Motor Systems Overview

• Overview of Motor Systems
• Rhea Kimpo, Ph.D.

Motor System Organization

• Descending systems involve upper motor neurons.
• The motor cortex is involved in planning, initiating, and directing voluntary movements.
• Brainstem centers control basic movements and postural control.
• The basal ganglia are responsible for gating proper initiation of movement.
• The cerebellum coordinates sensory motor during ongoing movements.
• Local circuit neurons integrate lower motor neuron signals.
• Motor neuron pools consist of lower motor neurons.
• The spinal cord and brainstem circuits receive sensory inputs and connect to skeletal muscles.

Lower Motor Neurons

• Lower motor neurons are located in the anterior horn of the spinal cord and certain cranial nerve nuclei.
• They innervate muscles.
• They consist of alpha and gamma motor neurons.
• Alpha motor neurons innervate extrafusal muscle fibers and generate muscle force, enabling muscle contraction.
• Gamma motor neurons innervate intrafusal muscle fibers within the muscle spindle.
• Gamma motor neurons contribute to the level of alpha motor neuron firing.
• Muscle spindles are fusiform shaped organs deep inside the extrafusal muscle fibers.
• Muscle spindles consist of intrafusal muscle fibers with sensory and motor innervation.
• Sensory receptors (sensitive to stretch) are located in the middle of each spindle with contractile fibers.
• Alpha and gamma motor neurons play roles in the monosynaptic stretch reflex arc.

Motor Unit

• A motor unit consists of a motor neuron and the muscle fibers it innervates.
• A single motor neuron can innervate 1 to 100 muscle fibers, varying the size of the motor unit.
• Areas of fine movement have more motor neurons and smaller motor units.
• Larger motor units generate greater force.
• Muscle force generation depends on:
  • Firing frequency of the alpha motor neuron (rate coding).
  • Activation of more motor units (recruitment).
• Motor units are recruited from smallest to largest.

Muscle Tone

• Muscle tone is the level of tension in a muscle at rest, which is due to the activity of alpha motor neurons.
• Gamma motor neurons are contribute to the activity of alpha motor neurons.
• Muscle tone is assessed clinically by testing a muscle's resistance to passive stretch.
• The level of activity in the stretch reflex arc is the primary determinant of muscle tone.

Monosynaptic Stretch Reflex

• Sensory apparatus in this reflex is in the muscle spindle.
• The reflex begins when a reflex hammer hits the patellar tendon, stretching it.
• Stretching activates the muscle spindles.
• Activation of 1a afferent nerve fibers projects into the posterior horn of the spinal cord.
• A sensory neuron synapses onto a motor neuron in the ventral horn.
• The motor neuron excites the quadriceps muscle and cause contraction and leg extension.
• Gamma motor neurons allow sensory stretch receptors to maintain sensitivity to stretch.
• Gamma motor neurons allow stretch receptors to remain sensitive regardless of muscle length.
• Tapping a tendon stretches extrafusal fibers.
• Sensory fibers are activated and send action potentials via afferent axons to the posterior spinal cord.
• Synapses form on lower motor neurons.
• Gamma motor neurons influence muscle tone and maintain sensory receptors to maintain their sensitivity.
• Damage to the muscle spindle affects tone.

Lower Motor Neuron Syndrome

• Neurological signs of damage include:
  • Flaccid paralysis
  • Hypotonia, atonia
  • Areflexia or hyporeflexia
  • Atrophy
  • Fasciculations

Upper Motor Neurons

• Upper motor neurons project and synapse on lower motor neurons and interneurons in the spinal cord.
• Reticular formation (brainstem)
• Vestibular nuclei
• Superior colliculus
• Red nucleus
• Motor cortex
• They maintain posture while sitting and moving (involuntary).
• They initiate movement (voluntary).
• Upper motor neurons influence muscle tone.
• Corticospinal and corticobulbar tracts are the pyramidal system.
• Extrapyramidal system includes all other pathways, basal nuclei, and cerebellar pathways.
• Tracts are named according to their origin and termination.

Medial and Lateral Systems

• The upper motor neurons in the lateral pathways innervate distal limb musculature.
• The upper motor neurons in the medial pathways innervate axial and proximal limb musculature.
• Medial pathways influence axial (trunk) and proximal limb muscles.
• Lateral pathways influence distal limbs.

Lateral Pathwaysdescend and terminate laterally

• Lateral pathways are involved in movements of the distal limbs.
• Lateral corticospinal tract innervates lower motor neurons (LMNs) in the spinal cord.
• Rubrospinal tract innervates LMNs in the cervical spinal cord, which innervate flexors of upper extremity
• Lateral corticospinal tract consists of upper motor neurons in the pre-central gyrus and paracentral lobule.
• Rubrospinal tract originates from red nucleus, cell bodies decussate and project to cervical spinal cord levels.

Medial Pathwaysdescent and terminate medially

• Medial pathways involved in innervation of trunk (axial) muscles and proximal limbs.
• Medial pathways maintain balance and position, especially during limb movement and orient gaze.
• Vestibulospinal tract innervates LMNs that excite the extensors (antigravity muscles).
• Tectospinal tract innervates LMNs in upper spinal cord and turns the head and visual gaze.
• Reticulospinal tracts innervate LMNs in spinal cord and enhance tone in antigravity muscles.
• Medial and lateral vestibulospinal tracts are considered medial pathways.
• Medial reticulospinal tracts have cell bodies in the pons.
• Lateral reticulospinal tracts have cell bodies in the medulla.

Motor Cortex

• The motor cortex initiates, coordinates, and plans voluntary motor movements.
• Cortices involved in motor activity include:
  • Primary motor cortex (Brodmann # 4)
  • Lateral premotor area (lateral Brodmann # 6)
  • Supplementary motor cortex (medial Brodmann # 6)
• Frontal eye fields, Broca's, somatosensory, and parietal cortices also influence motor activity.
• Primary motor cortex is mainly involves the execution of voluntary movement and fine control of muscles.
  • Lesions will have spastic paresis (UMN signs)
• Lateral premotor cortex is involved in preparation to move and sensorimotor integration.
• Supplementary motor cortex is involved in organizing or planning a sequence of muscle activation.
• Only the primary motor cortex is active when flexing the finger.
• Primary, lateral, and supplementary motor cortices are active when writing a letter.
• Only the supplementary motor cortex is active during the mental rehearsal of finger movements.
• A lesion in the lateral premotor cortex or supplementary motor cortex can lead to apraxia (disorder of motor control)

Corticospinal and Corticobulbar Tracts

• Corticospinal tracts originate in the motor cortex and project to the lower motor neurons in the spinal cord.
• Corticobulbar tracts originate in the motor cortex and project to the brainstem nuclei that innervate face.
• "Bulb" means brainstem.
• Both corticospinal and corticobulbar tracts originate contralateral to the lower motor neurons.
• A lesion in these tracts will cause contralateral signs/symptoms.
• Corticobulbar tracts are the upper motor neurons that innervate the trigeminal motor nucleus (V3), abducens nucleus (VI), facial motor nucleus (VII), nucleus ambiguus (IX, X), spinal accessory nucleus (XII), and hypoglossal nucleus (XI).
• The corticobulbar (UMN) influence on the cranial nerve nuclei involves bilateral innervation to upper face, contralateral innervation to lower face, contralateral innervation to nucleus ambiguus and hypoglossal nucleus, and ipsilateral innervation to spinal accessory nucleus.

Upper Motor Neuron (UMN) vs. Lower Motor Neuron (LMN) Lesion

• Upper motor neuron lesions (UMNLs) are in the corticobulbar tract and cause central facial palsy.
  • Symptoms include paresis of the contralateral lower quadrant of the face.
• Lower motor neuron lesions (LMNLs) are in the facial motor nucleus or its axons and cause Bell palsy.
  • Symptoms include ipsilateral facial paralysis.
• The protruded tongue deviates to the side contralateral to the lesion in UMNLs.
• The protruded tongue deviates to the same side (ipsilateral) as the lesion in LMNLs.

Decorticate vs. Decerebrate Rigidity

• Decorticate rigidity involves bilateral damage above the midbrain.
  • Arms are flexed because the rubrospinal tracts are still functioning.
  • Rubrospinal tract is composed of upper motor neuron axons (cell bodies in the red nucleus) that influence the flexors of the upper extremity.
• Decerebrate rigidity involves bilateral damage that includes the midbrain.
  • Arms are extended because the rubrospinal tracts are damaged.
• Spinal shock occurs immediately after a spinal cord injury.
  • Upper motor neuronal signs do not appear immediately.
  • Patient will experience flaccid paralysis and lack of reflexes that can last days to months.

Key traits of Upper and Lower Motor Neuron Lesions

• Upper motor neuron (UMN) lesions include:
  • Spastic paresis
  • Hypertonia
  • Hyperreflexia
  • Positive Babinski sign
  • Clonus
• Lower motor neuron (LMN) lesions include:
  • Flaccid paralysis
  • Hypotonia, atonia
  • Areflexia, hyporeflexia
  • Atrophy
  • Fasciculations

Overview of Motor System structures

• Corticospinal/lateral corticospinal tracts originate in the upper motor neurons in the motor cortex and innervate the lower motor neurons in the spinal cord.
• The basal nuclei pathway is a loop that begins and ends at the cerebral cortex and does not innervate LMN in the SC.
  • It has a direct pathway that facilitates movement and an indirect pathway that suppresses movement.
• The cerebellum has three functional modules: vestibulocerebellum, spinocerebellum, and pontocerebellum. Cerebellar pathways also do not directly innervate LMNs in the SC.
• Descending tracts from UMNs to LMNs involved in motor control include: rubrospinal tract, vestibulospinal tracts, tectospinal tract, reticulospinal tract, and corticobulbar tract.