The article discusses the role of the basal ganglia in goal-directed and habitual control, particularly in the context of Parkinson's disease. The basal ganglia, a group of subcortical nuclei, are crucial for movement control and are linked to various movement disorders. The 'direct versus indirect pathway' model describes the functional architecture of the basal ganglia, where the 'direct pathway' facilitates movement and the 'indirect pathway' inhibits movement. However, recent studies have revealed that the basal ganglia are divided into functionally segregated regions, with the rostromedial striatum regulating goal-directed control and the caudolateral striatum regulating habitual control. In Parkinson's disease, the progressive loss of dopamine in the posterior putamen, a region associated with habitual behavior, leads to a reliance on goal-directed control. This shift can result in behavioral difficulties, such as impaired automatic control and distorted output signals from habitual control circuits, which impede the expression of goal-directed actions. The article also explores the anatomical and functional organization of the basal ganglia, including the intrinsic and extrinsic connections, and the role of dopamine in modulating these circuits. The authors propose that the preferential loss of dopamine in sensorimotor territories may cause a significant deficit in habitual control, leading to difficulties in acquiring and expressing habitual actions. They suggest that patients with Parkinson's disease may have to rely increasingly on the slower, serial goal-directed control system, which can be disrupted by other goal-directed tasks. The article also discusses the implications of these findings for the interpretation of functional deficits in Parkinson's disease, including the impaired ability to perform automatic movements and the difficulty in initiating and executing movements. Finally, the article highlights the paradoxical nature of surgical lesions in treating Parkinson's disease, suggesting that they may work by blocking distorting signals from malfunctioning habitual control circuits, thereby improving goal-directed control. The review concludes by emphasizing the importance of understanding the intrinsic mechanisms underlying sensorimotor dysfunction in the basal ganglia for the development of novel therapeutic approaches.The article discusses the role of the basal ganglia in goal-directed and habitual control, particularly in the context of Parkinson's disease. The basal ganglia, a group of subcortical nuclei, are crucial for movement control and are linked to various movement disorders. The 'direct versus indirect pathway' model describes the functional architecture of the basal ganglia, where the 'direct pathway' facilitates movement and the 'indirect pathway' inhibits movement. However, recent studies have revealed that the basal ganglia are divided into functionally segregated regions, with the rostromedial striatum regulating goal-directed control and the caudolateral striatum regulating habitual control. In Parkinson's disease, the progressive loss of dopamine in the posterior putamen, a region associated with habitual behavior, leads to a reliance on goal-directed control. This shift can result in behavioral difficulties, such as impaired automatic control and distorted output signals from habitual control circuits, which impede the expression of goal-directed actions. The article also explores the anatomical and functional organization of the basal ganglia, including the intrinsic and extrinsic connections, and the role of dopamine in modulating these circuits. The authors propose that the preferential loss of dopamine in sensorimotor territories may cause a significant deficit in habitual control, leading to difficulties in acquiring and expressing habitual actions. They suggest that patients with Parkinson's disease may have to rely increasingly on the slower, serial goal-directed control system, which can be disrupted by other goal-directed tasks. The article also discusses the implications of these findings for the interpretation of functional deficits in Parkinson's disease, including the impaired ability to perform automatic movements and the difficulty in initiating and executing movements. Finally, the article highlights the paradoxical nature of surgical lesions in treating Parkinson's disease, suggesting that they may work by blocking distorting signals from malfunctioning habitual control circuits, thereby improving goal-directed control. The review concludes by emphasizing the importance of understanding the intrinsic mechanisms underlying sensorimotor dysfunction in the basal ganglia for the development of novel therapeutic approaches.