Somatosensory & Motor Control

Motor Units: Structures and Properties

• A motor unit (MU) consists of an alpha motor neuron and all the skeletal muscle fibers it innervates.
• It serves as the fundamental functional unit for muscle contraction.
• Force is controlled by:
  • Recruitment, which involves altering the number of active motor units (de/recruitment).
  • Rate coding, which changes the frequency of activation (MU discharge rate).

Motor Neuron Classifications and Muscle Fiber Characteristics

• Motor units are classified by contraction type and metabolic characteristics.
• Type I (S) Slow MU
  • Motor neuron: Slow (S) MN
  • Muscle fibers: Slow oxidative (SO)
  • Characteristics: Fatigue-resistant, low force production, slow contraction speed
• Type IIa (FR) Fatigue Resistant MU
  • Motor neuron: Fatigue-resistant (FR) MN
  • Muscle fibers: Fast oxidative glycolytic (FOG)
  • Characteristics: Intermediate fatigue resistance, moderate force production, faster contraction speed
• Type IIx (FF) Fast Fatigable MU
  • Motor neuron: Fast fatigable (FF) MN
  • Muscle fibers: Fast glycolytic (FG)
  • Characteristics: High force production, fast contraction speed, fatigues quickly
• Force modulation depends on:
  • Size Principle, where smaller, low-threshold motor neurons (Type I) are recruited first, followed by larger, high-threshold motor neurons (Type II).
  • Rate Coding, increasing the discharge rate leads to summation and tetanus.

Action Potential Generation and Neuromuscular Junction

• Action Potential Generation:
  • Summation of excitatory post-synaptic potentials (EPSPs) at the axon hillock leads to an action potential.
  • Myelination and saltatory conduction (AP jumps between Nodes of Ranvier) increase conduction velocity and reduce metabolic cost.
• Neuromuscular Junction (Synapse) and Neurotransmitters:
  • Action potential in the motor neuron leads to a 1:1 muscle fiber action potential.
  • Acetylcholine (ACh) is released from the motor neuron and binds to receptors on the muscle fiber.
  • Safety Factor, is 3-5x more ACh is released than needed to ensure muscle fiber activation.
• Effects of Neurotoxins:
  • Curare (d-Tubocurarine): Blocks ACh receptors, preventing muscle contraction.
  • Botox (Botulinum Toxin): Prevents ACh release, inhibiting muscle contraction.

Influence of Motor Unit Types on Muscle Contraction Properties

• Physiological behavior of motor units depends on both the motor neuron and the muscle fibers it innervates.
• Small, low-threshold motor neurons (Type I) innervate slow oxidative (SO) fibers, which are fatigue-resistant and good for sustained contractions.
• Large, high-threshold motor neurons (Type II) innervate fast-twitch fibers, which are optimized for quick, powerful contractions but fatigue quickly.
• Type I MUs lead to sustained, low-force contractions (e.g., posture, endurance).
• Fast-twitch (Type IIa, IIx) MUs lead to rapid, high-force contractions (e.g., sprinting, jumping).

Orderly Motor Unit Recruitment

• Henneman's Size Principle:
  • Motor units are recruited from smallest to largest.
  • Small motor neurons (low-threshold) innervate slow oxidative (SO) muscle fibers first.
  • Larger, high-threshold motor neurons are recruited only as force demands increase.
• Functional benefits:
  • Simplifies force modulation.
  • Ensures smooth force production.
  • Minimizes fatigue by activating fatigue-resistant fibers first.
• Limitations:
  • Motor unit selection cannot be voluntarily controlled.
• Recruitment Threshold:
  • The force needed to activate a motor unit.
  • Can change within a motor unit but the order of recruitment remains the same.
  • Slow contractions require low-threshold MUs, while fast contractions recruit high-threshold MUs earlier.

Motor Unit Behavior and Force Control

• Two main strategies for force control:
  • Recruitment – Increasing the number of active motor units.
  • Rate Coding – Increasing the firing rate of already active MUs.
• Force-Frequency Relationship:
  • The relationship is sigmoidal between firing rate and force output.
  • Slow vs. fast motor units have different rate-coding properties.
• Asynchronous MU Firing for Steady Force Output:
  • MUs fire at 8 Hz, yet a smooth contraction is maintained.
  • Each MU produces partially fused tetanus; when firing asynchronously, the net force remains steady.

Recording Motor Unit Activity with Electromyography (EMG)

• Electromyography (EMG) records electrical activity in muscles.
• How it works:
  • Electrodes detect action potentials from motor neurons and muscle fibers.
  • EMG signals reflect summed electrical activity from multiple MUs.
• Applications:
  • Used in research, clinical diagnosis, and biomechanics.
  • Measures muscle activation patterns, fatigue, and force output.

Electromyography (EMG) Types

• Electromyography (EMG):A method of recording muscle electrical activity.
• Two Types of EMG exist:
  • Surface EMG (sEMG):
    • Non-invasive, electrodes placed on the skin.
    • Captures global muscle activity.
    • Used for large muscles, movement analysis, and rehabilitation.
  • Indwelling EMG:
    • Invasive, uses fine-wire or needle electrodes inserted into the muscle.
    • Records single motor unit activity.
    • More precise but less comfortable.
    • Used for deep or small muscles and clinical research.

Afferent and Sensory Inputs

• Afferents carry sensory information from the periphery to the central nervous system (CNS).
• The cell body of afferent neurons is located in the dorsal root ganglion.
• Afferent fibers are classified based on their diameter with larger diameters resulting in faster conduction velocity.
• Classification:
  • Group Ia – Muscle spindles detect length & velocity changes.
  • Group II – Muscle spindles detect static length.
  • Group Ib – Golgi tendon organs detect tension.
  • Group III & IV – Free nerve endings to detect chemical and mechanical stimuli.
• Divergence: A single neuron synapses on multiple neurons.
• Convergence: Multiple neurons converge onto fewer neurons.
• Sensory inputs from muscle receptors help in movement coordination, proprioception, and reflex responses.

Anatomy and Physiology of Muscle Spindles

• Muscle spindles are sensory receptors embedded within skeletal muscle fibers.
• Structure:
  • Intrafusal muscle fibers inside the spindle vs. Extrafusal muscle fibers in the regular skeletal muscle.
  • Lie parallel to extrafusal fibers and detect muscle length changes.
• Types of Muscle Spindle Fibers:
  • Bag Fibers:
    • Bag 1 – Dynamic response to stretch.
    • Bag 2 – Static response to stretch.
  • Chain Fibers: Static response to stretch.
• Afferent Nerve Endings:
  • Primary (Ia) Afferents:
    • Innervate all spindle fibers (bag 1, bag 2, and chain).
    • Detect both length and velocity of stretch.
  • Secondary (II) Afferents:
    • Innervate bag 2 and chain fibers only.
    • Detect static length changes.
• Muscle spindle function:
  • When the muscle stretches, Ia and II afferents fire action potentials.
  • Ia afferents detect both velocity and length changes.
  • II afferents detect only length.
• Muscle spindles act as stretch receptors, providing information about muscle length and movement speed.

Fusimotor (Gamma) System

• Fusimotor (Gamma) System:
  • Unique because muscle spindles have their own motor supply (gamma motor neurons).
  • Gamma motor neurons adjust spindle sensitivity by keeping intrafusal fibers taut.
• Types of Gamma Motor Neurons:
  • Dynamic Gamma (γ-d):Increases spindle sensitivity to velocity changes.
  • Static Gamma (γ-s): Increases spindle sensitivity to static length changes.
• Function of the Gamma System:
  • When the muscle contracts, muscle spindles could become slack, making them ineffective.
  • Gamma activation prevents spindle unloading and ensures continued sensory feedback.
• Alpha-Gamma Co-Activation:
  • During voluntary movement, both alpha (extrafusal) and gamma (intrafusal) motor neurons fire together.
  • This maintains spindle sensitivity during contraction.
• The gamma system regulates muscle spindle sensitivity, ensuring continuous feedback during muscle contractions and movement.

Golgi Tendon Organs (GTOs) and Joint Receptors

• Golgi Tendon Organs (GTOs)
  • Location: Found at the junction between muscle and tendon.
  • Structure: Encapsulated bundles of collagen fibers and nerve endings.
  • Orientation: Arranged in series with muscle fibers.
  • Function:
    • Detect muscle tension and force production.
    • More sensitive to actively generated forces than passive stretch.
  • Protective mechanism:
    • When tension is too high, GTOs inhibit the agonist muscle to prevent damage (autogenic inhibition).
• Joint Receptors
  • Found in joint capsules and ligaments.
  • Provide feedback about joint position and movement.
  • Important for proprioception (awareness of limb position).
• GTOs regulate muscle force output, while joint receptors monitor limb position and movement.

Motor Feedback from GTOs and Joint Receptors

• GTOs Provide Motor Feedback:
  • Activated when muscle tension increases.
  • Feedback is sent to the spinal cord via Ib afferents.
  • Disynaptic inhibition: Ib afferents activate inhibitory interneurons, which inhibit the agonist muscle. Autogenic Inhibition Reflex:
  • If muscle force is too high, GTOs reduce force output to prevent injury.
  • Role in Low-Force Tasks: GTOs are also active at low forces, modulating force control for fine motor tasks.
• Joint Receptors in Motor Feedback:
  • Detect joint position and movement.
  • Help with balance and coordination.
  • Contribute to reflexive adjustments in posture.
• GTOs prevent excessive force production through inhibitory feedback, while joint receptors contribute to proprioception and balance.

Afferent Fibers Innervating GTOs and Joint Receptors

• Golgi Tendon Organs (GTOs):
  • Innervated by Group Ib afferents.
  • Fast conduction velocity due to large diameter.
  • Transmit information about muscle tension and force.
• Joint Receptors:
  • Innervated by Group II and III afferents.
  • Provide feedback about joint movement and position.
  • Ib afferents transmit force information from GTOs, while II and III afferents carry joint movement data.

Vestibular End Organs: Anatomy and Function

• The vestibular system detects head movement, orientation, and balance.
• Vestibular End Organs include:
  • Semicircular Canals (SCCs) – Detect Angular Acceleration
    • Three canals: Anterior, Posterior, and Horizontal SCC.
    • Structure: Filled with endolymph fluid.
    • Cupula houses hair cells.
    • Function: Detect angular acceleration when the head rotates.
  • Otolith Organs – Detect Linear Acceleration
    • Two structures: Utricle and Saccule
    • Utricle detects horizontal linear acceleration.
    • Saccule detects vertical linear acceleration.
    • Structure: Hair cells project into a gelatinous membrane.
    • Otoliths are embedded in the membrane.
    • Function: Detect linear acceleration and head tilt. Vestibular system detects rotational movements (angular acceleration) and linear acceleration and head tilt.

Vestibular Mechanoreceptors and Head Movement Coding

• Vestibular mechanoreceptors convert mechanical stimuli into neural signals which allow the brain to interpret head movement.
• Hair Cells as Mechanoreceptors:
  • Hair cells contain Kinocilium and Stereocilia.
  • How They Work:
    • Bending stereocilia toward the kinocilium depolarizes the hair cell leading to increased firing rate (excitation).
    • Bending stereocilia away from the kinocilium hyperpolarizes the hair cell leading to decreased firing rate (inhibition).
• Semicircular Canals (SCCs) – Coding Angular Acceleration:
  • At rest hair cells have a baseline firing rate.
  • During acceleration, movement increases firing rates.
  • During deceleration, movement decreases firing rates.
  • During Constant velocity, firing rates return to baseline.
• Left-Right Balance:
  • If the head rotates left, the left SCC is excited, and the right SCC is inhibited.
• Otolith Organs – Coding Linear Acceleration:
  • Head tilts cause otoliths to slide resulting in bent sterocilia.
  • This causes either depolarization (excitation) or hyperpolarization (inhibition), based on movement direction.
• Hair Cells, fluid movement, sterocilia bending allow for detection of angular and linear acceleration

Vestibular System Adaptations: Alcohol, BPPV, Ménière’s Disease

• Alcohol – “The Spins”
  • Mechanism: Alcohol thins the blood, changing the density of the cupula in the inner ear resulting in a false sense of motion.
  • Symptoms: Sensation of movement when stationary, dizziness, and imbalance.
• Benign Paroxysmal Positional Vertigo (BPPV)
  • Cause: Otoliths become dislodged from the otolith organs and move into a semicircular canal, causing abnormal fluid movement.
  • Pathophysiology: Canal becomes hypersensitive, leading to vertigo when lying down or changing head position.
  • Treatment: Epley Maneuver moves the crystals out of the semicircular canal.
• Ménière’s Disease
  • Cause: Idiopathic (unknown cause).
  • Pathophysiology: Excess fluid accumulation in the labyrinth disrupts hair cell function. Leads to decreased firing in the affected ear and increased firing in the unaffected ear, creating a false sense of head movement (spinning sensation).
  • Symptoms: Vertigo, Tinnitus, Hearing loss, Ear fullness or pressure.

Healthy vs. Pathological Vestibular Systems

• Healthy Vestibular System in Young Adults involves:
  • Semicircular Canals detecting angular acceleration using endolymph movement, with hair cells deflecting to cause depolarization or hyperpolarization.
  • Otolith Organs detect linear acceleration and head tilt via shifting otoliths and bending stereocilia. Condition | Mechanoreceptor Effect | Functional Impact
• -------- | ---------------------- | ---------------- Alcohol | Alters alters cupula density, disrupting balance | False sense of spinning even when still BPPV | Dislodged otoliths increase sensitivity | Triggered vertigo with head movement Ménière’s Disease | Excess endolymph pressure reduces vestibular function on one side | Unilateral vertigo, hearing loss, ear pressure
• Healthy adults accurately encode movement but alcohol, BPPV, and Ménière’s disease disrupt vestibular function and cause false signals result in dizziness and vertigo.

Mechanoreceptors, Thermoreceptors, and Nociceptors

Receptor Type | Function | Key Characteristics

• ------------- | -------- | ------------------ Mechanoreceptors | Detect mechanical changes like touch, pressure, and vibration | Includes cutaneous receptors, others Thermoreceptors | Detect temperature changes | More cold receptors than heat receptors (3:1 ratio) Nociceptors | Detect painful stimuli (from tissue damage) | Two types: A-fibers and C-fibers
• Mechanoreceptors perceive Touch, pressure, vibration.
• Thermoreceptors perceive Temperature changes.
• Nociceptors perceive Pain detection.

Cutaneous Receptor Adaptations

Cutaneous receptors adapt to continuous stimuli: Receptor Type | Adaptation Type | Response to Continuous Stimuli

• ------------- | --------------- | ------------------------------- Tonic Receptors | Slowly adapting | Sustained response to continuous stimuli Phasic Receptors | Rapidly adapting | Fire at the beginning and end of a stimulus but stop responding if it continues
• Tonic receptors provide continuous feedback.
• Phasic receptors respond to changes.

Spatial Extent and Variation in Density of Cutaneous Receptors

• Receptive Field pertains to the area of skin a sensory neuron responds to and it has a "hot spot" as the most sensitive area. Types of Cutaneous Receptive Fields: Receptor Type | Location | Field Size | Sensitivity
• ------------- | -------- | ---------- | ----------- Superficial Receptors (Type 1) | Near epidermis | Smaller receptive fields | High spatial resolution Deep Receptors (Type 2) | Deeper in the dermis | Larger receptive fields | Lower spatial resolution
• High receptor density = better touch discrimination. Low receptor density = poorer spatial resolution.
• Fingers have more densely packed mechanoreceptors whereas the Back and legs have larger receptive fields.

Anatomical Structure of Cutaneous Receptors

Cutaneous mechanoreceptors detect touch, pressure, vibration, and skin stretch differentiated by adaptation speed and location. Receptor | Location | Structure

• ------- | -------- | -------- Merkel Cells (SA1) | Superficial | Small, densely packed cells Meissner Corpuscles (FA1) | Superficial | Stacked flattened disks Ruffini Endings (SA2) | Deep | Branched fibers in a cylindrical capsule Pacinian Corpuscles (FA2) | Deep | Onion-like capsule Cutaneous receptors enable fine details, light touch, stretch, and vibrations based on depth and structure

Function and Role of Cutaneous Mechanoreceptors

• Each mechanoreceptor has a specific function related to touch perception. Receptor | Adaptation Type | Function | Sensitivity

• ------- | --------------- | -------- | ----------- Merkel Cells (SA1) | Slow adapting | Detects edges, curvature, and sustained pressure | Moderately sensitive Meissner Corpuscles (FA1) | Fast adapting | Detects stroking, motion, and low-frequency vibration | Very sensitive Ruffini Endings (SA2) | Slow adapting | Detects skin stretch and joint position | High threshold Pacinian Corpuscles (FA2) | Fast adapting | Detects vibration through objects | Extremely sensitive

• Slow-adapting receptors detect sustained pressure and stretch.

• Fast-adapting receptors detect motion and vibration.

• Merkel cells → Edges and shape (fine details). Meissner corpuscles → Motion and grip control. Ruffini endings → Skin stretch and hand position. Pacinian corpuscles → Vibration and tool use.

Questions cover somatosensory receptors like Pacinian corpuscles and motor control mechanisms. Explore how receptors enable grip, identify shapes, and adapt to stimuli. Understand motor unit recruitment during physical activities and fatigue prevention.