Post Midterm #2 Flashcards
spinal reflexes
Automatic stereotyped motor response in reaction to a sensory stimulus
- stimuli from peripheral receptors
- circuity within the spinal cord
basic components of the spinal reflex loop
- sensory neuron
- interneuron
- motor neuron
muscle spindles sense _ and work to _
sense stretch and work to excite against the agonist muscle
how are spinal reflexes mediated
spindle mediated (often referred to as stretch reflex)
how are spinal reflexes elicited and mediated
elicited by: stretch of muscle fibers
mediated by: muscle spindles via 1a afferent and ascend via dorsal column : Medial Lemniscal Tract
what is the goal of the spinal reflexes (stretch reflex)
maintain muscle length
what are spinal reflexes comprised of?
two simultaneous reflexes
- autogenic excitation
- reciprocal inhibition
Autogenic Excitation
amplification effect of single 1a afferents
monosynaptic reflex (occurs 20-30ms)
Autogenic excitation: 1a afferents diverge and project to:
- alpha motor neuron’s of the same muscle
- motor neurons of synergist
Reciprocal Inhibition goal
facilitate the activation of the agonist/synergist muscles -> inhibit antagonist muscle
Reciprocal Inhibition
1a afferents diverge onto 1a inhibitory interneuron
1a inhibitory interneuron projects onto alpha motor neuron of the antagonist muscle-> inhibits antagonist
Golgi tendon organs
- sense muscle tension
- work to inhibit the agonist muscle
GTO mediated spinal reflexes:
1b Inhibition Reflex
how is the 1b inhibition reflex elicited and mediated
elicited by: active tension in muscle fibres
mediated by: Golgi tendon organs via 1b afferent, ascend via dorsal column medial lemnical tract
Goal : relax/inhibit muscle
what reflexes are the GTO mediated comprised of
- autogenic inhibition
- reciprocal excitation
autogenic inhibition
- 1b afferent projects to 1b inhibitory interneuron
- 1b inhibitory interneuron projects to alpha motor neuron of agonist muscle (inhibits agonist)
*disynaptic reflex (occurs 40-50ms)
reciprocal excitation
to facilitate relaxation of agonist muscle-> activate the antagonist
*1b inhibitory interneuron diverges onto another inhibitory interneuron
secondary inhibitory interneuron projects onto alpha motor neuron of antagonist muscle -> facilitates antagonist muscle
facilitation via inhibition of inhibitor
cutaneous mediated spinal reflexes:pathways
- polysynaptic reflex pathways
polysynaptic reflex pathways goal
withdraw from painful stimulus
how are the polysynaptic reflex pathways elicited and mediated
elicited by: painful stimulus
mediated by: nociceptors (pain receptors) via A or C fibres , ascend via spinothalamic tract
goal of polysynaptic reflex pathways
withdraw from painful stimulus
polysynaptic reflex pathways elicited and mediated by
elicited by painful stimulus
mediated by nociceptors (via a or c fibers)
polysynaptic reflex pathways comprised of two simultaneous reflexes
flexor withdrawal reflex and crossed-extensor reflex
flexor withdrawal reflex
coordinated response in limb flexor muscles to withdraw from the pain
- A-fibres project to excitatory interneuron to excite flexor alpha motor neurons
- extensor motor neurons inhibited allow flexors to pull away from the pain A-fibres project to inhibitory interneuron
crossed extensor reflex
opposite response in opposite limb of the flexor reflex
- functions to stabilize body so other limb can move away from pain
crossed extensor reflex
A fibres project to excitatory interneuron: to excite extensor alpha motor neurosn and A fibres project to inhibitory interneuron: to inhibit flexor alpha motor neurons
flexor and crossed extensor reflex for
protective mechanism:
- flexor: withdraw from stimulus
- crossed-extension reflex: to stabilize body
stretch reflex take aways
autogenic excitation
reciprocal inhibition
1b inhibition reflex
autogenic inhibition
reciprocal excitation
flexor and crossed extensor reflex
flexor reflex: flexor=excited, extensor=inhibited
crossed-extensor: flexor= inhibited, extensors= excited
what is recurrent inhibition
negative feedback mechanism
- Acts as a limiter or governor to prevent over activity of the muscle
Recurrent inhibition rate of discharge is
proportional to the rate of discharge associated with motor neuron (increase MN activity=increased renshaw cell activity)
tetani
bacteria causing tetanus
- releases toxin which prevents Crenshaw cells from releasing Glycine
what does tetani prevent
prevents recurrent inhibition
- leading to hyperactivity of motor neurons
- severe persistent muscle activation
- tetanic spasm
pre-synaptic inhibition =
one pre-synaptic neuron inhibits another by releasing GABA
- leads to downstream decrease in post-synaptic neuron activity
pre synaptic inhibition is
communication via an axo-axonal synapse
- inhibition on the pre-synaptic neuron
inhibition on the pre-synaptic neuron causes
- Ca2+ channels can’t open
- decrease Ca2+ influx in presynaptic neuron
- reduction in neurotransmitter release onto post-synaptic neuron
can we train our reflexes through pre synaptic inhibition?
yes: use can train it to condition the Reflex depending on what the task requires
what are the three conditions we can train or reflexes through pre-synaptice inhibition
- control = reward after every stimulation
- H reflex up = reward when reflex increases
- H reflex down = reward when reflex decrease
vestibular end organs function
sense head motion and project information regarding head motion to vestibular nucleus
vestibular nucleus projects to
muscles in body to elicit reflexive movements to compensate for head motion
3 types of vestibular reflexes
- vestibule-ocular reflex
- vesibulocolic reflex
- vestibulospinal reflex
vestibulo-ocular reflex function and projection
stabilize gaze and project from vestibular organs to ocular muscles
Vesitublocolic reflex function and projection
function to stabilize head and project from vestibular end organs to muscles of the neck to bring back to neutral
vestibulospinal reflex function and projections
maintain upright balance and project from vestibular end organs to muscles of the limbs
electrical vestibular stimulation
small electrical currents activate vestibular afferents
- mimics vestibular affront activity we would see if vestibular end organs were actually sensing head motion
explain the physiology from electrical vestibular stimulation
central nervous system believes vestibular afferent activity is coming from the actual head motion (we think we are falling)
two methods of assessing standing balance in the involvement in different settings
- quiet standing (COM or COP)
- external perturbations (reactive balance control)
3 different context needed to maintain balance
- during quiet standing
- during unexpected perturbations
- during self-initiated movements
postural control
controlling body position in space to maintain stability and orientation
centre of mass
location where all the mass of the body is concentrated
centre of gravity
vertical projection of COM to ground
centre of pressure
point of application of vertical ground reaction force exerted on body
base of support
region bounded by body parts in contact with surface or surfaces
quiet standing
when trying to stand perfectly still with some body sway
how is amount of sway affected by body alignment
better alignment=less sway
stable posture exist if
vertical line of action of the force of gravity passes through whole body
when the body is aligned with line of gravity
- minimizes energy required to maintain balance
- maximizes stability
can the body be at equilibrium and stable even while strayed from exact point of equilibrium?
yes
a person has stable posture as long as
line of action of COG is within base of support
postural stability depends on
- base of support
- line of COG distance from edge
- height of COM increased or decreased2
sway is a
exploratory mechanism
standing balance requires..
constant sensory input to know where we are positioned in space
is sway cortical or subcortical
predominantly subcortically driven
contribution of each sensory sysytem is typically assessed by
- removing or altering/distorting sensory information available
- using patient populations where the sensory information absent or distorted
standing balance sensory contributions
1) vision
2) vestibular
3) proprioception
when there is no visual input, postural sway increases between
30-40%
with eyes closed COM displacement is,
greater, following linear translation of support surface
physical perturbation
- eyes closed, physical displacement
visual perturbation
ex) - sitting in a car, car next to you starts to move and you perceive that you are moving
is vision involved in quiet standing
yes
how do we know vision is involved in quiet standing
when we remove vision, there’s greater sway :
- indicated by greater movement of COP/COM
- altering of optic flow gives illusion that a person is swaying in one direction (they will move the COM in opposite direction)
Vestibular standing balance: head tilting
COP RMS increase with head tilt even when visual input remains constant
proprioception standing balance
reduced sensory feedback from legs and feet causing increased postural sway
methods of standing balance being effected by proprioception
- vibration to muscle
- cooling feet or applying anesthetic
- loss of limb or somatosensory inputs
how to aid standing balance through proprioception
add proprioceptive feedback with touch
- cutaneous sensory information from the hand can substitute loss of vestibular function
Blind individuals sensory abilities explained
blind participants have a SMALLER COP-COM displacement compared to sighted with eyes closed
COM
centre of mass
COP
centre of pressure
vestibular loss patients experience increased sway immediately after loss due to
adopting abnormal alignment and increase in sway behaviour
over time vestibular loss patients,
adapt to loss of vestibular info
de-afferented patients definition
all somatosensory information is lost
standing balance reduction in aging associated with
reduced muscle strength
reduced sensory function
increased postural sway
response to perturbations slower and greater with muscle activity
how does postural control system maintain a desired orientation and stability if there is an external perturbation
- postural control system comes into play in response to a destabilizing external force or perturbation
- uses feedback mechanisms where CNS responds to info during and after a movement to restore stability
muscle synergy
particular muscles work together in synergy to achieve the task
* can occur without voluntary control
2 main responses of reactive balance
- ankle strategy
- hip strategy
*two strategies activate opposite muscles
*can have a mixed (ankle + hip response)
ankle strategy
involves distal to proximal sequence of muscle activation
hip strategy
involves proximal to distal activation
reactive balance other strategies
- ankle strategy
- hip strategy
- suspensory strategy
- step strategy
reactive balance is
context-dependent
small balance perturbations result in use of
ankle strategy
larger perturbations result in use of
hip strategy and stepping strategy
when does strategy switch occur in reactive balance
- at different perturbation magnitudes depending on context
if support surface is narrowed, strategy used will be:
the hip strategy at a smaller perturbation magnitude
cerebellar disorder causes problems with
scaling response amplitudes (hypermetria)
cerebellar response,
response cannot scale properly to amplitudes,
- response is too large and too long so they overshoot and must activate antagonist
hypermetria
a condition of cerebellar dysfunction in which voluntary muscular movements tend to result in movement of bodily parts beyond the intended goal
reactive balance is
context dependent
locomotion
a controlled rhythmic act of moving our body from one place to another and involves repeated cycles of movement
locomotion involves sensory contribution from
visual, proprioceptive, and vestibular information
phases of the step cycle can be broken down into
stance and swing phases
stance
starts with heel contact,, is 60% of step cycle
*double support of first and last 10% of stance phase
swing
starts with toe-off (40% of step cycle)
locomotion different gaits
walking and running
walking
locomotion in which the legs will move in anti phase
- one foot or other is in contact with ground at all times
- includes a period of time when both feet are on ground at same time (DOUBLE SUPPORT)
- plantigrade (place whole sole of foot on ground)
running
locomotion in which the legs move in anti phase
- both feet never on the ground at the same time
- includes period when both feet off ground (FLIGHT PERIOD)
- Plantigrade and Digitigrade
plantigrade
slow jogging
digitigrade
only digits (toes) on ground sprinting
double support in walking
includes period of time when both feet are on the ground at the same time
flight period in running
period where both feet are off the ground
phases of the step cycle in running
stance, flight period, swing
walking phases of the step cycle
double support, stance, swing
Muscle __ as it produces force in eccentric muscle contraction
lengthens
walking locomotion
neural control of gait:
1) heel contact
2) toe-off and swing initiation
3) swing
heel contact neural control of gait explained
- decelerate foot and absorb impact eccentrically
- contract ankle dorsiflexors and contract knee extensors
neural control of gait: toe-off and swing initiation
- propulsion forward and forward acceleration of thigh is concentric
- contraction of plantar flexors and contraction of quadriceps (specifically rectus femoris)
neural control of gait: swing
- toe clearance= concentric
- forward deceleration of thigh= eccentric
- contraction of dorsiflexors
- contraction on hamstrings
does the cortex control the rhythmic nature of locomotion (muscle activity patterns)
no
How are the alternating patterns of muscle activities controlled for locomotion
- the alternating activity must result from spinal cord mechanisms from CPG
CPG central pattern generator
groups of neurons in the spinal cord organized to alternate rhythmic control of locomotion
CPGS are specialized for
a wide range of rhythmic activities: walking, swimming, breathing, swallowing, vomititng
targeted therapy for spinal cord injury rehab can be done through
gait recovery
is there such thing as spinal walking in humans
- children below 1 years old have no CORTICOSPINAL INPUT onto alpha motor neurons which control lower limb muscles
sensory modulation: sensory feedback is important for
- controlling phase transitions ( ex. stance to swing phase)
- correcting for unexpected disturbances (ex. stumbling corrective response)
- initiate walking
- regulating level of muscle activity
controlling phase making transitions from stance to swing: timing of transitions:
muscle spindles in hip flexor signal when swing phase should be initiated
- inhibit knee extensor and aid in onset of knee flexor activity
stumbling corrective response
stimulate cutaneous and muscle receptors
response depends on the phase of locomotion
- stimulate top of foot during swing to have automatic flexion response to step over the obstacle
- stimulate top of the foot during a stance to have extension of limb to push over obstacle, shortening/accelerating through the stance phase
