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

2018 ◽  
Author(s):  
Henry Railo ◽  
Henri Olkoniemi ◽  
Enni Eeronheimo ◽  
Oona Pääkkonen ◽  
Juho Joutsa ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Eye Movements ◽  
Eye Movement ◽  
Visual Information ◽  
Early Stage ◽  
Movement Control ◽  
Saccadic Eye Movements ◽  
Corollary Discharge ◽  
Motor Deficits

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.

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

PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e6038 ◽  
Author(s):  
Henry Railo ◽  
Henri Olkoniemi ◽  
Enni Eeronheimo ◽  
Oona Pääkkönen ◽  
Juho Joutsa ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Eye Movements ◽  
Eye Movement ◽  
Visual Information ◽  
Early Stage ◽  
Movement Control ◽  
Saccadic Eye Movements ◽  
Corollary Discharge ◽  
Motor Deficits

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 toward the second target, especially when eye movements were made toward 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 toward the second target. Our results provide tentative evidence that the motor deficits in PD may be partly due to deficits in internal monitoring of movements.

scholarly journals A neurocomputational model of the basal ganglia for the analysis of motor deficits after dopaminergic loss in Parkinson's disease

2021 ◽  
Author(s):  
Ilaria Gigi ◽  
Rosa Senatore ◽  
Angelo Marcelli
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Basal Ganglia ◽  
Motor Learning ◽  
Early Stage ◽  
Motor Task ◽  
Movement Control ◽  
Neural System ◽  
Motor Deficits ◽  
Cortical Function

The basal ganglia (BG) are part of a basic feedback circuit, regulating cortical function, such as voluntary movement control, via their influence on thalamocortical projections. BG disorders, namely Parkinson's disease (PD), characterized by the loss of neurons in the substantia nigra (SN), involve the progressive loss of motor functions. The process that leads to these neural alterations is still unknown. At the present, PD cannot be cured, but an early diagnosis (ED) could allow to better manage its symptoms and evolution. A branch of neuroscience research is currently investigating the possibility of using motor alterations, e.g. handwriting, caused by the disease as diagnostic signs in the early stage of the disease, expression of small entity of SN lesion. In the present work, we propose a neurocomputational model to investigate the behaviour of the simulated neural system after several degrees of lesion, with the aim of evaluating, if possible, which is the smallest lesion compromising motor learning. The performance of the network in learning a novel motor task has been analyzed, in physiological and pathological conditions. The proposed neural network proves that there may exist abnormalities of motor learning process, due to alterations in the BG, which do not yet involve the presence of symptoms typical of the confirmed diagnosis, since the network shows having some difficulties in motor learning already with 20% DA depletion.

scholarly journals Eye movement control during visual pursuit in Parkinson’s disease

PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e5442 ◽  
Author(s):  
Chia-Chien Wu ◽  
Bo Cao ◽  
Veena Dali ◽  
Celia Gagliardi ◽  
Olivier J. Barthelemy ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Eye Movement ◽  
Smooth Pursuit ◽  
Rating Scale ◽  
Movement Control ◽  
Saccadic Eye Movements ◽  
Control Group ◽  
Moving Target ◽  
Binocular Coordination

Background Prior studies of oculomotor function in Parkinson’s disease (PD) have either focused on saccades without considering smooth pursuit, or tested smooth pursuit while excluding saccades. The present study investigated the control of saccadic eye movements during pursuit tasksand assessed the quality of binocular coordinationas potential sensitive markers of PD. Methods Observers fixated on a central cross while a target moved toward it. Once the target reached the fixation cross, observers began to pursue the moving target. To further investigate binocular coordination, the moving target was presented on both eyes (binocular condition), or on one eye only (dichoptic condition). Results The PD group made more saccades than age-matched normal control adults (NC) both during fixation and pursuit. The difference between left and right gaze positions increased over time during the pursuit period for PD but not for NC. The findings were not related to age, as NC and young-adult control group (YC) performed similarly on most of the eye movement measures, and were not correlated with classical measures of PD severity (e.g., Unified Parkinson’s Disease Rating Scale (UPDRS) score). Discussion Our results suggest that PD may be associated with impairment not only in saccade inhibition, but also in binocular coordination during pursuit, and these aspects of dysfunction may be useful in PD diagnosis or tracking of disease course.

Association of the Non-Motor Burden with Patterns of Striatal Dopamine Loss in de novo Parkinson’s Disease

2020 ◽  
Vol 10 (4) ◽  
pp. 1541-1549
Author(s):  
Seok Jong Chung ◽  
Sangwon Lee ◽  
Han Soo Yoo ◽  
Yang Hyun Lee ◽  
Hye Sun Lee ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
De Novo ◽  
Early Stage ◽  
Striatal Dopamine ◽  
Motor Deficits ◽  
Dopamine Depletion ◽  
Severe Motor ◽  
Severe Group ◽  
Striatal Dopamine Depletion

Background: Striatal dopamine deficits play a key role in the pathogenesis of Parkinson’s disease (PD), and several non-motor symptoms (NMSs) have a dopaminergic component. Objective: To investigate the association between early NMS burden and the patterns of striatal dopamine depletion in patients with de novo PD. Methods: We consecutively recruited 255 patients with drug-naïve early-stage PD who underwent 18F-FP-CIT PET scans. The NMS burden of each patient was assessed using the NMS Questionnaire (NMSQuest), and patients were divided into the mild NMS burden (PDNMS-mild) (NMSQuest score <6; n = 91) and severe NMS burden groups (PDNMS-severe) (NMSQuest score >9; n = 90). We compared the striatal dopamine transporter (DAT) activity between the groups. Results: Patients in the PDNMS-severe group had more severe parkinsonian motor signs than those in the PDNMS-mild group, despite comparable DAT activity in the posterior putamen. DAT activity was more severely depleted in the PDNMS-severe group in the caudate and anterior putamen compared to that in the PDMNS-mild group. The inter-sub-regional ratio of the associative/limbic striatum to the sensorimotor striatum was lower in the PDNMS-severe group, although this value itself lacked fair accuracy for distinguishing between the patients with different NMS burdens. Conclusion: This study demonstrated that PD patients with severe NMS burden exhibited severe motor deficits and relatively diffuse dopamine depletion throughout the striatum. These findings suggest that the level of NMS burden could be associated with distinct patterns of striatal dopamine depletion, which could possibly indicate the overall pathological burden in PD.

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