Émotion et noyaux gris centraux (I) : que peut nous apprendre la maladie de Parkinson ? [Emotion and basal ganglia (I): what can we learn from Parkinson's disease?]. - Université de Rennes Access content directly
Journal Articles Revue Neurologique Year : 2012

Émotion et noyaux gris centraux (I) : que peut nous apprendre la maladie de Parkinson ? [Emotion and basal ganglia (I): what can we learn from Parkinson's disease?].

Abstract

Parkinson's disease provides a useful model for studying the neural substrates of emotional processing. The striato-thalamo-cortical circuits, like the mesolimbic dopamine system that modulates their function, are thought to be involved in emotional processing. As Parkinson's disease is histopathologically characterized by the selective, progressive and chronic degeneration of the nigrostriatal and mesocorticolimbic dopamine systems, it can therefore serve as a model for assessing the functional role of these circuits in humans. In the present review, after a definition of emotional processing from a multicomponential perspective, a synopsis of the emotional disturbances observed in Parkinson's disease is proposed. Note that the studies on the affective consequences of subthalamic nucleus deep brain stimulation in Parkinson's disease were excluded from this review because the subject of a companion paper in this issue. This review leads to the conclusion that several emotional components would be disrupted in Parkinson's disease: subjective feeling, neurophysiological activation, and motor expression. We then discuss the functional roles of the striato-thalamo-cortical and mesolimbic circuits, ending with the conclusion that both these pathways are indeed involved in emotional processing.
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Dates and versions

hal-01133877 , version 1 (20-03-2015)

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T Dondaine, J Péron. Émotion et noyaux gris centraux (I) : que peut nous apprendre la maladie de Parkinson ? [Emotion and basal ganglia (I): what can we learn from Parkinson's disease?].. Revue Neurologique, 2012, 168 (8-9), pp.634-41. ⟨10.1016/j.neurol.2012.06.013⟩. ⟨hal-01133877⟩
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