Motor Systems
Organization of Neural Structures Involved in the Control of Movement → Can be divided into four distinct subsystems, each of which makes a unique contribution to motor control
Spinal Cord + Brainstem
Upper motor neurons
Basal Ganglia
Cerebellum
Basal Ganglia and Cerebellum have no direct access to local circuits or lower motor neurons, control is indirect; regulating upper motor neurons
Motor Homunculus → Premotor Cortex + Primary Motor Cortex
Information Coding by Cortical Neurons
Edward V. Evarts developed the technique to record the motor cortical neurons from awake monkeys performing motor tasks
Examined changes in the firing rate of motor cortex neurons as the monkey flexed its wrist under different load conditions
Technique allowed a deeper understanding of how cortical motor areas contribute to specific motor behaviors
Evarts Experiment (1966, 1968)
When no load was applied: the neuron fired before and during the flexion movement
When a load-opposing flexion was applied: The neuronal activity increased
When a load assisting flexion was applied: activity decreased
In all conditions wrist displacement was the same, but neuronal activity changed as load changed
Conclusion: the cells were muscle like; the force, not displacement of the wrist, correlates with neuron firing
Georgopoulos Experiments (1982): How do M1 cells behave during reaching?
A monkey was trained to move a joystick in the direction indicated by alight
The activity of a single neuron was recorded during arm movement in each of the eight direction
Black lines indicate the discharge rates of individual primary motor cortex neurons
By combining the responses of all the neuron a population vector (red arrows) can be derived
Population vector represents the movement direction encoded by the simultaneous activity of the the entire population of recorded neurons
Neural Tuning in Motor Cortex Correlates to a LARGE number of movement parameters: force + movements
Force
Movements in 2D
Movements in 3D
Premotor Cortex
Lateral premotor area is concerned with movement selection
Lesions impair the ability to perform visually cued conditional tasks, even though they can still respond to the visual stimulus can perform the same movement in a different setting
Patients with this damage have difficulty learning to select a particular movement in response to a visual clue, even though they understand the instruction and can perform the movements
Individuals with lesions in the premotor cortex may also have difficulty performing movements in response to verbal commands
Cerebellum
Small brain
10% of the weight, but 50% of the neurons in the entire brain
Highly regular structure – circuit modules for distinct function performed by distinct functions performed by connections to different parts of the motor system
Function: coordination, balance, motor learning
Damage:
Dyssynergia (decomposition of synergistic multi-joint movement)
Dysmetria (inaccuracy in range and direction of movement)
Dysdiadochokinesia (irregular pattern of alternating movement)
Vestibulocerebullum: Maintains equilibrium and stance
Input: from vestibular system, output to motoneurons of axial muscles
Function: Regulation of movements that maintain posture and equilibrium
Damage: loss of equilibrium, wide stance “drunken sailor’s gait”
Spinocerebellum: Fine motor coordination (threading a needle)
Input: from motor context and the spinal cord
Function: compares motor command with movement feedback; sends correction to motor context
Damage: Decomposition of movement, inability to correct ongoing movement
Over or undershoot of target, timing deficit, slurred speech
Lateral Cerebellum: Motor learning, initiation of movement (cerebrocerebellum)
Input: From many areas in cerebral cortex
Output: motor context
Function: Cognition and timing
Damage: Loss of learned motor skills, delay in initiating movements
Basal Ganglia
Collection of subcortical nuclei consisting of:
Caudate nucleus and putamen (receive input from cortex)
Globus pallidus (internal/external, output to thalamus)
Subthalamic Nucleus
Substantia Nigra
Function: initiating and braking movements
Damage: Manifests as movement disorders
Huntington Disease
Selective atrophy of the caudate and putamen
Neurons that project to the external segment of the globus pallidus degenerate
In the absence of their normal inhibition, the external globus pallidus becomes abnormally active; reduces the excitatory output of the subthalamic nucleus to the internal segment of the globus pallidus, and inhibitory outflow of the basal ganglia is reduced
Without the restraining influence of the basal ganglia, upper motor neurons can be activated by inappropriate signals, resulting in undesired ballistic and choreiform movements
Cause: An autosomal dominant disorder (IT15) on non-sex chromosome 4 causing an CAG triplet repeat
Size of caudate and putamen is dramatically reduced
Symptoms: Chorea, abnormal involuntary writhing movements, behavioral or psychiatric disturbances, dementia, 15-20 years after onset
Parksinson’s Disease
The dopaminergic inputs provided by substantia nigra pars compacta are diminished
More difficult to generate inhibition form the caudata/putamen, resulting in sustained or increased tonic inhibition from the internal segment of the globus pallidus to the thalamus
Thalamic excitation of the motor cortex less likely
A failure of the disinhibition; reduced movement amplitude, movements are difficult to initiate, and terminate
Abnormal gene on chromosome 4 from either parent
Progressive loss of dopaminergic neurons in substantia nigra pars compacta
Symptoms:
tremors at rest, slowness of movement, minimal facial expressions
Akinesia (loss or extreme difficulty voluntary initiating a movement)
Walking, stooped posture
Paucity of movements
Dementia
The Muscular Junction
1. An AP in a motor neuron is propagated to the terminal
2. This local AP triggers the opening of voltage gated calcium channels and the subsequent entry of calcium ions into the terminal bouton
3. Calcium ions triggers release of acetylcholine by exocytosis from a potion of the vesicles
4. Ach diffuses across the space separating the nerve and muscle cells and binds with receptor-channels specific for it on the motor end plate of the muscle cell membrane
5. This binding brings about the opening of these nonspecific cation channels, leading to a relatively large movement of Na+ into the muscle cell compared to a smaller movement of K+ outward
6. The result is an end-plate potential. Local current flow occurs between the depolarized end plate and the adjacent membrane
7. This local current flow opens voltage dNa+ channels in the adjacent membrane
8. THe resultant Na+ entry reduces the potential to threshold, initiating an action potential, which is propagated throughout the muscle fiber
9. ACh is subsequently destroyed by acetylcholinesterase, an enzyme located on the motor-end plate membrane, terminating the muscle cell’s response
Motor Unit
A motor neuron and all muscle fibers it innervates
Each muscle fiber receives input from only one motor neuron, but each motor neuron can branch to contact several muscle fibers
Motor unit size varies by function:
Fine control (eye muscles): 1 motor neuron: 3-6 muscle fibers
Coarse control (calf muscle): 1 motor neuron: 2-3K muscle fibers
Motor neurons into motor pools
Each pool provides specific muscles these pools collect in bundles (motor nerves) and exit the spinal cord in the ventral horn/root
Size Principle: Motor Units are Recruited in a Fixed Order
Motor Neurons are recruited in rank order according to size
Smaller motor neurons are recruited before larger ones (at lower firing rates, the neurotransmitter is more effective on the smaller motor neuron
As the firing rate of the interneurons increases, the larger motor neurons are recruited
The number of active motor units and their rate of firing both increase with voluntary force
As the amount of voluntary force increases, the number and the rate of active motor units increase
Lowest threshold motor units which generate the least amount of force are recruited first
Corticospinal Tracts
Origin: primary motor cortex (30%), premotor (30%), somatosensory (30%)
About 1 million fingers in humans
90% of fibers cross at lower medulla
Right motor cortical areas control left side of the body, specially the distal muscles
10% do not cross
All are excitatory
Small diameter, slow conducting fibers
Cortical neurons that project down the spinal cord often synapse at several levels, and in several motor neurons
Neurons that project to proximal diverge more broadly than those that project to distal muscles
Motor Pools are organized within the spinal cord
Somatotopic organization of motor neuron pools in a cross section of the ventral horn at the cervical level of the spinal cord
Medial-lateral topographical relationship: Motor neurons innervating axial (proximal) musculature are located medially, whereas those innervating the distal musculature are located more laterally
Knee Jerk Reflex (Myostatic Reflex)
Monosynaptic component: From the spindle to the alpha motor neuron back to the muscle containing the spindle → excitatory loop
Disynaptic component: From the spindle to inhibitory interneurons, to the alpha motor neuron innervating the antagonistic muscle
Due to the tap, sensory neuron is triggered to fire at a higher frequency, which triggers higher firing in the extensor neuron and interneuron
Increase in firing in the interneuron causes a decrease in the firing of the flexor neuron
Proper performance of knee jerk shows that sensory fibers, the input to motor neurons and muscles are all functioning normally
One of the purposes of the reflex is to maintain upright posture in the face of permutations (ex: tripping)
The Myotatic/Stretch Reflex in Upper Limb
Stretching the muscle and spindle leads to an increase of activity in the afferents and the motor neurons that innervate the same muscle
Indirectly inhibit the motor neurons that innervate the antagonist muscle via interneuron
Example of reciprocal innervation – results in rapid contact of the stretch muscle and simultaneous relaxation of the antagonist muscle
The stretch operates as a negative feedback loop to regulate muscle length at a desired value → muscle tone
The appropriate muscle length is specified by the activity of descending upper motor neuron pathways that influence the lower motor neuron pool
Deviations from the desired length are sensed by the spindles that lead to changes in the activity of motor neurons
The Flexion-crossed Extension Reflex
Mediates the removal of a limb or finger from a painful stimuli
Consists of:
The withdrawal of the ipsilateral limb by activation of the ipsilateral flexors and reciprocal inhibition of the ipsilateral extension muscles
The opposite reaction in the contralateral limb; activation of the extension and reciprocal inhibition of the flexor muscles
Last part provides postural support during withdrawal of the affected limb