutsa, Valtteri Kaasinen
bioRxiv 245381; doi: https://doi.org/10.1101/245381
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Dopamine and eye movement control in Parkinson’s disease: deficits in corollary discharge signals?
Henry Railo, Henri Olkoniemi, Enni Eeronheimo, Oona Pääkkonen, Juho Joutsa, Valtteri Kaasinen
bioRxiv 245381; doi: https://doi.org/10.1101/245381

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