Test 5 Flashcards
upper motor nuerons
-cerebral cortex and branstem
-can only connect to muscle through lower motor neurons (which are directly connected to muscle)
Lower motor neurons
-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)
lower motor neurons can receive input from:
-upper motor neurons
-interneurons in spinal cord
-sensory input
distribution of motor neurons in the spinla cord
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
how are motor neurons in the spinal cord organized
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
What are the 2 primry types of lower motor neurons
alph motor neurons and gamma motor neurons
alpha motor neurons
directly trigger the contraction of muscles for movement
gamma motor neurons
regulate muscle tone and control sensitivity of muscle spindles
Alpha motor neurons: motor unit
motor neuron and all the fibers it innervates
alpha motor neurons: motor neuron pool
All the alpha motor neurons that innervate a single muscle
excitation contraction coupling
-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
sliding filament model of contraction
Ca2+ binding to troponin allows myosin heads to bind to actin-myosin heads then pivot, causing filament to slide.
fundemental properties of contraction: force length relationship
-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…
fundemental properties of contraction: force velocity relationship
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
Titin
“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)
residual force enhancement
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.
Titin-residual froce development
-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
EMG
-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
Application of EMG
-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
EMG limitations
-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).
Proprioception- neurons
group 1 sensory neurons- can be further subdivided into 1a and 1b axons
Proprioception: 1a axons
-Largest and fastest (myelinated)
-Excitatory synapes with spinal interneurons and directly on alpha motor neurons
-muscle spindles (mount of stretch)
Proprioception: 1b axons
-slightly smaller/slower
-inhibitory synpases with spinal intreneruons
-Golgi tendon organ (amount of force)
Muscle spindles
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)
the stretch refelc (myotatic reflex)
when a uscle is pulled (stretched), it pulls back (contracts)
-reists changes in muscle length
-important for maintaining limb position or posture
myosynpatic stretch reflex
-primary sensory neuron (1a-muscle spindle)
-primary motor nueron (alpha motor neuron)- reflexive
how could be confirm the function of this sensory neuron/structure?
the stretch reflex (myotatic reflex)
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
How muscle spindles stay response to stretch?
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
Fine tuning muscle length with the gamma loop
- 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) - Muscle spindle detects muscle is too long
3.Ia axons send signal to alpha motor neuron - Alpha motor nueron activate extrafusal fibers to shorten muscle
Gamma Bias
-Constant activity to keep intrafusal fiber taught
-Firing rate increases or decreases to compensate for changes in exrrafusal fiber length
Fusimotor gain
-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
Gamma (motor) loop
The loop between the muscle spindle (sensory fiber + gamma motor neruon) and muscle (alpha motor neuron)
Gamma bias
Base level of firing for the inrefusal fibers to keep sensor online
Fusimotor gain
Ramping up/fine tuning the sensitivity of this loop to identify small changes
fusimotr gain example
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
fusimotor gain- static response
-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
fusimotor gain- dynamic response
-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
static stretch
-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
dynamic stretching
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!)
Golgi tendon Organs
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
joint receptors
-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
The stretch shortening cycle (SSC)
Involces an eccentric stretching of the muscle, immediately followed by an enhanced concentric contraction
SSC potentiation- verticle jump example
jump height: squat vs contermovment jump
enhanced concetric contraction
mechanisms of ssc
1.Elastic energy
2.stretch reflex
3.neural potentiation
4.active state
5.mechanical potentiation
mechanisms of ssc: elastic energy
-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)
mechanisms of ssc: Stretch Reflex
-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?
mechanisms of ssc: neural potentiation
-Electromechanical delay
-Picking up the “slack” in the unit (force producing unit)
-30-110ms
mechanisms of ssc: active state
-Time for cross-bridge to build up force
-100ms-1s
mechanisms of ssc: mechanical potentiation
-residual force enhancement
Fast SSC
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
Slow SSC
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
Mechanics of the contractile unit: slow SSC allows for
- 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
spinal interneurons
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
interneurons receive input from
-prinmary sensory axons
-descending axons from brain
-collaterals of lower motor neuron axons
-other interneurons
Reciprocal inhibition
reflex arc using spinal interneurons to support simple monsynaptic reflexes (eg stretch reflex)
-contraction of one muscle accompanied by relaxation of its antagonist muscle.
Withdrawal reflex
reflex arc used to withdraw limb from aversive stimulus
-Excitatory input for multiple ipsilateral motor units
What about staying upright? when pull foot away
Crossed-extensor reflex
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
Central pattern generators
-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)
Central pattern generators: Controlled by two “half-centers” of spinal neurons
-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
subdivisions of central pattern generators
rythm generators and pattern generators
central pathway generators: Rythm generators
setting the timming of patterns to be generated
central pathway generators: pattern generators
sending the required pattern of muscles activations
central pattern generators: descending control
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
Gait retraining
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
central pattern generators sensory information can…
influence both rythm and pattern
central pattern generators: stepping in cats
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
central pattern generators adjustments
patterns are continually adjusted from higher and lower inputs
unconcious but can adapt conciously (brain)
crtitisims of CPG evidence
-most evidence from fictive movments
-reflexes possible explination
CPG- fictive movment
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
CPG- reflexes still present
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)
Directly activating a CPG
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?
Directly activating a CPG- why is this experiement not a definitive answer
- 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?
Evidence for CPGs in walking (humans)
-Animal models
-stepping reflexes in infants as foundtation for adult locomotion
-spontaneous or evoked activation patterns SCI patients
-Effective circuitry for controlling robotic locomotion
Evidence against CPGs in walking (humans)
-No direct locomotion example in humans (vs cats)
-most is “fictive”
-Could simply be reflex-based
do humans really use CPGs in walking- conclusion
-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)
Spinal cord injuries (SCI)
Produce sensory, motor, and/or autonomic disfunction
-complete vs incomplete
-Pararaplegia vs tetrapelgia (quadraplegia)
-Can be direct trauma or vascular insufficiency
Location of injury- complete: cervical
-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
Location of injury- complete: Thoracic
T1-T6: Loss of upper chest/back mucles, arms fully functional
T7-T12: Retain greater control/balance of core while standing
Location of injury- complete: Lumbar
L1-L5: loss of lower limb function and some bowel/bladder dysfunction
Location of injury- complete: Sacral
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
Spinal shock
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
Spinal shock - 4 distinct phases
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
Spinal shock and neuroplasticity
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
SCI and CPGs
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?
Grading spinal cord injuries: 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
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
Incomplete SCI; Brown-Sequard syndrome
-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
Incomplete SCI; Anterior cord syndrome
-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)
Incomplete SCI: Posterior Cord Syndrome
-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)
Incomplete SCI; Central cord syndrome
-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
