Test 5

Question 1

upper motor nuerons

Answer 1

-cerebral cortex and branstem
-can only connect to muscle through lower motor neurons (which are directly connected to muscle)

Question 2

Lower motor neurons

Answer 2

-ventral horn of spinal cord
-Direct connection to muscle
-axons exiton ventral root
-exit ventrally and join sensory fibers in spinal nerve (31 pairs classified into 4 segments (CTLSc)

Question 3

lower motor neurons can receive input from:

Answer 3

-upper motor neurons
-interneurons in spinal cord
-sensory input

Question 4

distribution of motor neurons in the spinla cord

Answer 4

not an even distribution
-cervical enlargment (C3-T1)
-Lumbar enlargement (L1-S3)
These areas contain most of the motor neurons for distal and proximal muscles

Question 5

how are motor neurons in the spinal cord organized

Answer 5

organized at leavh level by area and function of the muscle they innervate
therefore, generally:
-Axial muscles more meidal than distal muscles
-Flexore more posterior to extensors

Question 6

What are the 2 primry types of lower motor neurons

Answer 6

alph motor neurons and gamma motor neurons

Question 7

alpha motor neurons

Answer 7

directly trigger the contraction of muscles for movement

Question 8

gamma motor neurons

Answer 8

regulate muscle tone and control sensitivity of muscle spindles

Question 9

Alpha motor neurons: motor unit

Answer 9

motor neuron and all the fibers it innervates

Question 10

alpha motor neurons: motor neuron pool

Answer 10

All the alpha motor neurons that innervate a single muscle

Question 11

excitation contraction coupling

Answer 11

-Alpha motor nueron release ACh
-ACh produces large EPSP in muscle fiber (graded potential)
-EPSP evokes muscle action potential
-AP triggers Ca2+ release from SR
-Fiber contracts (sliding filament model)
-Ca2+ reuptake
-Fiber relaxes

Question 12

sliding filament model of contraction

Answer 12

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

Question 13

fundemental properties of contraction: force length relationship

Answer 13

-describe the relationship of isometric msucle fiber forces with its length (amount of stretch on non moving muscle)
-goldilocks zone for maximum number of cross bridges (not too short, not too long)
but most movement is not isometric…

Question 14

fundemental properties of contraction: force velocity relationship

Answer 14

fore output changes based on the speed it shortens (or lengthnens)
= dont need “recocked’ and attatched more often in a powerful position. Also can utilize elastic properties
=more difficult for corss bridges to cycle and they spend more time near end of power stroke

Question 15

Titin

Answer 15

“spring” on end of myosin filament (very small- can’t see it even with a microscope- have proven its existance theoretically)
provides elastic compoent in muscle fibers
-titin is the main source of passive force in a single fiber
-minimal source of passive force in complete muscle (tendon acts as main source)

Question 16

residual force enhancement

Answer 16

possible thanks to titin
-when an active muscle is stretched its isometric, steady-state force following the stretch os greater than the corresponding (same length, same activation) purely isometric contraction.
(stay activated throughout lengthening allowa greater force development?
-titin when relax get passive stretch-deosn’t impact subsequent force (loose pring) when 1s contract and keep contrated and stretch, change property of the spring- may bind to things and stiffen- much more forceful-produces extra force due to tighter spring.

Question 17

Titin-residual froce development

Answer 17

-titin appears to be an adjustable (tight vs loose0 spring which plays an important role in residual force enhancement
-muscle activation can lead to a change in stiffness and length in of this spring
so… titin can help increase force (+efficiency) in movements that involve activated/stretching muscles

Question 18

EMG

Answer 18

-The quantification of a muscle(s) electrical activity (sum of action potentials)
-bipolar electrodie configuration to record the dofference in elcetrical activity
-eg V1-V2

Question 19

Application of EMG

Answer 19

-Linear relationship to muscle force and activation in isomectric contractions
-Provides amplitude of mucle activation (level of recruitment) ie during walking gait
-Provides time of activation (activation pattern) ie during walking gait
-fatigue and advance analyses

Question 20

EMG limitations

Answer 20

-not a direct relationship to muscle force (espceially during motion)- force length and force velocity relationship can mess things up
-sensitive in differences in placment/processing
-surface EMG: cross talk between muscles, recording through skin/adipose- especially in regions like the forearm (lots of little muscle very close together).

Question 21

Proprioception- neurons

Answer 21

group 1 sensory neurons- can be further subdivided into 1a and 1b axons

Question 22

Proprioception: 1a axons

Answer 22

-Largest and fastest (myelinated)
-Excitatory synapes with spinal interneurons and directly on alpha motor neurons
-muscle spindles (mount of stretch)

Question 23

Proprioception: 1b axons

Answer 23

-slightly smaller/slower
-inhibitory synpases with spinal intreneruons
-Golgi tendon organ (amount of force)

Question 24

Muscle spindles

Answer 24

Sensory receptor- forst thought to be a ‘muscle bud”
Sits within a muscle to measure the change in length
-Small intrafusal muscle fibers (collect info)
-Parellel to primary muscle fibers (extrafusal)
-Wrapped within a sensory neurom (1a)

Question 25

the stretch refelc (myotatic reflex)

Answer 25

when a uscle is pulled (stretched), it pulls back (contracts) -reists changes in muscle length -important for maintaining limb position or posture

Question 26

myosynpatic stretch reflex

Answer 26

-primary sensory neuron (1a-muscle spindle) -primary motor nueron (alpha motor neuron)- reflexive how could be confirm the function of this sensory neuron/structure?

Question 27

the stretch reflex (myotatic reflex)

Answer 27

i) Muscle is stretched (extrafusal and intrafusal) ii) Ia depolarizes from stretch iii) Action potential propogrates along axon through dorsal root iv) Synapses with alpha motor nueron V) alpha motor neuron sends action potential to contract muscle

Question 28

How muscle spindles stay response to stretch?

Answer 28

Intrafusal fibers need the ability to contract, just like extrafusal fibers (or else get slack in the line) Gamma motor nuerons receive input from brain to keep intrafusal fiber taut

Question 29

Fine tuning muscle length with the gamma loop

Answer 29

1. Descending command from brain sets first estimate (how much activation is needed to do something) -Coactivation of both alpha and gamma motor neruons (tuning for the inital guess) 2. Muscle spindle detects muscle is too long 3.Ia axons send signal to alpha motor neuron 4. Alpha motor nueron activate extrafusal fibers to shorten muscle

Question 30

Gamma Bias

Answer 30

-Constant activity to keep intrafusal fiber taught -Firing rate increases or decreases to compensate for changes in exrrafusal fiber length

Question 31

Fusimotor gain

Answer 31

-Ability of the nervous system to adjust/tine tune the sensitivity to small changes -How can we improve fusimotor gain? Plyometrics (reacting quickly), balance training

Question 32

Gamma (motor) loop

Answer 32

The loop between the muscle spindle (sensory fiber + gamma motor neruon) and muscle (alpha motor neuron)

Question 33

Gamma bias

Answer 33

Base level of firing for the inrefusal fibers to keep sensor online

Question 34

Fusimotor gain

Answer 34

Ramping up/fine tuning the sensitivity of this loop to identify small changes

Question 35

fusimotr gain example

Answer 35

ability of the body to adapt to small changes- balance -so balance training can help increase the sensitivity, meaning we can quickly/easily react to small changes -- stretch reflex allows contraction to get us back straight after a deviation -improved fusimotor gain allows our system to be sensitive to small changes--> leading to small, efficient and accurate postural corrections

Question 36

fusimotor gain- static response

Answer 36

-Intrafusal fibers: nuclear chain and static nuclear bags -correct to static gamma motor neurons -type (group) II sensory fibers -primarily related to changes that are constant/predictable example: static stretch (20-30sec) -inhibitory

Question 37

fusimotor gain- dynamic response

Answer 37

-Intrafusal fibers: Dynamic nuclear bag (dynamic responses) -Dynamic gamma motor neurons -Type (group) Ia sensory fibers -primarly related to changes that are quick/unpredictatble example: stretch reflec -excitatory

Question 38

static stretch

Answer 38

-likely to reduce muscle performance (if immediately prior to exercise)- creating inhibitory stretch response -Improves flexivibility (may be required for specific tasks) Activating type II sensory fibers (static response) However, if static stretching is integrated into a full warm-up (aerobic, SS, DS, Sport-specific activities), there is no evidence to say its detrimental

Question 39

dynamic stretching

Answer 39

may increase muscle performance and sport specific perofrmance -activating type Ia sensory fibers (gynamic response) -Ramping up fusimotor gait--> improving response to quick/unpredictable muscle length changes (increased sensitivity of muscle- ready to go!)

Question 40

Golgi tendon Organs

Answer 40

sensory receptor -sensory neuron (Ib) intertwined within the collagen fibers of tendons -allows for the measure of force of contraction (strain of muscle) -Regulate msucle tension within optiomal range GTO fibers are in series rather than parallel- force must go directly through them Synapse with inhibitory interneurons- primarily helps to regulate muscle force. Allows for protection of overload as last resort

Question 41

joint receptors

Answer 41

-Many proprioceptive acons in joint tissues (signals from ligaments and joint capsule- ynovial fluid, tissue, cartilage) -Similar to mechanoreceptors found in skin, but respond to the position and movement in a joint- rapidly adapting so better at measuing dynamic movement -Improtant for stability and control of joints, but can be damaged with injury -Neuromuscular training/rehabilitation can improve this but complex interplay of many factors

Question 42

The stretch shortening cycle (SSC)

Answer 42

Involces an eccentric stretching of the muscle, immediately followed by an enhanced concentric contraction

Question 43

SSC potentiation- verticle jump example

Answer 43

jump height: squat vs contermovment jump enhanced concetric contraction

Question 44

mechanisms of ssc

Answer 44

1.Elastic energy 2.stretch reflex 3.neural potentiation 4.active state 5.mechanical potentiation

Question 45

mechanisms of ssc: elastic energy

Answer 45

-generated from all eleastic compenetnts, but tendons dominate the storage and release of elastic energy - >0.5s may negate all effects of elastic energy (lost to heat)

Question 46

mechanisms of ssc: Stretch Reflex

Answer 46

-Fast lengthening of muscle (eccentric 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 to maximize sensitivity of the reflex -How can we imrpove our fusomotor gain for the SSC?

Question 47

mechanisms of ssc: neural potentiation

Answer 47

-Electromechanical delay -Picking up the "slack" in the unit (force producing unit) -30-110ms

Question 48

mechanisms of ssc: active state

Answer 48

-Time for cross-bridge to build up force -100ms-1s

Question 49

mechanisms of ssc: mechanical potentiation

Answer 49

-residual force enhancement

Question 50

Fast SSC

Answer 50

Fast eccentric phase, with an explosive concentric phase -Stiff joint, high activation in eccentric, very little loss of force during amortizating -contract time <250ms Primary mechanisms: -Elastic energy and stretch reflex, as well as mechanical potentiation (ie., RFE) Swift movement utilizes both-to get max height

Question 51

Slow SSC

Answer 51

Slower eccentric phase, with less explosive concentric phase -Less stiff joint, longer contact times, greater neruomuscular activity in the concentric phase -Contact time >250ms Primary mechanisms: -Active state, neural potentiation, and mechanics of contractile component

Question 52

Mechanics of the contractile unit: slow SSC allows for

Answer 52

- more work to be donw by contractile until over a greater distance (work=force x distance)- squat further= increased distance -too fast it may "fall down" the power curve

Question 53

spinal interneurons

Answer 53

intricate network of interneurons can design simple to highly comples patterns of movmenet based on input from various locations most input to alpha motor neuros is mediated by a complex netwek of spinal interneurons

Question 54

interneurons receive input from

Answer 54

-prinmary sensory axons -descending axons from brain -collaterals of lower motor neuron axons -other interneurons

Question 55

Reciprocal inhibition

Answer 55

reflex arc using spinal interneurons to support simple monsynaptic reflexes (eg stretch reflex) -contraction of one muscle accompanied by relaxation of its antagonist muscle.

Question 56

Withdrawal reflex

Answer 56

reflex arc used to withdraw limb from aversive stimulus -Excitatory input for multiple ipsilateral motor units What about staying upright? when pull foot away

Question 57

Crossed-extensor reflex

Answer 57

Reflex arc for extensors and flexors om opposite side -Excitatory and inhibitory for ipsilateral and contraleral motor units Note all positive from the sensory neuron. It is the job of the interneurons to create other responses. -Pain on R-flex on R. at same time inhibitaory response-extensors (so don't get contract) on the other side... if flex R leg, then L needs to go opposite--> extensors excite and flexroes relax

Question 58

Central pattern generators

Answer 58

-Circuitry for many rythmic movements reside in spinal cord. Off & On (initiate pattern), during repetitive movement-don't want to think/ fire individually- offloads job to spinal cord. -complex network of sensory, motor and interneurons -evidence from animal spinal transections (lamp rays). Measured bursts of rythmic and coordinated activity arising for input (from SC) that was constant. SC in soultion that gets max firing (should see constant full firing) but see alternating activity (rythmic coordingated from central pattern generator)

Question 59

Central pattern generators: Controlled by two "half-centers" of spinal neurons

Answer 59

-Mutually inhibiting halves that produce alternating bursts of flexor and extensor activity -Rythmic activity will continue as long as input exists -Circuitry for walking resides in the lumbar/sacral spinal cord

Question 60

subdivisions of central pattern generators

Answer 60

rythm generators and pattern generators

Question 61

central pathway generators: Rythm generators

Answer 61

setting the timming of patterns to be generated

Question 62

central pathway generators: pattern generators

Answer 62

sending the required pattern of muscles activations

Question 63

central pattern generators: descending control

Answer 63

input from brain initiates and adapts central pattern generotros -can influence both rythm anf pattern generation neural pools ie injury, icy weather, tip toe walking

Question 64

Gait retraining

Answer 64

changing the mechanics of how you walk or run -easy to override motor patterns or central pattern generotors for short period very difficult to "rewrite" them- long term

Question 65

central pattern generators sensory information can...

Answer 65

influence both rythm and pattern

Question 66

central pattern generators: stepping in cats

Answer 66

procetion -amount of stretching an regulate the stance phase -cats can match speed of treadmill, through central pattern generators alone (after trained/electrical/drug stim) Sensory information from the skin: -stimulaton to dorsal side fo paw causes pattern with increased flexion to avoid a tripping hazzard (mov eit out of way) -only impacts during swing no input from brain its just the CPG

Question 67

central pattern generators adjustments

Answer 67

patterns are continually adjusted from higher and lower inputs unconcious but can adapt conciously (brain)

Question 68

crtitisims of CPG evidence

Answer 68

-most evidence from fictive movments -reflexes possible explination

Question 69

CPG- fictive movment

Answer 69

fictive movment: electrical activity suggestive of movment - electircal acitivty related to movment (in spinal cord) -primary source of evidence for CPGs -resemble locomotion but are not true locomotion

Question 70

CPG- reflexes still present

Answer 70

what if its reflexes doing all the work? We said the reflexes can "influence" the rythm and pattern of the CPG but.. brain isn't inputing- it just starts the system -what if the reflexes themselves are doing all the work? -Simulations suggest this is possible (in theory)

Question 71

Directly activating a CPG

Answer 71

Electrical stimulus of spinal cord in SCI patients -consistent stimulating leads to intermittent activating of muscles (fictive movment)- some flex/ext activation -why might the activation near the dorsal spinal roots and dorsal column be problematic to definitvely determing the existance of a CPG?

Question 72

Directly activating a CPG- why is this experiement not a definitive answer

Answer 72

1. Where is the stimulus -dorsal region of the SC (where msucle spindle and proprioceptie info comes in- could be sparking the reflex) -could just be providing fake peripheral stimulus (ie reflexive information) 2.Most didn't really look like walking -back to "fictive movement" -could it relate to other movments? can we recreate these pathways pharamacologically?

Question 73

Evidence for CPGs in walking (humans)

Answer 73

-Animal models -stepping reflexes in infants as foundtation for adult locomotion -spontaneous or evoked activation patterns SCI patients -Effective circuitry for controlling robotic locomotion

Question 74

Evidence against CPGs in walking (humans)

Answer 74

-No direct locomotion example in humans (vs cats) -most is "fictive" -Could simply be reflex-based

Question 75

do humans really use CPGs in walking- conclusion

Answer 75

-our interpretation is that taken together, these faces underpin the view that CPGs do exist int he human spinal cord -perhaps a better question for future research is to what extent do CPGs control out locomotion (lots of higher order control in humans vs ther animals)

Question 76

Spinal cord injuries (SCI)

Answer 76

Produce sensory, motor, and/or autonomic disfunction -complete vs incomplete -Pararaplegia vs tetrapelgia (quadraplegia) -Can be direct trauma or vascular insufficiency

Question 77

Location of injury- complete: cervical

Answer 77

-c1-c5: often fata- inability or difficulty breathing (diaphragm C3-C5) -C6-C8: retain head/neck movement, ability to breathe and speak, along with some arm movement

Question 78

Location of injury- complete: Thoracic

Answer 78

T1-T6: Loss of upper chest/back mucles, arms fully functional T7-T12: Retain greater control/balance of core while standing

Question 79

Location of injury- complete: Lumbar

Answer 79

L1-L5: loss of lower limb function and some bowel/bladder dysfunction

Question 80

Location of injury- complete: Sacral

Answer 80

S1-S5: most function in legs (ability to walk), loss of bowels/bladder function and some sexual function (still exists on reflexive function of injury is higher up (local control)- but if damage as S1-S5 reflexes are impacted and loose control

Question 81

Spinal shock

Answer 81

immmediate clinical findings following a SCI -temporary loss or depression of all or most spinal reflex acvitivty below the level of the lesion -Does not necessarily relate to the severity of the underlying SCI -4 distinct phases- from loss of reflex to return to hypersensitive and increased spasticity; can last 1-12months

Question 82

Spinal shock - 4 distinct phases

Answer 82

from loss of reflexes to gradua return to hypersensitive and increased spasticity--> relates to fine tuning length of muscles (gamma loop slide)- muscles tighter posty injury because of alpha-gamma coactivation- tells us how tight to contract. Descending control; infor lost with SCI- muscle spindles working in dark (doing nothing initially)- eventually alpha-gamma overactivates (hypersensitive to any stretch of muscle) get very sensitive spastic muscles -can last 1-12 months

Question 83

Spinal shock and neuroplasticity

Answer 83

extensive nerural reoganization nad plasticity has been demonstrated in SCI and associated with functional recovery -Occurs only in axons near cell body (local connections) -Long-distance axonal regeneration is stil not possible (ie motor cortex to alpha motor neuron) Paradigm shift to maximize this local effect through intensive training eg, weight-bearing activities, functional electrical stimulation, locomotor trianing

Question 84

SCI and CPGs

Answer 84

From what we know about CPGs, how might this relate to SCI? -In incomplete SCI see increased locomotor function in those that did assisted treadmill training while animals appear to be unable to get by quite well on sensory input, human remains much more dependent on supraspinal input to maintain the locomotor patterns Sensory feedback pathways can shape locomotion for animals, but insufficient in humans- kick start CPGs with neurotransmitter cocktail?

Question 85

Grading spinal cord injuries: american spinal cord injury association- impairment scale (AIS)

Answer 85

-describes a person's functional impairment following an SCI -Measures sensation at multiple points and key motions on both sides of the body Graded as A-E A-complete B-Sensory incomplete (no motor function) C-Motor incomplete (some sparing of motor function) d-Motor incomplete (has >50% muscle function) E-Normal

Question 86

Incomplete SCI; Brown-Sequard syndrome

Answer 86

-Damage to one half of the spinal cord (hemisection) -Trauma (penetrating injury) or compression (eg tumor) -Results in: Ipsilateral motor loss (coritcospinal) Ipsilateral touch, proprioception loss (DCML) contralateral pain and temperature loss (spinothalmnic) Recall: point of decussation for pattern of loss

Question 87

Incomplete SCI; Anterior cord syndrome

Answer 87

-Damage to the anterior (and lateral) SC -Severe flexion onjury or lack of blood supply -Results in: Bilteral motor loss (corticospinal) Retention of biteral touh/proprioception (DCML) Biteral pain and temperature loss (Spinothalmic) *everyhting gone except dorsal comlom (touch)

Question 88

Incomplete SCI: Posterior Cord Syndrome

Answer 88

-Damage to the posterior SC -Trauma (penetrating injury) or lack of blood supply -Results in: Retention of bilteral motor function (corticospinal) Bilateral tocuh/proprioception loss (DCML) Retention of bilateral pain and temperature (spinothalmic)

Question 89

Incomplete SCI; Central cord syndrome

Answer 89

-Damage to the central SC -Degenerative spinal canal narrowing, hyperflexion (often in cervical spine) -Results: Greater loss (deficits) in upper limb function Variable loss of bilateral touch/proprioception loss Greater loss (deficits) in upper limb pain and temperature * greater upper limb loss as pain information is organized in a manner which the information for upper limbs is located deeper