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Neural Control of Human Movement > Topic 5: Spinal Control of Human Movement > Flashcards

Topic 5: Spinal Control of Human Movement Flashcards

1
Q

Lower motor neurons

A

Axons in ventral horn of spinal cord
CAN RECEIVE INPUT FROM:
- upper motor neurons
- interneurons in spinal cord
- sensory input
Direct connection to muscle
Exit ventrally and join sensory fibers in spinal nerve
- 31 pairs classified in 4 segments (C-T-L-S-c)

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1
Q

Upper motor neurons

A
  • Cerebral cortex and brainstem
  • can only connect to the muscle through lower motor neurons
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2
Q

Distribution of Motor Neurons down the Spinal Cord

A

NOT EVEN DISTRIBUTION
- Cervical enlargement (C3 - T1)
- Lumbar enlargement (L1 - S3)
These areas contain most of the motor neurons for distal and proximal muscles

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3
Q

Distribution of motor neurons within the spinal cord

A

Organized at each level by area and function of the muscle they innervate
- Neurons corresponding to more proximal regions are more medial in spinal cord
- Flexors are more posterior compared to extensors

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4
Q

Alpha Motor Neuorn

A

Directly trigger the contraction of muscles for movement

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5
Q

Gamma Motor Neurons

A

Regulate muscle tone and control sensitivity of muscle spindles

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6
Q

Motor Unit

A

Alpha Motor neuron and all the muscle fibers it innervates

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7
Q

Motor neuron pool

A

All the alpha motor neurons that innervate a single muscle

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7
Q

Excitation-Contraction Coupling

A
  • Alpha motor neurons release ACh
  • ACh produces larger EPSP in muscle fiber
  • EPSP evokes muscle action potential
  • Action potential triggers Ca2+ release from SR
  • Fiber contracts (sliding filament model)
  • Ca2+ reuptake
  • Fiber relaxes
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8
Q

Sliding Filament Model of Contraction

A

Ca2+ binding to troponin allows myosin heads to bind to actin - myosin heads then pivot, causing filaments to slide

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9
Q

Force-Length Relationship

A
  • Describes the relationship of isometric contraction
  • Goldilocks zone for maximum number of CB formed
  • Too short = compact and no more shortening to occur to create force
  • Too long = Not enough CB overlap and can form to create force
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10
Q

Force- Velocity Relationship

A
  • Force output changes based on the speed it shortens (or lengthens)
  • The slower the movement the greater force produced
  • max power occurs where the product of velocity and force is the greatest
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11
Q

Titin

A
  • “spring” on end of myosin filaments
  • provides elastic component in muscle fibers
  • Main source of passive force in a single fiber
  • Minimal source of passive force in complete muscle
  • provides residual force enhancement
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12
Q

Residual Force enhancement

A

When an active muscle is stretched, its isometric, steady-state force following the stretch is greater than the corresponding purely isometric contraction
- Muscle activation can lead to a change in the stiffness and length of this spring

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13
Q

EMG

A
  • The quantification of a muscle(s) electrical activity (sum of AP)
  • Bipolar electrode configuration to record the difference in electrical activity
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14
Q

Applications of EMG

A
  • Linear relationship to muscle force in isometric contractions
  • provides amplitude of muscle activation (level of recruitment)
  • Provides timing of activation (activation patterns)
  • Fatigue and advance analysis
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15
Q

Limitations of EMG

A
  • Not a direct relationship to muscle force (especially during motion)
  • Sensitive to differences in placement/processing
  • Surface EMG: cross-talk between muscles, recording through skin/adipose
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16
Q

Ia axons

A
  • Largest and fastest
  • Excitatory synapses with spinal interneurons and directly on alpha motor neurons
  • Muscle spindles (amount of stretch)
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17
Q

Ib axons

A
  • Slightly smaller/slower
  • Inhibitory synapses with spinal interneurons
  • golgi tendon organ (amount of force)
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18
Q

Muscle spindles

A
  • Sensory receptor
  • Sits within a muscle to measure the change in length
  • small intrafusal muscle fibers
  • parallel to primary muscle fibers (extrafusal)
  • Wrapped with a sensory neuron (Ia)
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19
Q

The stretch reflex (Myotatic reflex)

A
  • When a muscle is pulled (stretched), it pulls back (contracts) - resists changes in muscle length to maintain limb position or posture
  • Monosynaptic stretch reflex - Primary sensory neuron (Ia muscle spindle) to primary motor neuron (alpha motor neuron)
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20
Q

Steps of the stretch reflex

A
  1. muscle is stretched (extrafusal and intrafusal)
  2. Ia depolarizes from stretch
  3. Action potential propagates along axon through dorsal root
  4. Synapses with alpha motor neuron
  5. Alpha motor neuron sends action potential to contract muscle
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21
Q

How do muscle spindles stay responsive to stretch

A
  • Intrafusal fibers need the ability to contract just like extrafusal fibers
  • gamma motor neurons receive input from brain to keep intrafusal fiber taut
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22
Q

Gamma Loop

A

The loop between the muscle spindle (sensory fiber + gamma motor neuron) and muscle (alpha motor neuron)
1. Descending command from brain sets first estimate
- coactivation of both alpha and gamma motor neurons (tuning for the initial guess)
2. Muscle spindle detects muscle is too long
3. Ia axons send signal to alpha motor neuron
4. Alpha motor neuron activate extrafusal fibers to shorten muscle

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23
Q

Gamma Bias

A
  • Base level firing for the intrafusal fibers to keep sensor “online”
  • Constant activity to keep intrafusal fiber taut
  • Firing rate simply increases or decreases to compensate for changes in extrafusal fiber length
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24
Q

Fusimotor gain

A
  • Ramping up/fine tuning the sensitivity of this loop to identify small changes
  • Ability of the nervous system to adjust/ fine tune the sensitivity to small changes
  • Can be improved through balance training and plyometric training
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25
Q

Static stretch response

A
  • Intrafusal fibers: nuclear chain and static nuclear bag
  • Static gamma motor neurons
  • type II sensory fibers
  • Primarily related to changes that are constant/predictable
  • Inhibitory response
26
Q

Dynamic stretch response

A
  • Intrafusal fibers: dynamic nuclear bag
  • Dynamic gamma motor neurons
  • Type Ia sensory fibers
  • Primary related to changes that are quick/unpredictable
  • Excitatory response
27
Q

Static stretching vs dynamic stretching

A

STATIC
- Likely to reduce muscle preformance (if immediately prior to exercise
- improves flexibility (may be required for specific tasks) - activating type II sensory fibers
DYNAMIC
- May increase muscle performance and sport specific performance
- activating type Ia sensory fibres
- ramping up fusimotor gait - improving response to quick/unpredictable muscle length changes

28
Q

Golgi Tendon ORgans

A
  • Sensory neuron (Ib) intertwined within the collagen fibers of tendons
  • Allows for the measure of force of contraction (strain of muscle)
  • Regulate muscle tension within optimal range
  • Arranged in serious rather than parallel (forces must go directly through them)
  • Synapses with inhibitory interneurons
  • Primary helps regulate muscle force
  • allows for a protection of overload as last resort
29
Q

Joint receptors

A
  • Many proprioceptive axons in joint tissues (ligament and joint capsule)
  • Similar to mechanoreceptors found in skin, but respond to the position and movement in a joint ( fast adapting, dynamic movement)
  • Important for stability and control of joints, but can be damaged with injury
  • Neuromuscular training/rehabilitation can improve this but complex interplay of many factors
30
Q

The stretch-shortening cycle

A

Involves an ECC stretching of the muscle, immediately followed by an enhanced CON contraction

31
Q

Mechanisms of the SCC

A
  1. Elastic Energy
  2. Stretch Reflex
  3. Neural Potentiation
  4. Active State
  5. Mechanical Potential
32
Q

Elastic Energy as a mechanism for the SSC

A

Generated from all elastic components, but tendons dominate the storage and release of elastic energy
- >0.5s may negate all effects of elastic energy

33
Q

Stretch Reflex as a mechanism of the SSC

A
  • Fast lengthening of muscle (ECC contraction)
  • Dynamic nuclear bag convey sensory information on the stretch of the muscle through type Ia sensory neurons
  • Firing rate is dependent on the speed/amount of stretch
  • Improved fusimotor gain can help maximize sensitivity of the reflex
34
Q

Neural Potentiation as a mechanism of the SSC

A
  • Electromechanical delay
  • Picking up the “slack” in the unit
  • 30 - 100 ms
35
Q

Active state as a mechanism of the SSC

A
  • Time for cross bridges to build up force
  • 100 ms - 1s
36
Q

Mechanical Potentiation as a mechanism of the SSC

A
  • Residual force enhancement
37
Q

Fast SSC

A

FAST ECC WITH EXPLOSIVE CON
- Stiff joint, high activation in ECC, very little loss of force during amortization
- Contact time <250 ms
- Primary mechanism: elastic energy and stretch reflex, as well as mechanical potentiation

38
Q

Slow SCC

A

SLOW ECC WITH LESS EXPLOSIVE CON
- Less stiff joint, longer contact times, greater neuromuscular activity in the CON phase
- Contact time >250ms
- Primary mechanisms: Active state, neural potentiation and mechanics of contractile component
- Allows for more work to be done by contractile unit over greater distance

39
Q

Reciprocal Inhibition

A

Reflex arc using spinal interneurons to support simple monosynaptic reflexes
- Contraction of one muscle accompanied by relaxation of its antagonist

40
Q

Withdrawal Reflex

A

Reflex arc used to withdraw limb from aversive stimulus
- Excitatory input for multiple ipsilateral motor units
- cause flexion

41
Q

Crossed-Extensor Reflex

A

Reflex arc for extensors and flexors on opposite side
- Excitatory and inhibitory for ipsilateral and contralateral motor units

42
Q

Central Pattern Generators

A
  • Circuitry for many rhythmic movements resides in spinal cord
  • complex network of sensory, motor, and interneurons
  • evidence from animal spinal transections (measured bursts of rhythmic and coordinated activity arising for input that was constant
43
Q

How do central pattern generators work

A

Controlled by two “half-centers” of spinal neurons
- Mutually inhibiting halves that produce alternating bursts of flexor and extensors activity
- Rhythmic activity will continue as long as input exists
- Circuitry for walking resides in the lumbar/sacral spinal cord

44
Q

Rhythm Generators

A

Setting the timing of patterns to be generated

45
Q

Pattern Generators

A

Sending required pattern of muscles activations

46
Q

Effect of input from brain on central pattern generators

A

Descending control initiates and adapts CPGs
- can influence both rhythm and pattern generation neural pools

47
Q

Gait Retraining

A

Changing the mechanics of how you walk or run
- easy to override motor patterns of CPGs
- Very difficult to “rewrite” them

48
Q

Stepping in cats

A

PROCEPTION
- amount of stretching can regulate the stance phase
- cats can match speed of treadmill, through CPG alone
SENSORY INFORMATION FORM THE SKIN
- Stimulus to dorsal side of paw causes pattern with increased flexion to avoid a tripping hazard

49
Q

Fictive Movement

A

Electrical activity suggestive of movement
- primary source of evidence for CPGs
- Resemble locomotion

50
Q

Directly activating a CPG in humans

A
  • Electrical stimulus of spinal cord in SCI
  • Consistent stimulation leads to intermittent activation of muscles
    NOT DIFINITIVE ANSWER
  • Could just be providing fake stimulus
  • fictive movement
51
Q

Evidence for CPG

A

Evidence for
- Animal models
- Stepping reflexes in infants as foundation for adult locomotion
- spontaneous or evoked activation patterns SCI patients
- Effective circuitry for controlling robotic locomotion
EVIDENCE AGAISNT
- No direct locomotion example in humans
- Most is fictive
- Could simply be reflex-based

52
Q

Injury at C1-C5

A

Often fatal - inability or difficulty breathing

53
Q

Injury at C6-C8

A

Retain head/neck movement, ability to breathe and speak, along with some arm movement

54
Q

Injury at T1-T6

A

Loss of upper chest/back muscles, arms fully functional

55
Q

Injury at T7-T12

A

Retain greater control/balance of core while sitting

56
Q

Injury at L1-L5

A

Loss of lower limb function and some bowel/bladder dysfunction

57
Q

Injury to S1-S5

A

Most function in legs (ability to walk), loss of bowels/bladder function and some sexual function

58
Q

Spinal Shock

A
  • Temporary loss or depression of all or most spinal reflex activity below the level of the lesion
  • Does not necessarily relate to the severity of the underlying SCI
    4 DISTINCT PHASES
  • loss of reflexes
  • gradual return
  • hypersensitivity
  • Spasticity
    Can last 1-12 months
59
Q

Spinal Shock and Neuroplasticity

A

Extensive neural reorganization and plasticity has been demonstrated in SCI and associated with functional recovery
- Occurs only in axons near cell body
- Long-distance axonal regeneration is still not possible
Paradigm shift to maximize this local effect through intensive training

60
Q

SCI and CPG

A
  • 0G training can be effective in increasing functionality but not completely retraining
  • Functionality measured 0 to 5 - improvement from 1 to 3 not 1 to 5
  • Sensory feedback pathways can shape locomotion for animals, but insufficient in humans
61
Q

Grading Spinal Cord Injuries

A
  • American Spinal Cord Injury Association - Impairment Scale (AIS)
  • Describes a person’s functional impairment following an SCI
  • Measures sensation at multiple points and key motions on both sides of the body
    GRADES AS A-E
  • A = complete
  • B = sensory incomplete
  • C = Motor incomplete (some sparing of motor function)
  • D = Motor incomplete ( 50% muscle function)
  • E = Normal
62
Q

Brown-Sequard Syndrome

A
  • Damage to one half of the spinal cord
  • Trauma (penetrating injury) or compression
  • Ipsilateral motor loss (corticospinal)
  • Ipsilateral touch, proprioception loss (DCML)
  • Contralateral pain and temperature loss (spinothalamic)
63
Q

Anterior Cord Syndrome

A
  • Damage to the anterior (and lateral) SC
  • Severe flexion injury or lack of blood supply
    Results in:
  • Bilateral motor loss (corticospinal)
  • Retention of bilateral touch/proprioception (DCML)
  • Bilateral pain and temperature loss (Spinothalamic)
64
Q

Posterior Cord Syndrome

A
  • Damage to the posterior SC
  • Trauma or lack of blood supply
    Results in:
  • Retention of bilateral motor function
  • Bilateral touch/proprioception loss (DCML
  • Retention of bilateral pain and temperature (spinothalamic)
65
Q

Central Cord Syndrome

A
  • Damage to the central SC
  • Degenerative spinal canal narrowing, hyperextension
    Results in:
  • Greater loss in upper limb function
  • Variable loss of bilateral touch/proprioception loss
  • Greater loss in upper limb pain and temperature

Neural Control of Human Movement (6 decks)

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