Unit 11: Spinal & Brain Control of Movement

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Last updated 4:49 PM on 9/16/26
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18 Terms

1
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LO: Describe each of the components of the somatic motor system

The somatic motor system controls voluntary muscle movement and consists of:

  • Skeletal muscles: the effectors that produce movement

  • Alpha motor neurons: located in the ventral horn of the spinal cord; directly synapse on muscle fibers to initiate contraction

    • release ACh

    • A single alpha motor neuron innervates MANY muscle fibers

    • Alpha motor neurons receive input from upper motor neurons in the motor cortex and from sensory neurons in the periphery

    • Excitation of this neuron ALWAYS causes contractions due to the release of ACh at the NMJ

  • Descending motor pathways: tracts from the brain that carry movement commands to spinal motor neurons

  • Interneurons: located in the spinal cord; help integrate sensory feedback and coordinate motor output


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LO: Demonstrate flexion & extension and describe how muscles coordinate these movements

Flexion: movement that decreases the angle between bones

Extension: movement that increases the angle between bones

Antagonist pairs

  • when one muscle contracts, the opposing muscle relaxes (reciprocal inhibition)

  • Coordination occurs through alpha motor neuron activation and spinal interneurons

Muscles

  • they pull, they don’t push

  • muscle contraction occurs due to the release of ACh

Motor neurons controlling flexors lie dorsal to extensors

Motor neurons controlling axial muscles lie medial to those controlling distal muscles


3
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LO: Identify axial, proximal and distal muscles

Axial Muscles

  • located along the trunk and head; maintain posture and balance

Proximal muscles

  • controls movement of shoulders, elbows, pelvis, and knees

Distal muscles

  • controls hands, feet, fingers, and toes

  • responsible for fine motor control and manipulation


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LO: Summarize key features of alpha motor neurons

Alpha Motor Neurons (AKA Lower Motor Neurons - LMN)

  • found in the ventral horn of the spinal cord (upper motor neurons in the primary motor cortex)

  • Only the LMN directly triggers muscle contraction through the release of ACH at the NMJ

  • Three inputs

    • dorsal root ganglion cells with axons that innervate a specialized sensory apparatus embedded within the muscle known as muscle spindle

    • Descending input from the upper motor neurons in the brain (motor cortex& brain stem)

    • interneurons in the spinal cord

  • Segmental Organization

    • neurons innervating the same muscle are grouped together in longitudinal columns across several spinal segments

  • Distribution:

    • medial ventral horn: controls axial muscles

    • intermediate ventral horn: controls proximal muscles

    • lateral ventral horn: controls distal muscles


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LO: Compare the terms motor unit and motor neuron pool

Motor unit

  • LMN & all muscle fibers it innervates (LMNs control the activity of many fibers)

Motor neuron pool

  • all alpha MN that innervates a single muscle


6
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LO: Summarize how the force of muscle contraction is controlled in a finely graded fashion

The CNS finely controls muscle force through three mechanisms

  1. Adjusting firing rate of motor neurons

  • each action potential from an alpha motor neuron release ACh at the NMJ, triggering a twitch

  • sustained contractions require a continuous stream of action potentials

  • higher firing rates cause temporal summation of twitches, increasing muscle tension and producing smoother, stronger contracts

  • thus, the frequency of motor neuron firing directly controls the strength and smoothness of contraction

  1. Recruiting additional synergistic motor units

  • Motor Unit - one alpha motor neuron and all the muscle fibers it innervates

  • by recruiting more motor units, total muscle tension increases

  • Motor unit size

    • large units (leg muscles) have about 1000 fibers per neuron causing coarse movements and a large force

    • small units (finger muscles) have 3 fibers per neurons causing fine, precise control

  • Muscles with many small motor units allow finer control by the CNS

  1. Recruiting motor units from smallest to largest

  • motor units are activated from smallest to largest

    • small alpha MN are easily excited by brain signals due to their geometry and physiology

  • ordered recruitment allows for fine control under light loads and a gradual increase in force as load increases

  • Known as Size Principle (Henneman)


7
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LO: Compare the different types of muscle fibers and motor units

Slow motor units (I)

  • slowly-fatiguing red fibers

  • contain slow-twitch (Type I) muscle fibers

  • fibers are red due to high myoglobin and mitochondria content

  • produce slow, steady, weak contractions, but resist fatigue

  • used for endurance and postural control

Fatigue-resistant fast fibers (IIa)

  • white fibers with moderate strength and fast contractions

  • contain fast-twitch oxidative (Type IIa) fibers

  • generate moderately strong, fast contractions

  • resistant to fatigue

  • used for repetitive movements like walking or swimming

Fast fatigable fibers (IIb)

  • fastest, strongest white fibers, but rapidly fatiguing

  • contain fast-twitch glycolytic (Type IIb) fibers

  • generate the strongest, fastest contractions

  • fatigue quickly during sustained activity

  • used for brief, powerful movements


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LO: Describe the process of excitation-contraction coupling

Excitation

  1. an action potential occurs in an alpha motor neuron axon

  2. ACh is released by the axon terminal of the alpha motor neuron at the NMJ

  3. Nicotine receptor channels in the sarcolemma open, and the postsynaptic sarcolemma depolarizes

  4. Voltage-gated sodium channels in the sarcolemma open and an action potential is generated in the muscle fiber, which sweeps down the sarcolemma and into the T tubules

  5. Depolarization of the T tubules causes Ca2+ release from the SR

Contraction

  1. Ca2+ binds to troponin

  2. Tropomyosin shifts position and myosin binding sites on actin are exposed

  3. Myosin heads bind actin

  4. Myosin heads pivot

  5. An ATP binds to each myosin head and it disengages from actin

  6. The cycle continues as long as Ca2+ and ATP are present

Relaxation

  1. As EPSPs end, the sarcolemma and T tubules return to their resting potentials 

  2. Ca2+ is sequestered by the SR by an ATP-driven pump

  3. Myosin binding sites on actin are covered by tropomyosin


9
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LO: Describe the molecular basis of muscle contraction

Sarcomere Structure

  • basic contractile unit between two Z lines

  • thin filaments (actin) anchored to Z lines; thick filaments (myosin) in between

  • Contraction = thin filaments slide past thick, shortening the sarcomere (sliding filament model)

Key Proteins

  • Actin: has myosin-binding sites

  • Myosin: uses ATP to bind, pivot, and pull actin

  • Tropomyosin: blocks binding sites at rest

  • Troponin: binds Ca2+, moves tropomyosin to expose actin sites

Cross-Bridge Cycle

  • Ca2+ bind troponin —> exposes actin sites

  • Myosin binds actin —> power stroke moves thin filament

  • ATP binds myosin —> detaches from actin

  • ATP hydrolyzed —> myosin re-cocks for next cycle

  • repeats while Ca2+ & ATP are present

Role of Calcium

  • released from sarcoplasmic reticulum upon excitation

  • triggers contraction via troponin - tropomyosin shift

  • pumped back into SR by ATP-driven pump for relaxation

Energy Use

  • ATP required for: cross-bridge cycling, detachment, and Ca2+ reuptake

  • without ATP —> myosin remains bound —> stiffness


10
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LO: Diagram the knee jerk reflex

Knee Jerk Reflex

  • tendon beneath your knee cap briefly stretches the quadriceps of your thigh, which then reflexively contract and cause your leg to extend

Muscle Spindle

  • stretch receptor, specialized muscle fibers

  • group la axons encircle (detection of muscle length-stretch)

la axon

  • detect muscle length

  • sensory receptor for proprioception

    • proprioception - sense of how our body is positioned and moving in space

    • thickest and most muelinated = fast conduction

    • synapse on alpha motor neurons & interneurons in spinal cord

Monosynaptic

  • only 1 synapse between sensory neuron and alpha motor neuron


11
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LO: Discuss the role of interneurons, reciprocal inhibition, and reflexes when you step on a tack

When You Step on a Tack

  1. Interneurons in the spinal cord connect sensory and motor neurons, coordinating reflexes through excitatory or inhibitory signals.

  2. Reciprocal inhibition: contraction of one muscle group is paired with relaxation of its antagonist via inhibitory interneurons.

  3. Flexor withdrawal reflex: painful stimulus activates nociceptors → excitatory interneurons → flexor muscles contract to withdraw the limb.

  4. Crossed-extensor reflex: opposite leg’s extensor muscles activate while flexors are inhibited to maintain balance.

  5. Together, these spinal reflexes allow rapid withdrawal from pain while stabilizing posture without cortical input.


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LO: Describe the components of the motor control hierarchy in terms of anatomy and function

Anatomy and Function

  1. Overview

    • Upper motor neurons in the cortex control lower motor neurons in the spinal cord to produce voluntary movement.

  2. Hierarchy of Control

    • Strategy (highest): Neocortex & basal ganglia — decide movement goals.

    • Tactics (middle): Motor cortex & cerebellum — plan and coordinate muscle activity.

    • Execution (lowest): Brainstem & spinal cord — activate motor neurons and adjust posture.

  3. Sensorimotor Integration

    • Sensory feedback guides and refines movement at all levels.

  4. Descending Pathways

    • Lateral: Controls voluntary distal movement.

    • Ventromedial: Controls posture and balance.

  5. Example

    • Stepping on a tack quietly shows cortical (upper motor neuron) control overriding reflexive spinal (lower motor neuron) actions.


13
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LO: Compare and contrast the lateral pathways and ventromedial pathways

  • Lateral Pathways

    • Includes: Corticospinal and Rubrospinal tracts

    • Function: Control voluntary, precise, and fractionated movements of distal muscles (hands, fingers).

    • Anatomy: Fibers decussate in the medulla (pyramidal decussation) → control the contralateral side of the body.

    • Damage: Loss of fine motor control; slower, less accurate voluntary movements.

  • Ventromedial Pathways

    • Includes: Vestibulospinal, Tectospinal, Pontine Reticulospinal, Medullary Reticulospinal tracts

    • Function: Maintain posture, balance, and head/eye coordination; control of axial and proximal muscles.

    • Anatomy: Mostly bilateral projections; work together to stabilize the body and head.

    • Damage: Impaired balance, posture, and coordination of head and trunk movements.


14
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LO: Predict the site or consequence of a lesion based on knowledge of the pathways and their function

  • Corticospinal (lateral) – Lesion → loss of fine, fractionated movements (fingers/hands); slower, less precise voluntary movement; contralateral deficit.

  • Rubrospinal (lateral) – Lesion → minor loss of coordination/fine motor control.

  • Vestibulospinal (ventromedial) – Lesion → poor balance, head stabilization problems.

  • Tectospinal (ventromedial) – Lesion → impaired head and eye orientation to stimuli.

  • Pontine reticulospinal (ventromedial) – Lesion → weakened antigravity reflexes; trouble maintaining posture.

  • Medullary reticulospinal (ventromedial) – Lesion → excessive rigidity; loss of reflexive posture relaxation.


15
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LO: Describe the organization and function of the motor cortex

  • Primary Motor Cortex (M1 / Area 4)

    • Precentral gyrus; contralateral body control; somatotopic map.

    • Betz cells = upper motor neurons to spinal cord.

    • Inputs: cortical areas & thalamus.

    • Encodes force and direction via population coding (many neurons collectively determine movement).

  • Secondary Motor Areas (Area 6: PMA & SMA)

    • Convert action plans into movement signals (how to act).

    • Receive input from prefrontal & posterior parietal cortex.

    • Maintain movement strategies until execution.

  • Higher-Level Cortical Inputs

    • Prefrontal Cortex: decides actions & outcomes.

    • Posterior Parietal Cortex: sensory info about body position for planning.

  • Execution Hierarchy

    • Plan: parietal & frontal lobes

    • Strategy: SMA/PMA (Area 6)

    • Tactics: M1 → brainstem & spinal cord → voluntary movement


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LO: Describe the organization and function of the posterior parietal cortex

  • Integrates sensory information (visual, somatosensory, vestibular) for spatial awareness and movement planning.

  • Works with premotor areas to transform sensory input into coordinated motor output.


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LO: Explain how movements are planned by the brain

  1. Goal-Directed Movement:

    • Requires knowledge of body position, plan selection, memory of plan, and execution.

  2. Cortical Areas:

    • Prefrontal Cortex: Decide what to do.

    • Posterior Parietal Cortex: Track where the body is.

    • Area 6 (SMA/PMA): Convert plan into how actions are performed; hold strategies.

    • Primary Motor Cortex (M1): Execute tactics; send signals to brainstem/spinal cord.

  3. Basal Ganglia Loop:

    • Cortex → basal ganglia → VLo (thalamus) → SMA → cortex.

    • Function: selection & initiation of voluntary movement.

    • Parkinson’s disease = impaired initiation due to dopaminergic loss.

  4. Hierarchy Summary:

    • Decisions (prefrontal/parietal) → Strategy (SMA/PMA) → Tactics/Execution (M1 & descending pathways).

    • Loops and sensory feedback ensure coordinated, goal-directed movement.


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LO: Discuss the cause of Parkinson’s disease and why it is called a basal ganglia disorder

  • Definition: Difficulty initiating voluntary movements due to basal ganglia dysfunction.

  • Symptoms: Hypokinesia, bradykinesia, akinesia, rigidity, resting tremor.

  • Cause: Degeneration of dopaminergic neurons in substantia nigra → less dopamine to striatum → increased thalamic inhibition → reduced SMA activation.

  • Treatment: L-DOPA (restores dopamine), Deep Brain Stimulation (modulates basal ganglia).

  • Epidemiology: ~1% of people >60; prevalence increases with age; slightly higher in males and certain regions.

Key Point: PD is a basal ganglia disorder because the basal ganglia normally select and initiate voluntary movement, and dopamine loss disrupts this.