This motor circuit “regulates muscle contraction, muscle force, multijoint movements, and sequencing of movements” throughout different pathways in the brain (Lundy-Ekman, 2013, p. 235). Interestingly enough, however, there is no direct output to lower motor neurons (LMNs). Rather, information about motor control that comes from the basal ganglia is transferred to LMNs through three different routes: the thalamus, the PPN, and the midbrain locomotor region (Lundy-Ekman, 2013, p. 235). In Huntington’s, the specific part of the basal ganglia that degenerates is the striatum, as well as the cerebral cortex. The job of the striatum is to send “inhibitory, GABA-mediated projections on to the ventral pallidum” which then brings the inhibitory output to the nucleus of the thalamus (Paradiso et al., 2008, p. 74). Because of the degeneration in this area, there is a decrease in signals from the output nuclei, which means that they do not get to the motor thalamus or PPN to inhibit their activity (Lundy-Ekman, 2013, p. 245). To compensate for this disinhibition, there is excessive output from the “motor areas of the cerebral cortex”, which is why chorea presents as a primary symptom (Lundy-Ekman, 2013, p. 245). The specific basal ganglia nuclei that is affected is the striatum, which is made up of the caudate and putamen and are the only areas of the basal ganglia that deal with motor control (Lundy-Ekman, 2013, p. 235). The putamen is responsible for receiving input from the premotor and motor cortex, and has much control over our movements, whereas the caudate head is not directly responsible for controlling movements (Lundy-Ekman, 2013, p. 235). Rather, the head of the caudate is responsible for decision-making and goal-directed behaviors, including “evaluating information for making perceptual decisions, planning, and choosing actions
This motor circuit “regulates muscle contraction, muscle force, multijoint movements, and sequencing of movements” throughout different pathways in the brain (Lundy-Ekman, 2013, p. 235). Interestingly enough, however, there is no direct output to lower motor neurons (LMNs). Rather, information about motor control that comes from the basal ganglia is transferred to LMNs through three different routes: the thalamus, the PPN, and the midbrain locomotor region (Lundy-Ekman, 2013, p. 235). In Huntington’s, the specific part of the basal ganglia that degenerates is the striatum, as well as the cerebral cortex. The job of the striatum is to send “inhibitory, GABA-mediated projections on to the ventral pallidum” which then brings the inhibitory output to the nucleus of the thalamus (Paradiso et al., 2008, p. 74). Because of the degeneration in this area, there is a decrease in signals from the output nuclei, which means that they do not get to the motor thalamus or PPN to inhibit their activity (Lundy-Ekman, 2013, p. 245). To compensate for this disinhibition, there is excessive output from the “motor areas of the cerebral cortex”, which is why chorea presents as a primary symptom (Lundy-Ekman, 2013, p. 245). The specific basal ganglia nuclei that is affected is the striatum, which is made up of the caudate and putamen and are the only areas of the basal ganglia that deal with motor control (Lundy-Ekman, 2013, p. 235). The putamen is responsible for receiving input from the premotor and motor cortex, and has much control over our movements, whereas the caudate head is not directly responsible for controlling movements (Lundy-Ekman, 2013, p. 235). Rather, the head of the caudate is responsible for decision-making and goal-directed behaviors, including “evaluating information for making perceptual decisions, planning, and choosing actions