PSL201Y1 Lecture Notes - Lecture 16: Central Pattern Generator, Cpg Site, Flat Feet

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Published on 10 Nov 2011
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PSY300H1F L16; Oct. 19, 2011
Central pattern generator (CPG)
• Reflexes can perform simple elements of movements,
but not complex patterns by selves – need central
organizing generator to plan&structure a functional
movement
• e.g. stretch reflexes cannot restore postural stability
after a perturbation: a centrally coordinated response is
required
• posture and movement are ‘programmed’ by CPGs
(central pattern generators), functional networks of
neurons
Locomotion: leg step cycle
• The step cycle of each leg during walking is
programmed by a network of neurons within the
intermediate zone of the lumbar cord
• properties of network: - vaguely known in most
animals
• 1) pacemaker neurons, diffuse excitation
automatically produce depolarization&hyperpolarization
in endless seq aqs long as given background excitation
(membrane in right ballpark) – due to ion channel pops
present interacting w each other, constantly alternating
• 2) reciprocal inhibition – built right in; flexors then
extensors…
• 3) phase-dependent reflexes – used when positive
influence on movement; turning off when working
against movement 2 phases subdivided into 2
phases
Swing when in air, not
supporting weight: F starts w
toe coming off ground (pure
flexion, leg suspended in air)
E1 when foot brought back
to ground (extension, mostly
passive – gravity doing work
so minimal muscle activity)
Stance when on ground,
supporting weight: E2 heel
strike, flat foot at end, weight
right over ball of foot, totally
supporting weight; E3 starts
when heel lifted off ground,
power stroke pushing against
substrate w big toe, then toe
comes off swing phase
‘Half-center’ structure
• CPG organized into 2 half-centers:
• 1) flexor burst generator drives flexor motor nuclei (1st
part of swing)
• 2) extensor burst generator drives extensors (down
ventral part of brain matter, active for longer than flexor
burst generator so CPG asymmetrical – very typical)
• mutually inhibit one another
• both spontaneously active when not inhibited so
inhibition determines where activity is, infinitely more
important than excitation in NS
Flexor burst generator
• Flexion phase of swing has a fixed duration, regardless
of speed of locomotion – ex. Always lift leg up at same
pace in initial swing, extensors cause changes afters
• flexor neurons network has a build-up of inhibition that
eventually stops the burst of action potentials after a
few ms end of activation of flexor motoneurons
• reciprocal inhibition of extensor burst network ceases
extensor network active
Generators – reciprocal inhibition, ossicilation – 1
active at a time; extend all way thru lumbar cord to
lower thoracic segments – long column, medial
location near central canal
Drive corresponding motor neurons on swing &
stance
Reflex loops operating on them – especially
Extensor Burst gen
Stretch flexes, cutaneous reflexes (extensive
thrust – reinform activity in extensor burst gen
while leg bearing weight)
Regulated by network:
Propriospinal (in spinal) – regulate reflex strength of
swing & stance
Spinoreticulothalamic neurons have pain-related
neurons near central canal – so when very painful
stimulus, tends to turn on some of these locomotor
networks
Stance Phase
• Variable duration depending on speed duration
• regulated by sensory feedback, important to
determine duration, stays in stance as long as
supporting weight so not internally determined by CPG
• phase-dependent reflexes:
• stretch reflex; gain increases to peak in E3 – loading
extensor muscles w body weight, stretching postural
muscles
• Golgi tendon reflex: mild positive feedback (instead of
normal neg) – action contraction activating golgi tendon
afferents
• extensor thrust: extension only during stance,
(reversed to flexion during swing phase); from
cutaneous mechanoreceptors in sole of foot, reinforce
extensor activity when pressure built from body weight
• During swing, no extensor thrust function, reflex
reverses fine
So is foot stimulated, get increased flexion than
normal, functional since means hit obstacle and
increase flexion to get over it instead of stepping
on hid
So dif connections in spinal cord, presynaptic
inhibition, easy for NS to change signal effect
Gain = output of reflex for given stimulus, always
giving same stimulus/stretch to muscle; fluctuates
dramatically
Strong during stance face, esp power stroke
Dramatically falls as get into swing no reflex
Strong during stance since loading extensor muscles
w body weight, so stretched; reflex helps adjust
muscle activity exactly to weight experiencing, so
CPG of spinal cord doesn’t have to exactly compute
how much activity required in muscle (impossible)
Adjustments that have to be made, otherwise
lurch all over
So the reflex makes fast, perfect accurate, fine
adjustment, micron level
Turn off in swing phase – exaggerated in human
since walk flat on feet not toes; tendency when lift
foot up for toe to drag against ground (cats don’t
have this probably since walk on toes)
So need to lift toes up (dorsal flexion), flexes
ankle extensor muscles but must be turned off
abruptly at onset of swing (since would move
foot down into ground on activation and prevent
movement, counterproductive)
EMG = electrical activity in muscle, 25-30% driven
by the stretch reflex, rest by pattern generator; so
reflex makes large contribution to counterbalance
loads exerted by muscles
Need for sensory control
• Essential to match muscle contraction to loading
conditions on the leg; these vary with every step and are
unpredictable
• reflexes provide automatic adjustment of extensor
contraction to load experienced
• sensory cues inform CPG for transitions when it is safe
to start next swing phase – when leg no longer bearing
weight
Transition to swing
• E3 phase stops (and thus disinhibits flexor burst
generator) only if:
• 1) leg is not bearing weight – extensor muscles not
stimulated
• 2) hip is extended – when removed all weight from leg
• 3) opposite/contralateral leg is in stance (bearing
weight)
• crossed projections thru commissural axons
(propriospinal connections) provide correct phaselinking
of CPGs on each side
Arm swings
• CPGs in cervical cord (neck region) program motion of
arms during walking
• flexion phase synchronous with contralateral flexion in
leg: diagonal pattern to cancel torque on trunk – so
when right leg lifted in flexion phase generate
counterclockwise torque, left arm is lifted and makes
opposite torque, torques cancel out across backbone
• phase-linking via propriospinal tracts (from one
segment of cord to another) - interconnections
Upper body balance
• Bipedal humans must produce postural compensations
in trunk and head to maintain stability on top of moving
legs
• takes a long time to learn how to walk on 2 legs; learn
how in 1 year, low better in next 15 yrs (inertia changes
as you grow)
• requires postural CPGs in reticular formation in
brainstem to coordinate upper body motion with spinal
step cycles
• spinally-injured patients cannot walk without trunk
support, lose these connections from spinal cord to
brainstem, CPGS still there so if on treadmill and support
upper body in harness then can walk using lumbar
Postural pattern
generators all in
brainstem, source of
reticulospinal tracts
Grps of neurons in nuc,
underneath 4th ventricle
Heavy projection down
spinal cord in ventral white
matter surrounding ventral
grey matter (containing all
motornuclei)
Bilateral projection, so on
both sides very potent
input for motor nuclei
Essential for programming
postural connections to
stay stable
Lost in spinal injury to
make bipedal locomotion
impossible
Keep head perfectly
stable on top of
trunk
Bobs up and down a
little btwn foot-falls
Angle of upright
position of head kept
constant, amazing,
other animals can’t;
ex. Pigeon heads bob
Bipedal Bird Waddle Penguins closest to us
but their whole body
bobs back and forth w
head
Mesencephalic locomotory region – executive level in
midbrain since not interested in details/patterns
•Midbrain ‘switch’ that turns on reticulospinal
locomotory CPGs, which then activate spinal CPGs
[locomotion starts with weight shift, i.e. postural change]
• governs speed of locomotion: the faster the rate of
impulses, the faster the locomotion; if fast enough then
break into a run (slightly different from walking, dif
neurons involved linking the two legs, dif pattern)
• not involved in pattern generation of muscle
contractions Located underneath
colliculi
Looking thru 4th
ventricle
MLR in reticular
formation, sort of
underneath inferior
colliculus deep inside
midbrain
Projects down to
postural nuc
Small direct
connection to
intermediate zone in
spinal cord – CPGs
Provides excitation of
whole system to start
locomotion
Postural Maintenance
• Organized in reticular formation of pons and medulla –
reticulospinal areas; correct gross perturbations, restore
balance and appropriate muscle activity, works up to
head from base of support (ex. Feet if standing, seat if
sitting) – logical progression
• relies on 3 sensory sources:
• 1) somatosensory; rapid, especially proprioceptive
(stretch receptors of muscles, golgi tendon receptors) –
detect deviations, some cutaneous; detect fine details
• 2) vestibular: rapid, upright gravitational reference
• 3) visual: slower system – so good in a predictable
mode for perturbations, but important vertical cues, and
motion cues in envt Look at centre of
deviation on force
platform
Looking at small area,
illustrate how posture
deviates in time
Most deviation in
anterior and posterior
– by toes and heels
Less deviation side to
side due to space
btwn feet
Even when deviating
far from optimal
centre of gravity, turn
around and pull back –
don’t fall flat on face
due to stretch reflex
making corrections to
keep you in centre
position, increasing
contractions to pull
you back – goes on all
the time
•many CPGs in brainstem – respiration, chewing, cyclic
patterns
Eye-head coordination – isn’t cyclic
• Movement to inspect novel visual stimulus is
programmed in superior colliculus
• computes how much (amplitude) & in what direction
gaze must be shifted to ‘foveate’ target
• sends same motor signal to extraocular and neck
motor centers
• sends same signal to neck & extraocular centres; so
eye-head coordination is function of VOR (does this fine
adjustment perfectly once turned on; impossible for s.
colliculus to do)
Collicular spatial map
• Position of activated cells in s. colliculus codes spatial
location of visual/auditory stimulus (localization
performed in i. colliculus, info dumped in the s. colliculus
map)
• where activity registered, specific pt in spatial map lit
up
• spatial map is calibrated for eyes/head facing straight
forward; calibrated started from centre 0 position –
assumes head/eyes at centre (sometimes skewed, so
cerebral cortex adjusts map)
• activated cells provide motor signal to shift gaze in
order to foveate stimulus.
Looking at one superior colliculus, right maps left
world of auditory & visual input
Centre of visual world straight ahead – anterior pole
where fixating
Upper half of opposite half on envt is medial half of
superior colliculus; lower half in lateral half
Horizontal meridian btwn upper & lower sides of
world; as get higher up get more medial (longitudinal
lines going up and down)
Medial lateral lines depict how far from midline
position/ fixation pole (2, 5, 10…) – lateral deviation
of anterior and posterior
Eyes driven to point of stimuli (pinpointed using
map), use VOR once head moves

Document Summary

Drive corresponding motor neurons on swing & Reflex loops operating on them especially. Stretch flexes, cutaneous reflexes (extensive thrust reinform activity in extensor burst gen while leg bearing weight) Propriospinal (in spinal) regulate reflex strength of swing & stance. Spinoreticulothalamic neurons have pain-related neurons near central canal so when very painful stimulus, tends to turn on some of these locomotor networks. So is foot stimulated, get increased flexion than normal, functional since means hit obstacle and increase flexion to get over it instead of stepping on hid. So dif connections in spinal cord, presynaptic inhibition, easy for ns to change signal effect. Swing when in air, not supporting weight: f starts w toe coming off ground (pure flexion, leg suspended in air) E1 when foot brought back to ground (extension, mostly passive gravity doing work so minimal muscle activity) Flexor burst generator: flexion phase of swing has a fixed duration, regardless of speed of locomotion ex.