Motor control is the study of how the nervous system controls movement. Movements can range from simple reflexes to complex actions. The primary purpose of the brain is to guide movement.
Reflexes: Simple, brief muscle activations (e.g., eyeblink, hiccup, finger twitch).
Acts/Action Patterns: Complex, sequential movements (e.g., honking a car horn, writing your name, playing guitar).
Motor Plan/Motor Program: A set of muscle commands established before an action occurs.
Two control mechanisms optimize accuracy and speed:
Maximizes speed by using pre-programmed instructions without external feedback. Ballistic movements are rapid and completed regardless of sensory feedback. No guiding external feedback.
Maximizes accuracy by using feedback from the controlled action to guide movements. Ramp movements are smooth, slower, and sustained, and are guided by feedback.
Nonprimary Motor Cortex: Initiates cortical processing.
Primary Motor Cortex: Initiates commands for action.
Brainstem: Integrates motor commands.
Cerebellum and Basal Ganglia: Tweak these systems.
Spinal Cord: Controls skeletal muscles.
Skeletal Muscles: Power movement.
Antagonists: Biceps and triceps are antagonists.
Balance:At rest, flexor and extensor muscles are balanced.
Tremor: Alternation of flexor-extensor (antagonist)/bicep-tricep contraction. Normally present, but debilitating if poorly regulated.
Motoneurons send their axons to innervate muscles. Action potentials travel along the motoneuron from the spinal cord to the muscle.
Neuromuscular Junction: Point where a motor neuron terminal and muscle fiber meet.
Acetylcholine: Neurotransmitter released at the neuromuscular junction.
Motor Unit: One motor neuron's axon and all its target fibers.
Fine Movements: Muscles that make fine, precise movements have only a few muscle fibers per axon.
Innervation Ratio: Examples include 1/3 and 1/13, which describe the ratio of motor neurons to muscle fibers.
1 axon and 3 fibers attached will produce fine movements
1 axon and 13 movements will NOT
Action of muscles is guided by sensory feedback:
Muscle Spindles: Responsive to muscle stretch.
Golgi Tendon Organs: Respond to muscle contraction, less to stretch.
Proprioception: Information about body movements and position.
Muscle spindles provide feedback on muscle length and stretch.
alpha-gamma Coactivation mechanism involving sensory neuron, \alpha motor neuron, and \gamma motor neuron.
Muscle is stretched.
Excitation of muscle spindle afferents. muscle spindles stretching and excite.
Excitation of \alpha -motoneurons. Beta and alpha neurons are excited.
Agonist muscle (biceps and triceps) stimulated to oppose stretch.
Antagonist muscle is inhibited. Muscle goes to relaxed state neither stretching or contractions.
This reflex prevents you from falling over when you extend your arm.
Impaired control of the stretch reflex. Motor cortex normally inhibits reflex behavior. When cortical input is cut off, spinal cord is released from inhibition, exaggerating reflexes. Hyperreflexia, Clonus.
Pyramidal System: Includes the primary motor cortex, and is responsible for voluntary movement.
Extrapyramidal System: Includes the basal ganglia and cerebellum, modulates and tweaks movements.
Upper Motor Neuron: From primary motor cortex to the medulla, where it crosses over (decussation), then down the spinal cord to the anterior horn cell (lower motoneuron).
Lower Motor Neuron: From spinal cord to muscle.
Primary motor cortex changes as a result of learning. Early music training results in expansion of motor cortex.
Learns and plans movement:
Supplementary Motor Area (SMA): Encodes sequences of movements during skill acquisition.
Premotor Cortex: Neurons fire just before performing an activity.
Includes the caudate nucleus, putamen, globus pallidus, subthalamic nucleus, and substantia nigra.
Guides movement through inhibition via Purkinje cells, which send inhibitory messages.
Primary motor cortex and basal ganglia are more involved in early phase of a movement than SMA and cerebellum.
Basal ganglia and cerebellum (extrapyramidal system) predict postural consequences of planned (pyramidal) movement and act to prevent loss of balance.
Gastronemius is activated before he lifts bell? Why? Because of extrapyrimidal movements.
Neural circuits generate rhythmic behaviors (e.g., walking) in the spinal cord.
A visual task that requires a simple choice and a button push involves a complex cascade of processes.
What is the current state of the body?
Should I move?
Select the motor plan.
Load the motor plan.
Execute the plan.
Feedback on how the plan is going. Change it?
Strength: Largely a pyramidal function (power).
Tone: Largely an extrapyramidal function (posture).
These are not independent.
Pyramidal damage causes weakness.
Extrapyramidal damage impairs movement control.
Primary disorder of muscle.
Dystrophin is a protein needed for normal muscle function, produced by the X chromosome. Patients make no dystrophin or an abnormal dystrophin molecule, leading to progressive degeneration of muscle.
Autoimmune disorder where patients develop antibodies to their own ACh receptors. This causes weakness of skeletal muscles that develops over the day and resolves with rest/sleep.
Poliovirus destroys spinal motoneurons and sometimes cranial motoneurons. There is no treatment for polio.
Lou Gehrig disease, degeneration of motoneurons and consequent loss of their target muscles. Fasciculations.
Spinal cord injuries result in paralysis; reflexes, sensation, and strength below the level of the injury are lost.
Higher-level (motor processing) disorder: inability to sequence movements, though no muscle paralysis exists. New acts are ramped (feedback-controlled) - slow, variable - frontal and parietal cortex. Well-learned acts are ballistic - fast, consistent - cortex and basal ganglia.
Tremor
Bradykinesia
Shuffling gait
Postural instability
Degeneration of dopamine cells in the substantia nigra, which project to the basal ganglia. L-dopa, a precursor to dopamine, improves symptoms. Environmental exposures, especially pesticides, contribute.
Progressive destruction of the caudate nucleus and putamen. Cerebral cortex also is impaired. The gene responsible (HTT) has a trinucleotide repeat (CAG). If CAG repeats too many times, the disease develops.
Cerebellar damage impairs motor control. Purkinje cells die. Causes include childhood tumors of the cerebellar vermis, alcoholism, and inherited degeneration of the cerebellum.
Abnormal sustained posture due to basal ganglia dysfunction.
Tics and Obsessive-Compulsive Disorder. Basal ganglia and cortex disorder. Clinical features: more common in boys, tics usually end by adulthood, tics affect face and shoulders more than hands and legs, coprolalia is rare in children.
Motor cortex damage, such as stroke, causes motor impairment. Weakness (paresis) of voluntary movements.