Transcript BN21 subcortical motor control

Subcortical Motor
Systems:
Cerebellum
& Basal Ganglia
Lecture 21
Motor Loops
Cortex  Subcortex  Cortex 
Spinal cord
 Cerebellum
 coordination of movement
 Basal Ganglia
 selection & initiation of voluntary
movements ~

Cerebellum
Nonmotor functions - memory/language
 Coordination of complex movements
 Programs ballistic movements
 no feedback during execution
 direction, force, & timing
 Motor learning
 shift from conscious  unconscious ~

Cerebellum: Anatomy
Folia & lobules
 analogous to sulci & gyri
 Vermis - along midline
 output  ventromedial pathway
 Hemispheres
 output  lateral pathway
 Deep cerebellar nuclei
 analogous to thalamus ~

Motor Loop Through Cerebellum

Lateral cerebellum
simplest circuit
20 million axons
 Cortex  pons & cerebellum
 Prefrontal, Motor, PPC
 Pons & Cerebellum  thalamus
 VLc - ventrolateral nucleus
 VLc  M1  lateral pathway ~

Prefrontal
M2
Lateral
Cerebellar
Motor Loop
M1
VLc
Distal Limbs
PPC
Pons,
Cerebellum
Cerebellum: Damage
Lesions - loss of motor coordination
 Dysynergia
 no simultaneous movement of joints

serial movement only
Dysmetric movements
 to wrong coordinates
 Alcohol intoxiction
 depression of cerebellar circuits ~

Basal Ganglia

Caudate nucleus
Putamen
Globus Pallidus
Striatum
Substantia Nigra
 Tegmentum
 Control slow movements
 Using immediate sensory
feedback ~

Striatum
Substantia
Nigra
Globus
Pallidus
Thalamus
Cross section of Tegmentum
Substantia
Nigra
Prefrontal
Basal
Ganglia
M2
VLo
M1
PPC
Basal
Ganglia
Motor Loop
Distal Limbs
Basal Ganglia
Movement Disorders
Parkinson’s Disease
1% of population
 Nigrostriatal pathway
 Substantia nigra neurons die
 Progressive loss
 Hypokinesia
 Rigidity
 Bradykinesia
 Akinesia ~

Cortex
+
+
Parkinson’s
Disease
Putamen
+
X
SMA
-
Substantia
Nigra
Globus
Pallidus
(GPi)
VLo
-
+
Subthalamic
Nucleus
Parkinson’s Disease: Treatment
Basal Ganglia - Cholinergic
 Substantia Nigra - Dopaminergic
 Drug Therapy
 L-DOPA
 Pallidectomy
 Tissue transplants ~

Huntington’s Disease (Chorea)

Rare
 onset 30-40s
early as 20s
Degeneration of Striatum
 Caudate
 Putamen
 GABA & ACh neurons ~

Symptoms
Khoros = dance
 Uncontrollable, jerky movements
 Dementia
 Progressive
eventually fatal ~

+
SMA
Putamen
X-
Huntington’s
Disease
VLo
-
++
GPe GPi
-
Subthalamic
Nucleus
Huntington’s Disease: Cause
Genetic disorder
 Single dominant gene on chromosome 4
 HD mutation unstable trinucleotide repeat - CAG
 # of repeats correlated w/ age of onset ~

Huntington’s Disease: Cause
HD gene  huntingtin
 3 forms
 mutated form binds to protein
 involved in energy production
 neuron starves
 Excitotoxicity contributes to degeneration
 glutamate  Nitric oxide (NO)
 Potential treatment::
Inhibit NO synthase ~

Hyperkinesia
Excessive movement
 Ballism
 violent, flinging movements
 Lesions in subthalamus
 less inhibition of VLo
 excitation of SMA ~

SMA
Striatum
+
Hyperkinesia
(e.g. ballism)
-
VLo
-
Globus
Pallidus
+
X
Subthalamic
Nucleus