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Brain Motor Control
Lesson 20
Hierarchical Control of Movement
Association cortices & Basal Ganglia
 strategy : goals & planning
 based on integration of sensory info
 Motor cortex & cerebellum
 tactics: activation of motor programs
 Spinal cord
 execution: activation of alpha motor
neurons ~

Sensorimotor Cortical System
Integration of sensory information
 and directed movements
 Anatomy
 Descending spinal tracts
 Lateral pathway

Pyramidal Motor System


Ventromedial pathway
Extrapyramidal pathway ~
SMA
Cortical Anatomy
M1
S1
PM
S1 - postcentral gyrus
 PPC - Posterior Parietal Cortex
 M1 - Precentral Gyrus
 Frontal Lobe
 somatotopic organization
 M2 - Secondary Motor Cortex
 SMA - Supplementary Motor Area
 PM - Premotor Cortex ~

PPC
Primary Motor Cortex
Somatotopic organization
 neurons have preferred direction
of movement
 Motor homunculus ~

M1: Coding Movement
Movement for limbs
 Neuron most active
 Preferred direction
 but active at 45 from preferred
 How is direction determined?
 Populations of M1 neurons
 Net activity of neurons with
different preferred directions
 vectors ~

M1: Coding Movement
Implications
1. Most M1 active for every
movement
2. Activity of each neuron
1 “vote”
*all votes NOT equal
3. direction determined by
averaging all votes ~

Motor Association Cortex
Motor area other than M1
 Premotor & Supplemental Motor Areas
 Active during preparation for movement
 Planning of movements
 Stimulation - complex movements
 motor programs
 Active during preparation for movement
 Planning of movements
 e.g. finger movements ~

Planning Movements
Targeting vs trigger stimulus
 recording activity of neurons
 active when movement planned
 for specific direction
 Different populations of neurons active
 during planning (targeting)
 & execution (trigger stimulus) ~



Simple finger flexion
 only M1 activation
Sequence of complex finger
movements
 M1 + SMA activation ~

Mental rehearsal of finger
movements
 only SMA activation ~
The Lateral Pathway
Voluntary movement
 distal limbs
 Corticospinal (Pyramidal) tract
 Primary pathway (> 1 million neurons)
 Contralateral control movement
 Cortico-rubrospinal tract
 Via red nucleus
 But some recovery if damage to
corticospinal ~

Spinal Cord: Lateral Pathway
Dorsal
Ventral
Corticospinal
tract
Corticorubrospinal
tract
Motor Loops
Cortex  Subcortex  Cortex 
Spinal cord
 Cerebellum
 coordination of movement
 Basal Ganglia
 selection & initiation of voluntary
movements
 Parallel Processing ~

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
Basal Ganglia

Caudate nucleus
Putamen
Globus Pallidus
Striatum
Substantia Nigra
 Tegmentum
 Control slow movements
 Using immediate sensory
feedback ~

Prefrontal
Basal
Ganglia
M2
VLo
M1
PPC
Basal
Ganglia
Motor Loop
Distal Limbs
Parkinson’s Disease
1% of population
 Nigrostriatal pathway
 Substantia nigra neurons die
 Progressive loss
 Hypokinesia
 Rigidity
 Bradykinesia
 Akinesia ~

Cortex
+
Parkinson’s
Disease
+
VA/VL
Striatum
X
- +
Substantia
Nigra
Direct
Indirect
-
GPe
-
GPi
+
-
Subthalamic
Nucleus
Parkinson’s Disease: Treatment
Basal Ganglia - Cholinergic
 Substantia Nigra - Dopaminergic
 Drug Therapy
 L-DOPA
 Pallidectomy
 Tissue transplants ~

Huntington’s Disease (Chorea)
Rare Genetic disorder
 Single dominant gene, chrom. 4
 onset 30-40s
 Progressive disease
 Uncontrollable, jerky movements
 Dementia
 Degeneration of Striatum
 Caudate & Putamen
  GABA & ACh neurons ~

Cortex
Direct
Indirect
+
Huntington’s
Disease
+
VA/VL
Striatum
-
GPe
-
GPi
- +
+
Substantia
Nigra
-
Subthalamic
Nucleus
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 ~
