Motor System: Lower Motor Neurons and Spinal Motor Function — Week 6

Motor control hierarchy

• Top Down

• Movement begins with a decision in the anterior part of the frontal lobe.

• Motor planning areas are activated next.

• Control circuits (cerebellum and basal ganglia) regulate activity in upper motor neuron (UMN)- refers to tracts.

• UMNs deliver signals to lower motor neurons (LMNs)- refers to motor neurons.

• LMNs transmit signals directly to skeletal muscles, eliciting contraction of muscle fibers.

• Voluntary movement is controlled from the top down: brain → spinal cord → muscle.

• Higher centers include: sensorimotor cortex, brainstem, thalamus, basal nuclei, cerebellum.

• Afferent neurons convey information from receptors in the periphery to the brainstem and spinal cord.

• Final common pathway is the motor neurons (LMNs) that connect to muscle fibers.

• This hierarchy links to typical reflexes and voluntary action through motor tracts (UMN) and spinal interneurons.

Motor System overview and hierarchy details

• Motor control hierarchy is described as three levels:

  • Highest level: decision making and planning (cortex, basal ganglia, cerebellum interactions).

  • Middle level: brainstem pathways and planning outputs that modulate UMN activity.

  • Local level: spinal circuits and LMNs forming the final common pathway to muscles.

• The organization emphasizes a top-down control of movement via UMNs and LMNs with integration by brainstem and cerebellar/basal ganglia circuits.

Motor Units and Innervation

• A motor unit = one motor neuron + all the muscle fibers it innervates.

• Each individual muscle fiber is innervated by exactly one efferent neuron (LMN).

• A given muscle contains many motor units; a single LMN can innervate hundreds to thousands of fibers.

• Large muscles used for powerful movements (e.g., gastrocnemius) are controlled by hundreds of LMNs.

• Each LMN’s axon branches to multiple fibers; thus, a single unit can produce a sizable force.

Distinctions between motor units (Three types)

• Motor units are classified into three groups based on physiological/biochemical properties of the neuron and its muscle fibers:

  • Small motor neurons innervate few fibers; form small, low-force motor units; slow contraction; fatigue-resistant.

  • Large motor neurons innervate many fibers; form large, high-force motor units; fast force production but fatigue quickly.

  • A third class sits between these two extremes: fast fatigue-resistant (FR) motor units.

• The classification enables the nervous system to tailor force output to the task.

Characteristics of motor unit types

1) Slow (S) motor units

• Innervate small, red muscle fibers.

• Contract slowly and generate small forces.

• Resistant to fatigue; important for sustained activities (e.g., maintaining upright posture).
  2) Fast fatigable (FF) motor units

• Innervate larger, pale muscle fibers.

• Generate large forces quickly but fatigue easily.

• Important for brief, high-force actions (e.g., running, jumping).
  3) Fast fatigue-resistant (FR) motor units

• Properties lie between S and FF.

• Balance between force and fatigue resistance.

Initiation of muscle contraction

• Contraction is produced when actin slides relative to myosin.

• The cross-bridge cycle involves repeated attachment, swiveling (power stroke), and detachment of myosin heads.

• This sliding of actin and myosin shortens the sarcomere, producing contraction.

• Visual resources mentioned (e.g., YouTube animations) illustrate cross-bridge cycling and sarcomere dynamics.

Skeletal muscle structure (sarcomere and filaments)

• A muscle fiber contains many myofibrils.

• A myofibril section between two Z lines is a sarcomere.

• Sarcomere components:

  • Actin: thin filament attached to the Z line.

  • Myosin: thick filament attached to the M line.

  • Titin: elastic filament anchoring the M line to the Z line.

• The sarcomere’s organization determines contractile properties and force generation.

Titin and sarcomere function

• Titin actions (illustrated by Fig. 13-03):

  • A titin molecule prevents the sarcomere from being pulled apart when stretched.

  • At normal sarcomere lengths, titin helps maintain the position of myosin in the center of the sarcomere.

• Titin contributes to passive elasticity and restoring force during stretch.

Contraction mechanism details

• Contraction occurs via actin-myosin interactions where myosin heads bind to actin, swivel to pull actin toward the center, then detach and rebind for another cycle.

• Repeated cross-bridge cycling shortens the sarcomere and generates force.

• The process is energy-dependent and regulated by calcium and ATP availability in muscle fibers.

Total muscle resistance to stretch and muscle tone

• Total resistance to stretch is determined by:

  • Active contraction (cross-bridge cycling).

  • Titin’s passive stiffness.

  • Weak, non-covalent actin-myosin bonds that resist stretch without active cycling.

• Muscle tone is the resistance to stretch in a resting muscle (clinically assessed via passive range of motion).

• Normal resting muscle tone is minimal resistance to passive stretch and is provided by titin and weak actin-myosin bonds.

Actin–myosin bonds and their effect on stretch resistance

• Actin–and–myosin bond states:

  • Strong bonds: myosin heads swivel, pulling actin and shortening the sarcomere (active contraction).

  • Weak bonds: actin and myosin are attached, but lack of rotation means the sarcomere length remains unchanged; however, many weak bonds increase resistance to stretch.

• The balance between strong and weak bonds contributes to the muscle’s overall tone and stiffness.

Adaptation of sarcomeres to muscle length

• Sarcomere number adapts to resting length through immobilization history:

  • Shortened muscles: sarcomeres disappear from ends; adaptation allows generation of force at a shorter length.

  • Lengthened muscles: new sarcomeres are added to accommodate longer length.

• Consequences:

  • Shortened muscles quickly reach elastic limits when stretched.

  • Lengthened muscles can add sarcomeres to maintain function over a wider range.

Contracture: adaptive shortening of the muscle–tendon unit

• Contracture refers to adaptive shortening of muscle-tendon units.

• Causes include paresis, prolonged immobility, spasticity, and muscle imbalances.

• Consequences include loss of sarcomeres and stiffer connective tissues, reducing range of motion.

Lower motor neurons (LMNs)

• LMNs are the final common pathway to skeletal muscle.

• Two types exist:

  • Alpha (α) motor neurons: project to extrafusal muscle fibers; large cell bodies in the ventral horn; large, myelinated axons; normally release enough acetylcholine (ACh) to activate all innervated fibers.

  • Gamma (γ) motor neurons: project to intrafusal fibers of the muscle spindle; mediate spindle sensitivity and tone adjustments.

• Both α and γ motor neurons have cell bodies in the ventral horn of the spinal cord.

Alpha–gamma co-activation

• Co-activation ensures that muscle spindles remain sensitive to stretch when extrafusal fibers contract.

• This maintains proprioceptive feedback during active movement.

Generation of tension and force control

• Muscles adjust tension via two mechanisms:

  • Motor unit recruitment: adjust the number of active motor units.

  • Rate coding: adjust the firing rate of motor neurons.

• The CNS follows the size principle during force gradation:

  • Recruitment proceeds from small (low-threshold) motor units to large (high-threshold) motor units as force demand increases.

• This orderly recruitment optimizes energy use and smooths force output.

Spinal circuits and reflexes

• Phasic stretch reflex (myotatic reflex):

  • A quick tendon stretch activates type Ia afferents from the muscle spindle.

  • Ia afferents cause monosynaptic excitation of the stretched muscle’s α-motor neurons.

  • Result: abrupt contraction of the stretched muscle to resist stretch.

• Reciprocal inhibition:

  • When a muscle is activated, inhibitory interneurons suppress antagonist muscles to facilitate movement.

• Withdrawal reflex:

  • In response to painful cutaneous stimuli, multiple coordinated muscle activations occur to withdraw from the stimulus.

  • Involves multiple synapses across several spinal segments and motor pools.

Disorders of motor neurons

• Causes of motor neuron damage include:

  • Trauma, infection (e.g., poliomyelitis), degenerative or vascular disorders, tumors.

• Consequences of LMN damage (cell bodies or axons destroyed):

  • Loss of reflexes

  • Muscle atrophy

  • Paresis or paralysis

  • Abnormal muscle tone: flaccidity

  • Fibrillations

Involuntary muscle contractions

• Fibrillation:

  • Brief contraction of a single muscle fiber; not visible on the skin.

  • Occurs when a muscle fiber loses contact with its innervating axon.

  • Detected as fibrillation potentials on needle EMG.

• Fasciculation:

  • Quick twitch of muscle fibers within a single motor unit; visible on the skin.

  • Caused by spontaneous depolarization of the motor neuron, activating the entire motor unit.

  • Fasciculation: (brief contractions of small muscle fiber groups; visible under the skin)

  • Fibrilations (brief contrations of single muslce fibers; not visibal on skin- only detectable with EMG testing)

  • Hypertonia- flaccidyty

  • Hypertonia: spadivity and rgiisdity

Polio and its effects on alpha motor neurons (illustrative progression)

• Figure sequence describes:

  • A) Healthy motor units with normal innervation.

  • B) Acute polio: death of some neurons leads to muscle fiber atrophy.

  • C) Recovery: collateral sprouting by surviving neurons reinnervates surviving fibers.

  • D) Postpolio syndrome: overextended surviving neurons cannot sustain the excessive distal branches; newer distal branches atrophy, leaving some fibers denervated.

• Clinical relevance: poliomyelitis can cause acute neuron loss with potential partial reinnervation, but long-term compensatory changes may lead to late post-polio symptoms.

Electrodiagnostic studies (nerve conduction and EMG)

• Techniques involve stimulating a nerve and recording responses from a target muscle to assess nerve and muscle health.

• Typical measurements include:

  • Distal latency (time from stimulation to onset of muscle response).

  • Proximal latency (when applicable, between two stimulation sites).

  • Amplitude of recorded response (reflects number of fibers activated).

  • Conduction velocity (speed of impulse along the nerve).

• Example layout from slides: stimulating electrode at the wrist and elbow with recording electrode over the abductor pollicis brevis; norms provided for the median nerve (latency in ms, amplitude in mV, velocity in m/s). Values vary by nerve and limb segment.

• Interpreting results:

  • Prolonged distal latency or reduced amplitude may indicate demyelination or axonal loss.

  • Abnormal conduction velocity suggests nervopathies.

Connections to foundational principles and real-world relevance

• The motor system illustrates the classic nervous system organization: decision-making centers code plans, planning circuits tune movement, and LMNs execute precise contractions.

• The brain–spinal cord–muscle axis exemplifies the final common pathway concept: regardless of plan, the LMN-to-muscle connection is the end point for motor output.

• The “size principle” provides a unifying rule for how the CNS scales force efficiently and smoothly, relevant to motor learning, rehabilitation, and robotics control analogies.

• Understanding muscle architecture (sarcomeres, titin, actin–myosin interactions) is essential for grasping conditions like contractures, postural control, and adaptations to immobilization.

• Reflex circuits (phasic stretch, reciprocal inhibition, withdrawal) underpin quick, automatic responses to maintain posture, protect tissue, and coordinate rapid movements.

• Pathology discussions (LMN injury, polio, fibrillations, fasciculations) are clinically important for diagnosing motor neuron disorders and interpreting electrodiagnostic tests.

Formulas and key notation

• Motor unit: a single neuron and all the muscle fibers it innervates. Notation: MU = (LMN, {muscle fibers innervated})

• Sarcomere organization (structural relations):

  • Z line —— Actin (thin filament) —— Titin —— Myosin (thick filament) —— M line

• Contraction mechanism (conceptual):

  • Actin slides over myosin via cross-bridge cycling: attaches → power stroke → detaches → re-attach

• Tension generation mechanisms (quantitative ideas):

  • Motor unit recruitment: increase number of active MUs

  • Rate coding: increase firing rate of active MUs

• Size principle (recruitment order):

  • Recruitment proceeds from small-to-large motor units as force demands rise

• Muscle tone contributors: titin elasticity + weak actin–myosin bonds + minimal active contraction at rest

Practical implications for study and exams

• Remember the hierarchy: decision centers → planning/circuit regulation → UMN tracts → LMNs → muscles.

• Distinguish alpha vs gamma LMNs and the purpose of co-activation for spindle sensitivity.

• Differentiate S, FR, FF motor units and their functional roles in posture vs rapid high-force actions.

• Understand how sarcomere length and sarcomere number adaptation impact muscle function when immobilized or stretched.

• Be able to explain reflexes and their neural wiring (monosynaptic stretch reflex, reciprocal inhibition, withdrawal reflex).

• Recognize clinical signs of LMN damage and how electrodiagnostic tests help localize lesions.

• Relate muscle physiology (cross-bridge cycling, titin) to clinical phenomena like muscle tone and contractures.