L6 Flashcards
posture and locomotor control
- righting reflex in decerebrated frog vs spinally-transected
- scratch reflex
present i D but not s-t
scratch = pressent in both = brainstem mediated.
function of postural and locomotor control
control positions of body segments in stable relation to each other and to move the body over varying terrain
main postural reflexes: stretch placing hopping vestibular righting neck
s = muscle stretch
p - object in way, move foot around and place
h - shift in centre of gravity, catch self w foot.
v - head acceleration
r- gravity and pressure on body
n - head movements
response to stretch reflex? integrated?
resist stretch
spinal cord
placing - response? integrated?
lift and place foot forward
spinal cord
hooping response? integrated?
step to catch self
spinal cord, brainstem
vestibular response? integrated?
stabilize head, extend limb in reaction to acceleration
- midbrain
righting response? integrated?
right body
brainstem
neck
think yoga moves
head back, open arms and chest
head forward = contract, close chest.
head left = extend ipsilateral side.
brainstem
context-dependence and adaptation of postural stretch-reflexes: maintain postural stability
ankle extensor stretch = reduce body sway if foot is displaced horizontally, so CNS augments = less sway.
toe-up rotation = destabilizing. CNS attenuates in successive trials. more sway.
context -dependence and adaptation controlled by?
postural muscles activated involuntarily because voluntary movement of limbs
controlled by cerebellum and brainstem reticular fromation. - back actviated before grab something with hand.
stable, variable-speed movement across unpredicatble terrain
solution?
complex cyclical coordination of muscles
adaptation w vision, proprioception, skin receptor feedback
automaticity to “free” higher centers in CNS
locomotor step cycle & muscle activity
stance - extensor
swing = flexor
transition: bi-functional muscles
digitigrade gait
vs plantigrade
walk on toes
walk on flat foot
first basic question:
neural network that sequences muscles in mammalian locomotion in the spinal cord or supraspinal centres?
clinical conditions evidence for supraspinal pattern generation
stroke: poor, absent flexion of hip.
spinal cord injury: paralysis below level of spinal transection
PD: inability to initiate locomotion, suffling steps
cereballar ataxis: unsteady gait, scissoring, high-stepping.
graham browns experiment in cats
anesthetized cats decerebrated, abolishing consciousness.
- leg flexor, extensor could still generate alternating, rhtyhmic movments in response to strong sensory input & elec stim of brainstem.
CPG - in spinal cord
experimental evidence supporting spinal pattern generation
- activating spinal cord below complete transection can elicit locomotr rhyth,
= needs descending drive
clinical evidence support spinal pattern generation
locomotor rhyth, elicited in parapalegic with spinal cord transections with e.stim, clondifine, cyproheptidine.
clondidine- mediate presynatpic inhibition, reduce spasticity and facilitate locomotion.
recovery from cerebellar damage, cortical damage can walk normal.
experimental evidence that descending drive in important
high decerebrate cats - intact midbrain adapt to speed. caudal transections cannot.
- e. stim in MLR of midbrain of decerebrate promotes locomotion. can increase step cycle rate and locomotor velocity.
TMS affects leg flexor more than extensor
neurons rhythmically co-activated with leg muscles, indicating pattern generation role.
second basic question:
locomotor CPG entirely within CNS or sensory afferents part of it?
hypothesis: intrinsic mechanism capable of generating locomotor pattern without sensory input.
- command neurons = activity spontaneously bursts in rhyth,. elicit and coordinate rhythmical activity of neurons controlling limb muscles in absence of sensory input.
experimental evidence for basic rhythm generator in CNS
- rhythmical activity of leg muscles elicited in de-afferented animals.
experimental evidence for CPG being entirely in spinal cord
fictive locomotion: rhythmic activity in decerebrated animals. require IV drugs or steady electrical stimulation of sensory nerve roots to provide generalized CNS excitation.
clinical evidence that sensory contributes to locomotor pattern generation
gait in de-afferented abnormal. incorrect timing, muscle sequencing
experimental evidence that sensory afferent contributes
stretch reflexes - sensory. affect muscle activation
reflex responses modify locomotor pattern
bule-based phase swtiching = phase transitions between swing and stance phases triggered by sensory input
if-then sensory-triggered rules for gait
swing onset: if stance, extensor force low, leg extended, contralateral foot on ground THEN flex and swing
stumble: IF in swing, skin stimulus THEN swing forward and place.
BUT IF in stance and skin stimulus THEN maintain ground contact
backward gait: IF stance, extensor force low, hip flexed forward and contralateral foot on ground THEN flex and swing back.
third basic Q
answer?
is spinal locomotor CPG localized or distributed along several segments?
generated by single segment of lumbar and sacral spinal cord, even half of single segment. rostral segments set rhythm generated by caudal segments.
overall conclusions of control system
CPG in spinal cord. strong modulation from descending and sensory inputs.
gait initiated by descending drive from BG and hypothalamus.
desired velocity of body may be basic descending command signal.
-
decerebrate locomotive cats. highly cerebrate, walk spontaneously if treadmill starts = increased stimulation of midbrain = increase speed.
gait velocity command from BG and hypo, mediated by MLR. different CPG neurons, force feedback.
different neurons in CPG responsible for?
speed of movement, duration of phases.
which muscles activated, how strongly activated.
