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KIN 313 - Neurointegration of Human Movement > Midterm 2 Study > Flashcards

Midterm 2 Study Flashcards

1
Q

Where is Glabrous Skin Located?

A
  • Non Hairy Skin
  • I.e. Lips, palms of hands, etc.
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2
Q

How many Types of Receptors are in Glabrous Skin?

A
  • 4
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3
Q

How are Receptors Classified?

A
  • Receptive Field Size
  • Responses to sustained stimulation/indentation of skin (adaption rates)
  • Spike train regularity
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4
Q

What is the 5th Receptor?

A
  • Hair Receptor
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5
Q

What is the structure of a Hair Receptor?

A
  • Loses Myelin
  • Wraps around the hair follicle as free nerve ending
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6
Q

What does a hair receptor do?

A
  • Responds to bending of hair
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7
Q

What are the four Receptors found in Glabrous Skin?

A
  • Merkel Disk/Cell
  • Meissner’s Corpuscle
  • Ruffini Ending
  • Pacinian Corpuscle
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8
Q

Where are Merkel Disk/Cells located?

A
  • Very Close to the skin surface
  • In epidermis on the peak/dome of connective tissue
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9
Q

What causes Merkel Cells to be deformed?

A
  • Indentation of skin
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10
Q

What happens when a Merkel Cell experiences indentation of the skin?

A
  • The cell is pinched and if enough leakiness it generates AP
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11
Q

How is a Merkel Cell classified?

A

Slowly Adapting Type 1 Receptor

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12
Q

What happens to a Merkel Cell if an indentation is held?

A
  • It continues to fire AP
  • It has an irregular discharge, sputters a bit
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13
Q

What does a Merkel Cell code for?

A
  • Velocity and Magnitude of Indentation
  • Velocity during indentation
  • Discharge rate that’s proportional to the magnitude of indentation
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14
Q

What is the threshold for a Merkel Cell? What is it highly sensitive to?

A

Threshold
- Moderately Low (30um)
Sensitive
- To Edges and Curvature

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15
Q

Where are Meissner’s Corpuscle Receptors located?

A
  • Right under ridges (in the valleys) in the epidermis
  • Very Close to skin Surface
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16
Q

What type of receptor is a Meissner’s Corpuscle?

A
  • Fast Adapting Type 1
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17
Q

What is the Structure of a Meissner’s Corpuscle?

A
  • Connective Tissue Ending
  • Located in valleys of the epidermis
  • Close to skin surface
  • Grouping of Connective Tissue that Spirals around
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18
Q

What causes a Meissner’s Corpuscle Receptor to Fire?

A
  • Pushing/Distorting the connective tissue
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19
Q

What do the Meissner’s Corpuscle Receptors Code for?

A
  • Velocity of skin indentation
  • Motion across Skin
  • Love Texture
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20
Q

Give an example of when a Meissner’s Corpuscle Receptor would give high bursts of AP

A
  • Running nails over receptive field
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21
Q

What is the Threshold of a Meissner’s Corpuscle Cell?

A
  • Low Threshold (6um)
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22
Q

What Receptor Cell makes of the highest percentage in the hand? What are they sensitive to?

A

Location
- 40% of receptors in the hand are Meissner’s Corpuscle
Sensitive
- to Low Frequency Vibrations (40-50Hz, i.e. phone)

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23
Q

Where are the Ruffini Endings located?

A
  • in the deep dermis layer
  • Buried in Collagen of connective tissue
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24
Q

Describe the Structure of a Ruffini Ending Receptor

A
  • Deep in Dermis
  • Buried in Collagen
  • Axon shrapnels and weaves amongst collagen
  • Lies parallel to surface
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25
Q

What causes distortion of the Ruffini Endings?

A
  • Stretching and Pulling on capsule
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26
Q

What type of discharge does a Ruffini Ending have?

A
  • Regular discharge when stimulated
  • 1/3 have background discharge
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27
Q

What type of Receptor is a Ruffini Ending?

A
  • Slowly Adapting Type II
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28
Q

What is the Threshold of a Ruffini Ending?

A
  • High Threshold to indentation (300um)
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29
Q

What causes Ruffini Endings to Fire?

A
  • Hard and Deep indentation
  • Sensitive to lateral skin stretch
  • Skin stretch must line up with receptors
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30
Q

What is an example of when a Ruffini Ending would be firing?

A
  • Walking (sheer skin pattern through feet)
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31
Q

What do Ruffini Endings Code For?

A
  • a bit for velocity
  • Fire like a clock during indentation
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32
Q

Do non-human primates contain Ruffini Ending Receptors?

A
  • NO
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33
Q

What type of receptor is a Pacinian Corpuscle?

A
  • Rapidly Adapting Type II
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34
Q

Where are Pacinian Corpuscle Receptors located?

A
  • Very Deep in Collagen of Dermis
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35
Q

Describe the Structure of a Pacinian Corpuscle

A
  • Very Deep in Collagen of Dermis
  • Connected to a single axon
  • Myelinated nerve ending that comes in, and loses its myelin right where it enters multilayered connective tissue (like an onion)
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36
Q

What is the Threshold of a Pacinian corpuscle Receptor?

A
  • Very low threshold (0.08um)
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37
Q

What is the most common Receptor in the body

A
  • Pacinian Corpuscle
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38
Q

What do the Pacinian Corpuscle Receptor Cells Code for?

A
  • Acceleration: change in indentation rates
  • High-Frequency Vibrations (300-400Hz)
  • Microacceleraions with ground
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39
Q

What is an example of when a Pacinian corpuscle receptor would be helpful?

A
  • Walking in heels versus sneakers will have different frequency characteristics
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40
Q

How does Pacinian Corpuscle Receptors Vibration Sensitivity work?

A
  • Concentrically arranged fluid-filled lamellae around sensory nerve terminal
  • Fluid between layers of connective tissue filters out low frequencies
  • High Frequencies reach the axon
  • Transducers of acceleration
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41
Q

What are Pacinian Corpuscle Receptors built for?

A
  • being an accelerometer in joints, skin, and mesentery of gut
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42
Q

What are Pacinian corpuscles very sensitive to?

A
  • alternating inputs, such as mechanical vibrations
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43
Q

What does each cycle of vibrations do to a Pacinian Corpuscle do?

A
  • Generates an AP
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44
Q

What do the 4 Receptors have in common?

A
  • All tied to a single axon
  • all are smaller than 1a and 1b, closer to spindle secondary size
  • All Roughly the same in nature
  • all classic mechanoreceptors that rely on deformation
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45
Q

What is Mechanotransduction?

A
  • The process whereby mechanical energy gets converted to voltage change in sensory afferent neurons
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46
Q

What is common about how the 4 receptors work?

A
  • all classic mechanoreceptors, rely on deformation
  • ending has many channels, deformation causes membrane shift
  • membrane shift causes AP generation
  • All work with voltage changes
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47
Q

What is the one type of receptor cell that gets deformed?

A
  • Slowly adapting type I (Merkel Cell)
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48
Q

What is a Cutaneous Receptive Field?

A
  • The region of skin that is capable of driving a response in a particular neuron
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49
Q

What is unique about type II receptor’s cutaneous receptive fields?

A
  • Large, obscure borders
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50
Q

Do the different Cutaneous Receptive Fields Overlap?

A
  • Yes
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51
Q

Describe a Cutaneous Receptive Field

A
  • Area of stimulation for a particular neuron (receptor cell)
  • Central sensitivity, like a bullseye target
  • Relative densities vary across different skin regions
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52
Q

What Receptors have higher Cutaneous Receptive Field Densities in the tips of fingers?

A
  • Slow-Adapting Type I (Merkel)
  • Fast-Adapting Type I (Meissner’s Corpuscle)
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53
Q

Which Receptors have more equally Distributed Cutaneous Receptive Field Densities?

A
  • Slow-Adapting type II (Ruffini Endings)
  • Fast-Adapting Type II (Pacinian corpuscle)
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54
Q

What do the cutaneous receptive fields of Type I FA & Type I SA receptors have in common?

A
  • small receptive fields, with sharp borders
  • almost half in the hands are on the finger tips
  • Edge Sensitive
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55
Q

What is the difference between the cutaneous receptive fields of Type 1 FA & Type 1 SA receptors?

A
  • Type 1 FA has a more equally distributed gradient
  • Type 1 SA has gradient towards hand
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56
Q

Describe the Cutaneous Receptive Field for Type II FA (Pacinian Corpuscles)

A
  • Huge receptive Field
  • Very Low threshold
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57
Q

Describe the cutaneous receptive field for Type II SA (Ruffini Endings)

A
  • Large receptive field
  • tied to skin stretch
  • sensitive to lateral skin strain
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58
Q

How are fingertips able to pick up small objects like pins?

A
  • High Density of Type I receptors (especially Meissner’s
  • Incredible resolution of tactile information
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59
Q

How do the size and shape of objects get coded for when holding them?

A
  • SA1s (Merkel)
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60
Q

What happens to FA receptors during sustained contact?

A
  • They go quiet
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61
Q

How do Merkel (SA1s) code for the curvature of an object?

A
  • Using the Receptors as a population
  • Varying the size and shape of an object over the receptive field changes the coding
  • smaller probe are has higher discharge rate with fewer receptors
  • Larger probe has lower discharge rate but more receptors are active
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62
Q

Why do we not need a large number of FA2 and SA2 receptors?

A
  • Very Large Receptive Fields
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63
Q

What is the functional role of the Merkel Cells (SA1)?

A
  • Senses edges, curvature and texture
  • Contact information as you tap i.e. phone
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64
Q

What is the functional role of Meissner’s corpuscle?

A
  • Motion Detection and grip control
  • Knowing how slippery something is on contact
  • i.e. holding glass of beer
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65
Q

What is the functional role of Ruffini Endings?

A
  • Skin stretch, skin strain pattern
  • can help gauge how far apart your fingers are
  • Proprioception of the hand
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66
Q

What is the functional role of the Pacinian corpuscle receptors?

A
  • feeling through objects, perception of finer texture
  • information about contact i.e. walking cane
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67
Q

How do you test the control of grip force?

A
  • Record glabrous skin receptors during pinch grasp using microneurography
  • task: grab and hold the object
  • Vary: weight, interface, or if the object in air or on ground
  • Monitor: acceleration, grasp force, sheer on object
  • Results: see what happens when ‘load’ is increased by monitoring the activity of skin receptors as load pulls them down
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68
Q

How do we code for accidental slips (of object)?

A

When the object moves relative to you
- detected by accelerometer
- Both FA2 and SA1 receptors respond to microslips between object and skin

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69
Q

How do FA2 (Pacinian) respond to microslips between an object and the skin?

A
  • Upon contact FA2 discharges
    Slip do to inefficient grip strength
  • FA2 senses the acceleration of object
  • FA2 Fires
  • Response is increase in grip force relative to load
  • response is unconscious
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70
Q

How does SA1 (Merkel) code for microslips between an object and skin?

A
  • Brief acceleration during microslip
  • Instant SA1 burst
  • Continue to fire while increasing grip to force ratio
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71
Q

How many unconscious automatic channels correct microslips?

A
  • 2 FA2 and SA1
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72
Q

How do FA1s respond to different surfaces?

A

Slipperiness
- Not-slippery: few spikes
- Slippery: high activity
Velocity of Grab
- Code as a population for slow
Surface type
- change in interface between skin and object (sandpaper vs suede vs silk)

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73
Q

How do FA1 (Meissner’s) react to slippery surfaces?

A
  • Higher activity and discharge
  • ridges in fingertips move up and down on contact, slippery objects have more movement
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74
Q

What do FA1’s tell you about an object when grabbing it?

A
  • When you make contact
  • How fast you make contact
  • How slippery the thing is you are grabbing
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75
Q

When can FA1’s be critical?

A
  • During walking to help adjust for slippery surfaces
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76
Q

What is a limb matching task?

A
  • Closed eyes and matching position and speed of on limb to other limbs
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77
Q

What are the sources of Proprioception and Kinesthesis?

A
  • Muscle Spindle
  • Skin
  • Joints
  • GTO
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78
Q

How does a muscle spindle contribute to proprioception and kinesthesis?

A
  • Velocity and length of the muscle
  • reflexively onto motor neurons and up to the brain
  • Primary and secondary: two pipelines dedicated to change in muscle length
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79
Q

How does the skin help with proprioception and kinesthesis?

A
  • length and velocity of skin stretch
  • onset of movement
  • acceleration
  • changes its length around a joint, skin strain (ruffini)
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80
Q

How do Joint help with proprioception and kinesthesis?

A
  • Pressure
  • contraction
  • sensitivity
  • reflexes: tuning the gamma system in the spindle
  • can modulate joint receptors
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81
Q

How do Golgi Tendon Organs help with proprioception and Kinesthesis?

A
  • Tension and Force Sensing
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82
Q

Is Kinesthesis Conscious? how?

A

Yes
- Involves an interpretation/judgment of where you are in space

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83
Q

What are the four main contributors to Kinesthesis? What do they contribute?

A
  • Sense of Position and Movement of Limbs: position relative to you and world around you, how fast they are moving
  • Sense of Tension and Force: GTO to some extent
  • Sense of Effort and Heaviness: Force output stays the same/ fatigue requires more effort
  • Sensations of Body Image and Posture: clinical conditions to pain, distortion
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84
Q

Is proprioception conscious? why?

A

More Reflexive
- Happens before you know to prevent you from falling over

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85
Q

What is some early evidence of a somatosensory role in proprioception and kinesthesis?

A
  • Dorsal Rhizotomy in animals
  • Human Deafferented Subjects
  • Clinical Conditions
  • Vitamin B6 Toxicity in Cat
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86
Q

How does Dorsal Rhizotomy in animals support the somatosensory role in proprioception and kinesthesis?

A
  • fine motor control disappeared: movement deteriorates
  • reflex orientates within spinal cord
  • tactile information not getting to brain
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87
Q

What is a dorsal rhizotomy

A

surgical removal of dorsal root afferent input

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88
Q

How do humans who have been deafferented support somatosensory role in proprioception and kinestheis?

A
  • Familiar tasks remain intact
  • New tasks are difficult
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89
Q

How does Guillain-Barre Syndrome support the somatosensory role in proprioception and kinesthesis?

A
  • Woman lost vocal proprioception and sounded deaf
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90
Q

What is Gullain-Barre Syndrome?

A
  • loss of sensation (motor, sensory, or both)
  • or increase in pain due to demyelination
  • can recover
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91
Q

What does a Vitamin B6 toxicity in cats do?

A
  • Leads to large fibre neuropathy (loss of proprioceptive inputs)
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92
Q

How does vitamin B6 toxicity in cats support a somatosensory role in proprioception and kinesthesis?

A
  • 1as, secondaries, 1bs, afferents from joints and skin demyelinate
  • loss of sensory information
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93
Q

What happens when the code for somatosensory is interrupted?

A
  • a dramatic reduction in control and perception of movement
  • code is critical for performing normal movements
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94
Q

How are cortical projections for 1a afferents important for kinesthesis?

A

3rd neuron projection
- medial lemniscus pathway carries information all the way to the cortex
- use information for proprioception and kinesthesis
- muscle spindles very useful for providing code on length and velocity

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95
Q

What is strong evidence that muscle spindles play a conscious role in position/movement sense?

A
  • Illusion of muscle lengthening when vibrating
  • Joint and skin receptors arent activated while this is happening
  • has to be on the muscle itself, if it isn’t the illusion disappears
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96
Q

What are some examples using vibrations to create an illusion of movement? what do they show?

A
  • Pinocchio effect
  • Falling Forward/Backwards
    Shows evidence of selectively attending to muscle spindle feedback to determine where you are in space
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97
Q

How do you produce the Pinocchio Effect?

A
  • Grab nose / close eyes
  • vibrate bicep: makes it feel like elbow extend
  • nose must grow to maintain contact
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98
Q

How do you produce the falling forward illusion?

A
  • bilaterally vibrate tricpes surae tendons in standing position
  • illusion of tricep extend and lengthen
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99
Q

How do you activate the falling backwards illusion?

A
  • light source
  • vibrate Achille’s tendon
  • light source moves vertically upward
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100
Q

What did the Assigned Readin #3 Discuss?

A

For fast movements, muscle spindles in the agonist may go quiet / become unloaded
- extrafusal muscle shortening faster than .2 resting length/s may result in muscle spindle unloaded, even with gamma drive
- If the agonist muscle spindle is unable to code for position/movement, then antagonist muscle does

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101
Q

What happens to your finger proprioception when you isolate the finger and selectively remove sensation?

A
  • Limited loss in proprioception
  • Muscle spindle afferent feedback intact in forearm muscles
102
Q

What happens when you pull on the muscle tendons during a carpel tunnel surgery?

A
  • People perceive finger movement depending on direction pulled
  • activates spindles and interpret discharge as movement
103
Q

What is evidence that muscle spindles are involved in proprioception?

A
  • Vibration Illusions
  • Removal of all Senses other than Spindles, still have proprioception
104
Q

What happens to proprioception after a total joint replacement? What does it say about joint receptors?

A
  • No evidence of a significant decrease in joint position sense
  • Joint receptors are not essential for proprioception in this case
105
Q

What experiment showed people that skin was involved in proprioception?

A

Isolate muscle tendons and mechanically move the finger. Remove joint receptors, and test proprioception with only skin receptors active. Decreased, but still active.

106
Q

What is an experiment that shows that joint receptors are used in proprioception?

A

Inject dextran to joint, joint swells and activates joint receptors. This resulted in higher detection in proprioception, specifically for the hand.

107
Q

What do we know about joint and skin receptors in the hand regarding proprioception?

A

Joint
- Definitely play a role in the hand
Skin
- Skin strain around a joint is involved (Ruffini Endings)

108
Q

When can SA2’s be recorded on the back of the hand?

A

During Flexion and Extension Movement
- Codes for lateral skin stretch

109
Q

What happens when you push on a Ruffini Ending? What about when you stretch the skin?

A

Push
- Regular discharge
Stretch
- Increase firing rate (codes for finger position)

110
Q

What does the map of SA2s on the front and back of the wrist do?

A
  • Measures skin strain when you flex or extend
  • I.e. throwing a baseball pitch
111
Q

What is the Problem for SA2?

A
  • Doesn’t distinguish which finger is firing when moving two individually, just says it was moving
112
Q

Does each finger have a subpopulation of FA1’s? what happens when that a finger moves?

A

Yes
- The population associated with that subpopulation fires

113
Q

What is similar about SA2’s and FA1s? What is different?

A

Same
- similar code
Different
- FA1’s tells which finger is firing

114
Q

What is evidence that you pay more attention to skin strain pattern on back of the hand over what the spindles tell you?

A

Using ring block to selectively remove joint, skin, spindle receptor feedback. Move finger and they can tell it moves but cant feel it. Stretch skin and make you think finger was flexed when extended - vice versa.

115
Q

What does Functional Knee Bracing do to proprioception?

A

Facilitates Skin Strain around knee joint
- increases proprioceptive awareness and accuracy
*useful if there is a deficit

116
Q

What do pressure undergarments do for proprioception?

A

Creates skin strain pattern
- helps tell more accurately how you’re moving
- i.e. how hips are rotating
- modifies cutaneous feedback

117
Q

What are the problems with codes from muscle spindles? how can it be identified?

A

Problems
- Ambiguous Nature to code
- Code is changed by the gamma system
- Has Gamma bias
Identification
- Gamma system sends efference copy to cortex/cerebellum
- Subtract gamma bias from afferent feedback
- now you have the code

118
Q

How does your brain compare and analyze movement?

A

Copy of motor command goes to sensory centers
- for comparison and error detection

119
Q

What happens when you send a central command to extrafusal fibres?

A

Get a bunch of Afferent Feedback to the sensory cortex associated with that movement
- GTO feedback on twitch force
- Spindles on muscle length and velocity
- Skin/joint receptors

120
Q

What is a corollary discharge?

A
  • When you make a contraction and send a copy of the motor command to the sensory centres
121
Q

How do we correct errors in movement?

A

Compare corollary discharge with afferent feedback at the sensory cortex and make a correction

122
Q

What are the different classifications of Joint Receptors? what are they based on?

A

4 subtypes
- based on type of axon connected to

123
Q

What are the four subtypes of joint receptors/

A
  • I
  • II
  • III
  • IV
124
Q

What Joint Receptors are mechanoreceptors? what are their characteristics?

A

Subtypes I, II, III
- larger
- Myelinated Axons

125
Q

What Joint Receptor is a Nocireceptor? What does is code for?

126
Q

Where are the Joint Receptors located? where are they not located?

A

Located
- Joint Capsule
- Joint Ligaments
- Loose Articular Tissue
Not Located
- Cartilaginous surfaces
- Synovial Membranes

127
Q

Where are Type IV joint receptors located?

A

Small nerve endings
- within bone, surface tissue of bone
- Not in Joint Capsule

128
Q

Where are Type III Joint Receptors Located?

A

Part of External Ligament (tibial collateral)
- lots of them

129
Q

Where Are Type I Joint receptors located?

A
  • Superficial layers of capsule
  • Denser in proximal joints
  • Denser in Cervical Spine (vs Lumbar)
130
Q

Describe Type I Joint Receptor Threshold/firing

A
  • Low THreshold
  • Slow Adapting
  • Fires as soon as stretch starts
  • continues firing throughout stretch
131
Q

Describe the Type I Joint Receptor structure

A
  • Globular or Ovoid Corpuscles
  • As it gets in tissue, loses myelin and branches that imbed
132
Q

Where are Type II Joint Receptors Located?

A
  • Deep layers in capsule and articular fat pads
  • More in distal articulations
133
Q

Describe Type II Joint Receptor Threshold/Firing

A
  • Low Threshold
  • Rapid adapting
  • Fires only during transitions (transient)
134
Q

What is the structure of Type II Joint Receptors?

A
  • Elongated
  • Cylindrical Corpuscle
  • Modified Pacinian Corpuscles
  • Axon is in middle of numerous layers
135
Q

What are Type III Joint Receptors known as?

A
  • Golgi Receptors
136
Q

Where are Type III Joint Receptors Located?

A
  • Intrinsic and Extrinsic Joint Ligaments
  • Embed in ligaments
137
Q

Describe the Type III Joint Receptor threshold/firing

A
  • High Threshold
  • Slow Adapting
  • Takes a lot of tension to fire, will continue to fire if tension maintained
138
Q

What is the structure of Type III Joint Receptors?

A
  • Fusiform Corpuscles (identical to GTO)
  • Embedded in ligaments
139
Q

What is the Neural Code?

A
  • Respond to extreme limits and joint pressure (swelling or compression)
140
Q

How do Joint Receptors code for joint position?

A
  • Fire in limited way
  • Respond mainly to extremes
  • Respond to joint pressure
  • code ambiguously for joint movements
  • Respond to both flexion and extension (not specific to what is occurring)
141
Q

What is an example of the ambiguity of Joint Receptor Coding?

A

Metatarsal Phalangeal Joint
- Increase discharge when held in flexion (velocity and static code of position of joint)
- Extension fired the same way

142
Q

How does the firing rate of Joint Receptors at different joint angles contribute to their ambiguity?

A
  • Don’t Fire at midrange
  • Has inverted U-shape as extension is continued
  • Same firing rate at two different points
  • Does not help physiologically define range/angle
143
Q

What implies that Joint Receptors have a strong connection to higher-order sensory neurons?

A
  • Joint afferents reach the supraspinal centre
  • Stimulation of Joint afferents evoke distinct sensation of rotation, deep pressure and well defined somatosensory evoked potentials
144
Q

What Joint Receptors have strong projections on Alpha MN?

A
  • High Threshold (mainly nocirecptors)
145
Q

what Joint Receptors have a weak and infrequent effect on Alpha MN?

A
  • Low threshold (mechanosensive)
146
Q

What is an indication of protective muscle reflexes in knee ligaments?

A
  • Require heavy stretching for measurable EMG activity
147
Q

Which is more influenced by low threshold joint afferents? Alpha MN or Gamma MN?

148
Q

What causes strong excitatory and inhibitory effects on static and dynamic Gamma MN?

A
  • Low threshold Joint Mechanoreceptors
149
Q

How can Joint Receptors indirectly influence muscular control and proprioception?

A

JR excites or inhibits static and dynamic gamma MN
- Gamma modulates spindle behavior
- muscle spindle plays a key role in reflexive control of muscles and movement, position sense

150
Q

Why does a damaged Joint Receptor decrease proprioception?

A

JR feedback to gamma MN which codes for velocity and static
- Damaged JR results in loss of regulation of muscle spindle (it doesn’t know what to code for)

151
Q

What is an example of the simple monosynaptic reflex?

A
  • Drinking from a mug
  • add to the load
  • stretches biceps and activates spindles
  • feedback from spindle to MNP of biceps
  • Causes contraction to correct for increased load
152
Q

What is a massive convergence?

A
  • A large amount of spindles in muscle
  • All go back and connect up with every single MN in muscle
153
Q

What is a massive divergence?

A
  • Every Spindle connects to every neuron in the MNP
154
Q

How fast is the simple monosynaptic reflex?

A
  • Quick, rapid corrects in 22ms
155
Q

Describe the Simple monosynaptic reflex in the anterior arm

A
  • Very strong connections to MNs in biceps
  • Weaker connection to MNs in other muscles that flex (brachialis, brachioradialis) `
156
Q

What is the Hoffman (H) Reflex?

A
  • EMG response
  • An artificial copy of the monosynaptic reflex
  • Requires artificial stimulus
157
Q

What nerve can the Hoffman Reflex stimulate?

158
Q

What is the Hoffman Reflex used for?

A
  • To test the level of excitability of a MNP
159
Q

How can the Hoffman Reflex vary in certain populations?

A
  • Hypo or Hyper
160
Q

What is the Pulse rate for the Hoffman Reflex?

A
  • 1ms pulse/ 5s
161
Q

What was the Hoffman Reflex intended for?

A
  • Artificially set up APs that go to spinal cord and come back as part of reflex
  • Electrically activate 1a afferents and alpha motor neurons
162
Q

Why do both 1a afferents and alpha motor neurons activate during the Hoffman Reflex?

A
  • They are the largest diameter axons (most sensitive)
  • cross-sectional size of axon is critical
162
Q

Why do both 1a afferents and alpha motor neurons activate during the Hoffman Reflex?

A
  • They are the largest diameter axons (most sensitive)
  • cross-sectional size of axon is critical
163
Q

What is the largest axon in the peripheral nerve?

A
  • 1a Afferents
164
Q

Why did Hoffman test the strength of the monosynaptic reflex?

A
  • to see if it was stronger or weaker in certain populations
  • To test the excitability of different MNP
165
Q

What happened when Hoffman turned up the current?

A
  • Excite progressively smaller diameter axons
  • At high level, it directly stimulated largest diameter motor neurons axons
166
Q

What is the highest threshold MN?

A
  • Big axons that connect to biggest cell bodies
167
Q

What two reasons are there for a change in the Hoffman Reflex if the current is kept the same?

A
  • Strength of coupling between 1a afferent and MN
  • MNP changed its state
168
Q

What is Orthodromic?

A
  • The correct direction of potential travel for afferent and efferent
169
Q

What is the Orthodromic current for 1a afferents?

A
  • AP goes along axon into the spinal cord
170
Q

What happens if during an Orthodromic 1a Afferent there is sufficient EPSPs onto the MNP?

A
  • Lowest threshold MN will fire
  • AP goes to nerve
171
Q

How long does it take for an H-reflex to occur?

A
  • 30-33ms after stimulus
172
Q

What is the Orthodromic direction for an Alpha motor neuron?

A
  • Ap goes down the muscle
173
Q

What is an Antidromic Current? How can this happen?

A
  • Backwards Propagation of the potential
  • Stimulate the nerve in the middle
  • No refractory period
174
Q

What is an Antidromic path for a 1a Afferent?

A
  • AP goes back down to muscle spindle
  • dissipates
175
Q

What is the path of an antidromic current in alpha motor neurons?

A
  • AP goes back up towards the cell bodies
176
Q

What is the relationship between the H-reflex and the M-wave?

A
  • Increasing Current Increases H-reflex
  • Increasing H-reflex activates M-wave
  • As M-wave increases, H-reflex decreases
  • At M-max, H-reflex disappears
177
Q

Why does the H-reflex get smaller as the M-wave increases?

A
  • Due to Anti and Orthodromic Activation in the nerves
  • Antidromic AP of Motor Neuron causes depolarization and hyperpolarization of cell body
  • Brief Period MN cannot be activated
178
Q

What does a plot of M-wave and H-reflex amplitudes measure?

A
  • Peak-to-peak amplitude of the response
  • M-wave starts to recruit more and more MN until max
  • H-reflex grows until antidromic consequence causes it to disappear
179
Q

How to tell if you are always hitting the nerve with the same stimulus?

A
  • M-wave is present and stable
  • Close to Solid H-reflex
180
Q

How would you know if you are not hitting the nerve with the same stimulus?

A
  • H-reflex start to grow and change
181
Q

What happens if the H-reflex changes while the M-wave is constant?

A
  • Change in MNP excitability or
  • Strength of synapse changed
182
Q

Whats the Difference between activating a T-reflex and H-reflex?

A

H-reflex
- Electrically stimulated
T-reflex
- Activate spindle by tapping the tendon

183
Q

Which is totally dependent on a transducer? H-reflex or T-reflex?

A

T-reflex
- requires spindle to generate AP, H-reflex does not

184
Q

What is the size of the T-reflex dependent on?

A

The size of the tap
- Larger tap equals bigger volley of APs from spindle

185
Q

How does a small contraction influence a T-reflex? why?

A

Larger one
- lowest threshold MUs are above the threshold, rest are right near

186
Q

Describe a reflex

A
  • Automatic motor response to sensory stimulus
  • Evoked from stimulation of peripheral receptors
    -widespread effect on MNP
  • Adaptable depending on context/task/state
187
Q

What does a reflex involve?

A
  • Sensory Neuron
  • Interneuron
  • Motorneuron
188
Q

What is the exception to the Reflex circuitry?

A

Monosynaptic Stretch Reflex
- 1a afferent directly to MN

189
Q

Where can there be an influence on a Reflex?

A
  • First Synapse between afferent and interneuron
  • other connections at interneuron
  • where the interneuron connects to MN
  • IPSP or EPSP Interneuron
190
Q

What is Autogenic Excitation?

A
  • When the 1a afferents project to all the MN of the same muscle
191
Q

what is a Reciprocal Inhibition of a Reflex? Example?

A

Homonymous Stretch Reflex that also connects to 1a inhibitory interneuron
- disynaptic reflex (1 IPSP and 1 EPSP)
- Creates balance across the joint
Example
- Bicep fires
- Tricep Inhibited

192
Q

What is an Autogenic Inhibition? What is an example?

A

AI
- When a reflex inhibits its own muscle
Example
- 1b (GTO) inhibition
- active muscle activates GTO
- 1b afferent enters spinal cord has disynaptic to MN
- MN goes back to the original muscle
- GTO senses tension and force
- GTO uses 1b inhibitory interneuron to inhibit

193
Q

Why is the 1b Inhibitiroy Interneuron misnamed?

A
  • Because it can be both faciliatory and inhibitory
194
Q

What does the 1b inhibitory interneuron connect to other than the 1b pathways? What is this an example of?

A
  • Joint Afferents
  • Cutaneous Afferents
  • Descending Inputs
    Example of Convergence
195
Q

Why is it good to have an interneuron?

A

So you can make a contraction without it being prevented
- Interneuron can prevent large IPSP from stoping EPSPs from GTO

196
Q

What does 1b feedback have a facilitatory effect on?

A

-Antagonist MNs

197
Q

How does the 1b inhibitory interneuron excite an antagonist MN?

A

Facilitates by Inhibiting inhibition (passive)
- Release IPSP onto interneuron
- Interneuron goes to mnp of antagonist
- IPSP inhibits the inhibition on the antagonist MN

198
Q

What is the Flexor (withdrawal) Reflex?

A

Protective reflex that coordinates activation of limb flexor muscles

199
Q

How does the Flexor Reflex work? (two ways)

A

The interneuron connects to another interneuron that connects to MNP
- IPSP onto MNP = prevents muscle extending further into stimulus
Connects via 2 interneurons with EPSP on MNP of muscle to flex away from stimulus
- goes to everything that can flex away (major divergence)

200
Q

What is the Crossed-Extension Reflex?

A

In opposite limb
- Activation of extensors
- Inhibition of Flexors

201
Q

How can reflex responses be modulated?

A
  • Through interactions at different components of the reflex arc
202
Q

Where do mechanisms to modulate reflex responses occur?

A
  • Peripheral inputs (reflex connecting to reflex)
  • Descending inputs (brainstem, cortex, etc)
203
Q

What mechanisms can be used to modulate reflex responses?

A

Excitability of MN
- make really negative (prevent reflex)
Change sensitivity of interneurons
- severe negative, no 1b inhibition
Change MNP excitability

204
Q

Wha tis a Renshaw Cell?

A
  • Interneuron located really close to the alpha MNP
205
Q

How is a Renshaw cell activated?

A
  • Collateral from alpha MN (EPSP)
206
Q

What do R-cells Project to?

A
  • Motor Neurons
  • 1a Inhibitory interneurons
  • Gamma motorneurons (weakly)
  • other R-cells (weakly)
207
Q

What do R-cells receive input from?

A
  • Descending pathways
  • Cutaneous afferents
  • Type II afferents
208
Q

Is a Renshaw Cell inhibitory or excitatory?

A
  • Inhibitory
209
Q

What does the R-cell do?

A
  • Biases own MN not to fire
  • Remove inhibition to the antagonist
210
Q

What is Axo-axonal synapse? How does work? What does it do?

A

When presynaptic neuron connects to post synaptic neuron
- Selective inhibition of only the presynaptic neuron
Used
- Chlorine Conductance
- Decrease the size of propagated AP
- Decrease Ca release, decrease NT release, Decrease EPSP
Do
- Enables a change in the input-output relationship
- Helps to control monosynaptic reflex

211
Q

What is the Latency Response length of pre-programmed reactions compared to monosynaptic response and voluntary reaction times?

A
  • Shorter than Voluntary reaction times
  • Longer than a monosynaptic response
212
Q

Example of how Pre-programmed reactions work?

A

Stretch Wrist
- stretch all forearm flexors
- M1 is monosynaptic reflex
- M2-3 is a big burst in EMG between M1 and voluntary response
- M2-3 can be preprogrammed

213
Q

What does the pre-programmed reactions involve? what does it travel via?

A

Involves
- Parallel spinal and supraspinal pathways
Travels
- via dorsal column medial lemniscus pathway

214
Q

Is the M2-3 Response Transcortical?

215
Q

Where does evidence come from for the Pre-programmed reactions? What is that evidence?

A

Klippel-Feil Patients
- Bifid movements (one side of cortex drives both sides upper body)
Evidence
- Stretch right hand, M2-3 response right and left wrist
- Stretch one side causes preprogrammed response out of bilateral muscle

216
Q

Are rhythmic movements still possible following a complete transection of the spinal cord? How

A

Yes
- circuitry resides in the spinal cord
- rhythmic movement generated distal to lesion

217
Q

what is central rhythm generation an inherent characteristic of?

A
  • spinal cord
218
Q

What is the Central Pattern Generator (CPG)?

A

EMG and Kinematic Pattern that looks normal due to rhythmic patterns generated by the spinal cord
- No Brain Involement

219
Q

What is an oscillator involved in Central Pattern Generator?

A

Group of interneurons
- When they start going, create rhymical oscillating pattern within spinal cord

220
Q

What is the Half Centre Model?

A

Interneuron excites flexor and inhibits extensor
- collateral comes back at itself with IPSP and briefly inhibit other side before terminated
- Same input can excite the other side, and oscillate back and forth

221
Q

How does Central Pattern Generator work for Walking?

A
  • Supraspinal input hits spinal cord
  • CPG starts, dont have to physically think about moving
  • Creates scaffolding for locomotion
222
Q

What happens after an injury or disease that inhibits descending inputs? Example?

A

No Supraspinal Input
- Intact CPG, still have rudimentary walking
Example
- Kids born with corticospinal tract demyelination
- pick up, the legs oscillate

223
Q

What is sensory feedback for regarding locomotion?

A
  • Initiating walking
  • controlling phase transitions
  • Regulating the level of muscle activity
  • correcting for unexpected disturbances
224
Q

How does sensory feedback help regulate level of muscle activity during locomotion?

A
  • CPG tells you the pattern
  • Afferent feedback is highly involved in tuning MNP
225
Q

How does sensory feedback help correct for unexpected disturbances in locomotion?

A

Stumbling-corrective response
- afferent feedback layers on CPG so when you trip you keep walking

226
Q

How does sensory feedback help control phase transitions when walking?

A

Stretch of hip flexors - muscle spindles
- determine how far hip is going to extension
Unloading of extensor muscle -GTO
- Monitor force required to put out to stay upright
Use load to determine when its safe to transition

227
Q

Explain the Stumbling-corrective Response

A

Encounter obstacle during swing phase
- automatic flexion response to step over
- All in spinal cord
If during stance phase
- extension of limb

228
Q

What is a Phase-dependent Reflex reversal?

A

Response to the obstacle depends on the phase
- stim of top foot during swing, flexion of limb
- Stim top foot during stance, extension of limb
Same stimulus leads to different responses, depending on phase of locomotion
- Afferent driven

229
Q

Where are Golgi Tendon Organs located?

A
  • Tendon Junctions
  • In Series
230
Q

What is the Structure of GTO?

A
  • capsule (1mm by 0.1mm)
  • 10-20 muscle fibers
231
Q

What afferent fiber innervates the Golgi Tendon Organ?

A
  • 1b Afferent
232
Q

Describe the Extrafusal Muscle Fibers of GTO

A
  • each belongs to different motor unit
  • not all muscle fibers associated with GTO
233
Q

What do GTOs do?

A
  • Muscle Receptors that provide feedback to the CNS about muscle force and tension
234
Q

Describe the sensory innervation of GTOs

A
  • Single 1b afferent (2% of GTOs have 2 ib afferents)
  • Nerve endings interdigitate among collagen fibers
235
Q

Are GTOs designed to monitor force production on active or passive force generation?

A
  • Active Muscle
236
Q

What will each GTO’s discharge rate scale with increasing force in muscle?

237
Q

What was the setup for Assigned Reading #3?

A
  • 4m/4f university students (blindfolded ex. 1)
  • Vibrations of 95Hz amplitude 2mm (measured by accelerometer)
  • Angle of arm recorded by potentiometers
238
Q

What was the setup of experiment 1 of Reading #3?

A
  • Right limb moved to fixed targets (20,40,60%)
  • Moves at 60degrees / second
  • Match with left limb
  • Conditions (no vibrations, antagonist vibration, agonist vibration)
239
Q

What was the results of Experiment 1 of Reading #3?

A
  • Antagonist muscle vibrations caused an overshoot in perceived movement magnitude
  • Overshoot was same for all three target distances
240
Q

What was the setup for Experiment 2 of Reading #3?

A
  • Right arm flexed to line up middle finger to visual target
  • Match with other arm
  • Three conditions (no vibrate, vibrate antagonist, vibrate agonist)
241
Q

What were the results of experiment 2 of Reading #3?

A
  • Antagonist vibration resulted in overshoot
242
Q

What was the purpose of the experiment in Reading #4?

A
  • Why illusions of movement when non movement happens and no sensory Feedback
243
Q

Describe how the experiment was performed in Assigned Reading #4

A

First
- Participants accuracy of effort level tested
Second
- Participants matching of wrist position was tested
Third
- BP cuff used to block motor and sensory function of arm
- Participants asked to make effortful extension or flexion
- Participants perceived position of wrist was recorded

244
Q

What did participants in Reading #4 perceive with effortful movement of an isolated and paralyzed wrist? why?

A

Perception
- perceived extension or flexion in direction of effort
Reason
- No afferetn feedback
- Paying attention to the command of effort and interpreting it as sensation of movement

245
Q

What were the results of the experiment done in Reading #4? what is this evidence of?

A

Results
- Error matching limb position
- Error dependent on effort direction
- Error dependent on the magnitude of effort
Evidence
- Kinesthesis is not just sensory, motor plays a role

246
Q

What was the purpose of the experiment in Assigned Reading #5?

A
  • Use height or possible postural perturbation to increase threat
  • compare H/T reflexes to see if level of threat changes spinal reflexes
247
Q

How did they control the H-reflex generated in Reading #5?

A
  • Tap Achille’s with load cell to ensure force is the same
248
Q

What does measuring the T-reflex and H-reflex together in Reading #5 say?

A
  • inform about the excitability of MNP
  • Inform about strength or monosynaptic connection
  • T-reflex will inform spindle activity
249
Q

What might have caused the different peak to peak amplitude of the T-reflex during high and low levels for Reading #5? What does an unchanged H-reflex tell you about this?

A

Potential Causes
- Change in MNP excitability
- Strength of synapse increased
- Spindle changed sensitivity (gamma system)
H-reflex
- No change in MNP excitability
- No change in strength of synapse
- Spindle had to change sensitivity

KIN 313 - Neurointegration of Human Movement (5 decks)

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