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18 Cards in this Set

  • Front
  • Back
Describe the blood supply to the basal ganglia
medial striate from anterior cerebral artery, lateral striate and anterior choridal from middle cerebral, branches of PCA
What is the net result of signaling through the direct pathway
the thalamus is disinhibited, movement is facilitaed
What is the net result of signaling through the indirect pathway
The thalamus inhibited and movement is inhibited
Describe the role of the nigrostriatal pathway in basal ganglia function
Dopaminergic synapses to the stratum acting on both the direct and indirect pathways. The D1 receptors of the direct pathway for an excitatory synapse that ultimately facilitates movement. The D2 receptors of the indirect pathway form an inhibitory synapse that also leads to movement (inhibit the inhibitory pathway)
Extrinsic inputs to the basal ganglia terminate mainly in the striatum. Where do thse inputs come from?
1. cerebral cortex (corticostriatal pathway) 2. Intralaminar nuclei of the thalamus (thalamostriate pathway)
Describe the output from the basal ganglia
Output arises from inhibitory (GABA) synapses from the GPi and SNr to the thalamus motor nuclei (VA/VL) and the superior colliculus of the midbrain (SNr)
What is the function of the subthalamic nucleus
Recieves input from the motor and premotor cortices, relay in the indirect pathway. It receivs an inhibitory synapse from the GPe and then provides a excitatory stimulus to the GPi/SNr.
What is the usual cause of basal ganglia disorder? Sxs?
Usually a disruption of transmitter metabolism. Sxs include involuntary movements, akinesia and bradykinesia, changes in posture, muslce tone, and muscular rigidity.
What is the cause or Parkinson's disease? How does this affect basal ganglia function? What sxs woudl be expected
Degeneartion of dopaminergic cells in the SNC leads to a decrease in the ability to facilitate movement. The result is a hypokinetic movement disroder with tremor at rest, rigidty, and bradykinesia
What is the cause of hemiballismus? How does this affect the basal ganglia? What sxs would you expect?
Caused by a lesion of the contralateral subthalamic nucleus. This lesion disrupts the STN's excitatory synapse onto the GPi/SNr so the inhibition that the GPi/SNr provides to the thalamus is decreased.
How do the basal ganglia and cerebellum differ in terms of: input from the spinal cord
cerebellum= direct input via spinocerebellar tracts; basal ganglia=none
How do the basal ganglia and cerebellum differ in terms of: output to the spinal cord
Neither system has direct output to the spinal cord, they relay through DCN or teh thalamus
How do the basal ganglia and cerebellum differ in terms of: input from the cortex
Cerebellum=indirect input form cortex via the pons (corticopontine tract); basal ganglia=direct input from cortex
How do the basal ganglia and cerebellum differ in terms of: projects to the cortex
both systems project to the cortex via the thalamus
How do the basal ganglia and cerebellum differ in terms of: output inhibitory vs. exhibitory
The output from the by the DCN is excitatory (note purkinje to DCN is inhibitory), the output from the basal ganglia to the thalamus is inhibitory
How do the basal ganglia and cerebellum differ in terms of: their effect on movement
Cerebellum-coordinates the execution of movements, compares intended with executed; Basal ganglia-planning and execution of complex motor strategies, amplitude and velocity of movements
How do the basal ganglia and cerebellum differ in terms of: the localization of lesions
Cerebellum=ipsilateral symptions; Basal ganglia=often contralateral symptoms but an be bilateral
How do the basal ganglia and cerebellum differ in terms of: the sxs of lesions
cerebellum-ataxia, impaired balance, intentional tremor; basal ganglia-hyper/hypo kinesia, resting tremor