The basal ganglia (BG) receives input at the striatum from the cortex and provides output from the pallidum, in particular the globus pallidus internal (GPi) via the ventral anterior and lateral (VA/VL) thalamic nuclei to the cortex – forming a motor loop.1,2 There are two major pathways in this motor loop, the direct and indirect pathways.1,2
The direct pathway originates in the cortex, projecting to the striatum of the BG which consists of the caudate and putamen nuclei.1,2 The striatum projects to and inhibits the GPi which has tonic inhibitory connections to the VA/VL nuclei of the thalamus and finally back to the motor and premotor cortex.1
Activation of the direct pathway initiates voluntary movement, by releasing upper motor neurons in the cortex from inhibition.1,2 The globus pallidus, internal and external, are made up of medium spiny GABA-ergic neurons which have tonically active inhibitory effects on the VA/VL thalamic nuclei.1,2 In the direct pathway the tonic inhibitory GPi neurons are inhibited by the striatum, leading to disinhibition of the VA/VL thalamic nuclei and facilitation of cortical activity and movement.1,2 The indirect pathway also originates in the cortex and projects to the BG striatum. From here it projects to the globus pallidus external (GPe), through the subthalamic nucleus (STN) and onto the GPi.1,2 The GPi then projects to the VA/VL thalamic nuclei and back to the motor and premotor cortex.1 Activation of the indirect pathway decreases motor output from the cortex, suppressing movement, by increasing inhibition of upper motor neurons in the cortex.1,2 The striatum inhibits the GPe’s tonically inhibitory effects on the STN.1,2 The STN has excitatory projections to the GPi, the release of GPe inhibition leads to increased excitation from the STN on the GPi.1,2 This increases inhibition of the GPi on the VA/VL thalamic nuclei and cortical activity is not induced.1,2 The BG’s role is to select and initiate voluntary movements, as well as suppress unnecessary movements and control adequate amounts of movement.1 Movement is initiated when disinhibition of the thalamus is achieved, via the direct pathway.1,2 The indirect and direct pathways of the motor-loop work together to fine tune and provide adequate amounts of appropriate movement.1,2 The substantia nigra pars compacta (SN) modulates the BG motor loops.1 It …show more content…
Huntington’s disease is a hyperkinetic genetic disorder characterised by degradation of the tonic inhibitory medium spiny neurons of the striatum which project to the GPe in the indirect pathway.1,3 The loss of inhibitory input from these neurons results in enhanced activity of the GPe.1,3 As a result, the GPe inhibits the STN and reduces its excitatory input to the GPi.1,2 The GPi’s inhibitory effects on the VA/VL thalamic nuclei is not enhanced and the inhibitory outflow of the BG is reduced.1,3 Upper motor neurons are not adequately inhibited, there is increased excitation to the motor cortex and inappropriate, ‘ballistic’ movement results.1,3
Hemiballismus is characterised by violent, involuntary movements of the limbs, usually on one side of the body, and occurs due to damage to the STN involved in the indirect pathway.1,3 Damage to the STN removes or reduces its excitatory input to the GPi, which normally enhances its inhibitory effects.1,3 The inhibitory connections from the GPi to the VA/VL thalamic nuclei are not enhanced.1,3 Thus, the upper motor neurons discharge abnormally as they are not adequately inhibited when movements are
The direct pathway originates in the cortex, projecting to the striatum of the BG which consists of the caudate and putamen nuclei.1,2 The striatum projects to and inhibits the GPi which has tonic inhibitory connections to the VA/VL nuclei of the thalamus and finally back to the motor and premotor cortex.1
Activation of the direct pathway initiates voluntary movement, by releasing upper motor neurons in the cortex from inhibition.1,2 The globus pallidus, internal and external, are made up of medium spiny GABA-ergic neurons which have tonically active inhibitory effects on the VA/VL thalamic nuclei.1,2 In the direct pathway the tonic inhibitory GPi neurons are inhibited by the striatum, leading to disinhibition of the VA/VL thalamic nuclei and facilitation of cortical activity and movement.1,2 The indirect pathway also originates in the cortex and projects to the BG striatum. From here it projects to the globus pallidus external (GPe), through the subthalamic nucleus (STN) and onto the GPi.1,2 The GPi then projects to the VA/VL thalamic nuclei and back to the motor and premotor cortex.1 Activation of the indirect pathway decreases motor output from the cortex, suppressing movement, by increasing inhibition of upper motor neurons in the cortex.1,2 The striatum inhibits the GPe’s tonically inhibitory effects on the STN.1,2 The STN has excitatory projections to the GPi, the release of GPe inhibition leads to increased excitation from the STN on the GPi.1,2 This increases inhibition of the GPi on the VA/VL thalamic nuclei and cortical activity is not induced.1,2 The BG’s role is to select and initiate voluntary movements, as well as suppress unnecessary movements and control adequate amounts of movement.1 Movement is initiated when disinhibition of the thalamus is achieved, via the direct pathway.1,2 The indirect and direct pathways of the motor-loop work together to fine tune and provide adequate amounts of appropriate movement.1,2 The substantia nigra pars compacta (SN) modulates the BG motor loops.1 It …show more content…
Huntington’s disease is a hyperkinetic genetic disorder characterised by degradation of the tonic inhibitory medium spiny neurons of the striatum which project to the GPe in the indirect pathway.1,3 The loss of inhibitory input from these neurons results in enhanced activity of the GPe.1,3 As a result, the GPe inhibits the STN and reduces its excitatory input to the GPi.1,2 The GPi’s inhibitory effects on the VA/VL thalamic nuclei is not enhanced and the inhibitory outflow of the BG is reduced.1,3 Upper motor neurons are not adequately inhibited, there is increased excitation to the motor cortex and inappropriate, ‘ballistic’ movement results.1,3
Hemiballismus is characterised by violent, involuntary movements of the limbs, usually on one side of the body, and occurs due to damage to the STN involved in the indirect pathway.1,3 Damage to the STN removes or reduces its excitatory input to the GPi, which normally enhances its inhibitory effects.1,3 The inhibitory connections from the GPi to the VA/VL thalamic nuclei are not enhanced.1,3 Thus, the upper motor neurons discharge abnormally as they are not adequately inhibited when movements are