Recent research has found that perceptual deficits exist in Parkinson???s disease (PD), yet the link between perception and movement impairments is not well understood. Inaccurate estimation of distance has the potential to be an underlying cause of movement impairments. Alternatively, those with PD may not be able to perceive their own movements accurately. The main objective of this thesis was to evaluate (1) whether distance estimation is influenced by static perception compared to perception during movement in PD, (2) how visual motion processing contributes to distance estimation during movement, and (3) how dopaminergic medication contributes to these distance estimation deficits. Thirty-seven participants (19 individuals with PD, 18 age-matched healthy control participants (HC) estimated distance to a remembered target in a total of 48 trials, in 4 randomized blocks. Estimation conditions included: (i) no motion: participants pointed with a laser, (ii) motion: participants walked to the estimated position, (iii) visual motion (wheelchair): participants were pushed in a wheelchair while they gave their estimate, (iv) visual motion (VR): participants completed their distance estimate while seated and viewed themselves (as if they were walking) in VR. PD patients completed this protocol twice; once OFF and once ON dopaminergic medication. Participants were matched for age, distance acuity, Modified Mini Mental State Exam (3MS), spatial working memory and motor planning ability. In Study 1 (no motion vs. motion), individuals with PD and healthy control participants did not differ in judgment accuracy during the no motion condition. However, those with PD did have greater amounts of error compared to healthy control participants while estimating distance during the motion condition. Similarly, those with PD significantly underestimated the target position compared to healthy control participants during the motion condition only. Individuals with PD demonstrated greater variability overall. In Study 2, error did not differ between PD and HC groups during visual motion perception (wheelchair). Interestingly, the HC group tended to perform significantly worse than those with PD in the VR condition. Overall, across both studies there was no significant influence of dopaminergic medication in any of the conditions. Individuals with PD demonstrated distance estimation deficits only when required to move through their environment. In contrast to estimations made with movement, neither static estimation nor estimations made with visual motion revealed significant differences between the two groups. Thus perceptual estimation deficits appear to occur only during movement, which may be suggestive of an underlying sensory processing deficit which leads to a problem integrating vision and self-motion information.

Recent research has found that perceptual deficits exist in Parkinson’s disease (PD), yet the link between perception and movement impairments is not well understood. Inaccurate estimation of distance has the potential to be an underlying cause of movement impairments. Alternatively, those with PD may not be able to perceive their own movements accurately. The main objective of this thesis was to evaluate (1) whether distance estimation is influenced by static perception compared to perception during movement in PD, (2) how visual motion processing contributes to distance estimation during movement, and (3) how dopaminergic medication contributes to these distance estimation deficits. Thirty-seven participants (19 individuals with PD, 18 age-matched healthy control participants (HC) estimated distance to a remembered target in a total of 48 trials, in 4 randomized blocks. Estimation conditions included: (i) no motion: participants pointed with a laser, (ii) motion: participants walked to the estimated position, (iii) visual motion (wheelchair): participants were pushed in a wheelchair while they gave their estimate, (iv) visual motion (VR): participants completed their distance estimate while seated and viewed themselves (as if they were walking) in VR. PD patients completed this protocol twice; once OFF and once ON dopaminergic medication. Participants were matched for age, distance acuity, Modified Mini Mental State Exam (3MS), spatial working memory and motor planning ability. In Study 1 (no motion vs. motion), individuals with PD and healthy control participants did not differ in judgment accuracy during the no motion condition. However, those with PD did have greater amounts of error compared to healthy control participants while estimating distance during the motion condition. Similarly, those with PD significantly underestimated the target position compared to healthy control participants during the motion condition only. Individuals with PD demonstrated greater variability overall. In Study 2, error did not differ between PD and HC groups during visual motion perception (wheelchair). Interestingly, the HC group tended to perform significantly worse than those with PD in the VR condition. Overall, across both studies there was no significant influence of dopaminergic medication in any of the conditions. Individuals with PD demonstrated distance estimation deficits only when required to move through their environment. In contrast to estimations made with movement, neither static estimation nor estimations made with visual motion revealed significant differences between the two groups. Thus perceptual estimation deficits appear to occur only during movement, which may be suggestive of an underlying sensory processing deficit which leads to a problem integrating vision and self-motion information.

La maladie de Parkinson est une affection neurodégénérative principalement associée à la dégénérescence progressive des neurones dopaminergiques du mésencéphale provoquant un dysfonctionnement des noyaux gris centraux. En parallèle de symptômes moteurs bien connus, cette affection entraîne également l’émergence de déficits émotionnels impactant en outre l’expression et la reconnaissance des émotions. Ici, se pose la question d’un déficit de reconnaissance des émotions faciales chez les patients parkinsoniens lié au moins en partie aux troubles moteurs. En effet, selon les théories de simulation des émotions, copier les émotions de l’autre nous permettrait de mieux les reconnaître. Ce serait le rôle du mimétisme facial. Automatique et inconscient, ce phénomène est caractérisé par des réactions musculaires congruentes à l’émotion exprimée par autrui. Dans ce contexte, une perturbation des capacités motrices pourrait conduire à une altération des capacités de reconnaissance des émotions. Or, l’un des symptômes moteurs les plus fréquents dans la maladie de Parkinson, l’amimie faciale, consiste en une perte de la mobilité des muscles du visage. Ainsi, nous avons examiné l’efficience du mimétisme facial dans la maladie de Parkinson, son influence sur la qualité du processus de reconnaissance des émotions, ainsi que l’effet du traitement dopaminergique antiparkinsonien sur ces processus. Pour cela, nous avons développé un paradigme permettant l’évaluation simultanée des capacités de reconnaissance et de mimétisme (corrugator supercilii, zygomaticus major et orbicularis oculi) d’émotions exprimées sur des visages dynamiques (joie, colère, neutre). Cette expérience a été proposée à un groupe de patients parkinsoniens comparé à un groupe de sujets sains témoins. Nos résultats supportent l’hypothèse selon laquelle le déficit de reconnaissance des émotions chez le patient parkinsonien pourrait résulter d’un système « bruité » au sein duquel le mimétisme facial participerait. Cependant, l’altération du mimétisme facial dans la maladie de Parkinson et son influence sur la reconnaissance des émotions dépendraient des muscles impliqués dans l’expression à reconnaître. En effet, ce serait davantage le relâchement du corrugateur plutôt que les contractions du zygomatique ou de l’orbiculaire de l’œil qui nous aiderait à bien reconnaître les expressions de joie. D’un autre côté, rien ne nous permet ici de confirmer l’influence du mimétisme facial sur la reconnaissance des expressions de colère. Enfin, nous avons proposé cette expérience à des patients en condition de traitement habituel et après une interruption temporaire de traitement. Les résultats préliminaires de cette étude apportent des éléments en faveur d’un effet bénéfique du traitement dopaminergique tant sur la reconnaissance des émotions que sur les capacités de mimétisme. L’hypothèse d’un effet bénéfique dit « périphérique » sur la reconnaissance des émotions par restauration du mimétisme facial reste à tester à ce jour. Nous discutons l’ensemble de ces résultats selon les conceptions récentes sur le rôle des noyaux gris centraux et sous l’angle de l’hypothèse de feedback facial. / Parkinson’s disease is a neurodegenerative condition primarily resulting from a dysfunction of the basal ganglia following a progressive loss of midbrain dopamine neurons. Alongside the well-known motor symptoms, PD patients also suffer from emotional disorders including difficulties to recognize and to produce facial emotions. Here, there is a question whether the emotion recognition impairments in Parkinson’s disease could be in part related to motor symptoms. Indeed, according to embodied simulation theory, understanding other people’s emotions would be fostered by facial mimicry. Automatic and non-conscious, facial mimicry is characterized by congruent valence-related facial responses to the emotion expressed by others. In this context, disturbed motor processing could lead to impairments in emotion recognition. Yet, one of the most distinctive clinical features in Parkinson’s disease is facial amimia, a reduction in facial expressiveness. Thus, we studied the ability to mimic facial expression in Parkinson’s disease, its effective influence on emotion recognition as well as the effect of dopamine replacement therapy both on emotion recognition and facial mimicry. For these purposes, we investigated electromyographic responses (corrugator supercilii, zygomaticus major and orbicularis oculi) to facial emotion among patients suffering from Parkinson’s disease and healthy participants in a facial emotion recognition paradigm (joy, anger, neutral). Our results showed that the facial emotion processing in Parkinson’s disease could be swung from a normal to a pathological, noisy, functioning because of a weaker signal-to-noise ratio. Besides, facial mimicry could have a beneficial effect on the recognition of emotion. Nevertheless, the negative impact of Parkinson’s disease on facial mimicry and its influence on emotion recognition would depend on the muscles involved in the production of the emotional expression to decode. Indeed, the corrugator relaxation would be a stronger predictor of the recognition of joy expressions than the zygomatic or orbicularis contractions. On the other hand, we cannot conclude here that the corrugator reactions foster the recognition of anger. Furthermore, we proposed this experiment to a group of patients under dopamine replacement therapy but also during a temporary withdrawal from treatment. The preliminary results are in favour of a beneficial effect of dopaminergic medication on both emotion recognition and facial mimicry. The potential positive “peripheral” impact of dopamine replacement therapy on emotion recognition through restoration of facial mimicry has still to be tested. We discussed these findings in the light of recent considerations about the role of basal ganglia-based circuits and embodied simulation theory ending with the results’ clinical significances.