MEDI258 lecture notes PDF

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MEDI258 (Human Neuromechani) Spring Semester 2021 Subject Coordinator: Jon Shemmell [email protected]

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LECTURE NOT WEEK 1 Recap: Generating Force w/ Muscle Neuromechanics: explain human motion via body dynamics, muscles, sensory organs & CNS Applications: exercise prescription, prosthetic design, humanoid robot design Encompasses: reflex control, spinal cord control (locomotion), voluntary movement, neural adaptations driving movement change * recap muscle function & structure * → sarcomere = smallest unit of contraction EMG = electromyography Excitation/contraction coupling: 1-3. Muscle fibre AP → fibre → activates sarcoplasmic reticulum 4. Calcium released 5. Calcium reuptake (sarcoplasm) 6. Calcium attach to Troponin → change actin filament structure 7. ATP binds to myosin head → detaches from actin Cross-bridge Cycle 1. Myosin head attached to actin filament 2. ATP bind → myosin → detaches from filament 3. Calcium bind → troponin (m→a) & ATP hydrolysed → power stroke (2pN force) 4. ADP released → myosin returns to base state EMG → measuring muscle force

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Differential amplifier captures signals (v2)

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Wave of negativity (depolarisation)

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Related to muscle force

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Determine amount of activity relative to time

Smallest unit of independent control = motor unit ●

Large muscle = ↑ innervation number

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Small muscle = ↓ innervation number

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High dexterity = ↓ innervation number ○

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Fewer fibres associated w/ every motor neuron

Low dexterity = ↑ innervation number ○

Highest control = 1:1

Type I: slow oxidative (ATP) Type IIA: fast oxidative (ATP) Type IIX: fast glycolic

Type S: slow, fatigue resistant (type I) Type FR: fast fatigue resistant (type IIA) Type FF: fast, fatigable (type IIX)

WEEK 2 Recap: Muscle Mechanics ●

Muscle length effects strength: ○

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Needs to have filament interaction to produce force ■

No actin overlap

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Actin & myosin overlap

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High shortening → ↓ time for myosin to interact w/ actin → ↓ force

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0 (isometric) → ↑ % force production

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Contractile element = sarcomere

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Parallel elastic element (CT) ○

In line...force = sum of fibre forces

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Low contraction speed

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Series elastic element (CT) ○

Passive = tendon

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Active = w/in sarcomeres

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Head to tail...force = average of each fibre

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High speed contraction

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Muscles have diff combos of series & parallel

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High penetration levels → slows velocity → allows for ↑ force

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>10% tendon stretch = damage ○

Tendon not very elastic

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Stiffness relationship → tendon = ↑ stiff ∴ can store lots of elastic energy

Joint Mechanics ●

Most muscles contribute to >1 axis of rotation

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Compensate for off axis torques

Stretch-Shortening Cycle ●

High force, dynamic movement

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Work = force x displacement (positive work)

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4 ways of contribution ○

Storage and release of elastic energy (mechanical model)

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Increased time for muscle force development

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Reflex action (neurophysiological model)

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Force potentiation

Reflexes (sensing muscle actions) ●

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5 common elements ○

Sensory receptor

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Afferent neuron

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CNS processing (through 1 or more synapses)

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Efferent neuron

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Muscle

Muscle receptors located in spindles ○

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Encapsulated nerve endings

WEEK 3 Recap: Reflex Neuromechanics Role of Reflexes in Complex Movements 3 levels of complexity 1. Spinal 2. Automatic behaviours → complex circuits 3. Voluntary actions Withdrawal Reflex → Protective ●

Nociceptor (pain)

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Skin

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Afferent impulses transmitted → excitatory interneuron

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Motor neurons of flexor muscles activated

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Motor neuron of extensor muscles inhibited

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Distal segment drawn away from pain source

Crossed Extensor Reflex (Extension of ^) ●

Extension of withdrawal reflex (WR)

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More complex than WR

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Initiated by same stimulus as WR ○

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Occur simultaneously

WR + excitatory interneurons activate motor neurons of opposite limb extensor muscle

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Flexor muscle of opposite limb inhibited

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Limb opposite to painful stimulus extends

Reflective Stability → response to enviro stimulant ●

Transcortical Stretch Reflex

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SR transmitted to sensorimotor cortex

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Motor response transmitted → via corticospinal tract to same muscle as spinal stretch reflex

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Latent as longer pathway

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Reflex observed in both arms (bilaterally-projecting corticospinal neurons)

Know likelihood of instability is high? 1. Change reflex sensitivity (bigger response) → feedback 2. Change ‘preparatory set’ (higher gain) → feed-forward/feedback 3. Co-contraction early (↑ limb stiffness) → feed-forward 4. Change posture (widen BOS, ↓ COM) → feed-forward 5. Respond to postural ‘errors’ early ∴ maintain balance Research Q’s To what extent are reflexes flexible? ●

Sensitivity dependant on stretch

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Reflexes modulated according to amount of stability provided by environment

How smart are reflexes in 3D situations? ●

Can reflexes change amplitude depending on the direction of instability? ○

Eg. surfing: more stability on longitudinal axis of board

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Eg. screwdriver: ↑ stability in direction screwdriver is being pushed, ↓ in all other directions

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Amplitude change dependant on: ○

Amount of ongoing muscle activity

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Direction of perturbation (↑ stretch = ↑ response)

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Direction of instability from robot

∴ reflexes are very smart

How might preparatory set assist postural stability?

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P set can influence both cortical reflexes & subcortical StartReact responses

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Co-contraction ↑ as enviro stability ↓

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Ankle → ↑ in intrinsic stability = dependent on feed-forward

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Upper limbs → reflexes = appear to play ↑ role

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Stretch reflexes can reach cortex

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Transcortical = slower, flexibility tunes

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Stability produced by co-contraction (lower limb)

Automatic Postural Reactions X3 coordinative strategies (posture correction) 1. Ankle strategy → (small disturbance) 2. Knee strategy → long/fast perturbations 3. Stepping → knee/hip bend (greater forces) ●

Related to functional needs

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Involve more muscle

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Too latent to be a reflex

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Brainstem generation

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feedback/feedforward

Anticipatory Postural Adjustments (APAs) ●

Feed-forward

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Anticipating off center COM

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Early activation of postural muscles

Voluntary Control → interactions w/ reflexes ●

Cortex = regulate all lower motor circuits

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Reciprocal inhibition

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Regulate reflex sensitivity ○

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Muscle synergies → group of muscles activated in synchrony w/ fixed relative gain ○

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Conditioning stimulus = ↓ muscle activity (response)

Reduce control (flexibility)

Spinal reflexes regulated by descending motor commands

Reflex Abnormalities ●

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Spasticity ○

Common w/ stroke, cerebral palsy, MS

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↑ in muscle tone → produces resistance to movement

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Reflex role in ^ ○

Reduced output from motor sensors

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Normal communication ↓

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Stretch reflex = hyperactive

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Produces force resisting movement (velocity dependant)

Adulthood → spinal reflexes regulate ○

injury/disease can ↓ output from motor cortex → spinal cord = ↓ inhibition & reflex modulation

WEEK 4 Recap: Gait Evolution of Upright Gait (locomotion) ●

Locomote bipedally (evolved from quadrupedalism)

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Advantages of bipedalism

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Energy efficient

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↑ ability to see predators

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display/warning

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Allows non-locomotor forelimb use

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Improved thermoregulation

Disadvantages (trade off) ○

Less stable

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> obvious to predators

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Exposes vulnerable body parts

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Slower over short distances

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Single limb injuries = > disabling

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Energetically expensive

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> loading on: spine, pelvis, hip, knees, ankles

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Climbing > difficult

Implications of bipedalism ○

Force production & absorption changes

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Large upper body mass = undesirable

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Strong pelvis/hip muscles required

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↑ reliance on vestibular system

Upright Gait Adaptations ●

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Foramen magnum position ○

In humans = under skull vertex

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In hominids = back of skull

Spinal curvature ○

Additional lumbar curve (maintain posture)

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Pelvic shape change

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Leg structure change ○

Femur angle > in humans

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Feet below pelvis

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↑ shearing forces @ HOF

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Change in mass distribution

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Change in foot structure

Kinematics of Walking (quantify gait) ●

Stance 60%

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Swing 40% ○

20% = double support phase

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Stride length: initial contact to initial contact of same leg (distance between)

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Step length: distance between heel contact of right leg → heel contact of left leg

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Temporal variables ○

Stride duration

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Step duration

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Cadence (steps/min)

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Speed ■

Cadence x step length

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Stride length x stride duration

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Width of BoS (midpoint of each heel)

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Degree of toe out (stability seeking): normal = 7 degrees

Joint Angles ●

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Measure displacement of joint from neutral anatomical position

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Ankle during walking ○

Phase 1: Slight plantarflexion (during contact)

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Phase 2: Passive dorsiflexion

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Phase 3: Active plantarflexion (propulsion)

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Phase 4: Active dorsiflexion (during leg swing)

Knee during walking ○

Phase 1: Flexion (after contact)

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Phase 2: Extension (support)

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Phase 3: Flexion (propulsion)

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Phase 4: Further flexion (ground clearance)

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Phase 5: Extension (pre- contact)

Hip during walking ○

Phase 1: Extension (loading and trunk translation)

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Phase 2: Flexion (propulsion)

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Phase 3: Slight extension (pre- contact)

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Frontal plane = rotation (pelvic drop/tilt)

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Transverse plane = rotation of pelvis about spinal axis

Gait Economy ●

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Minimise vertical CoG displacement ○

Lateral pelvic tilt

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Knee flexion (timing)

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Interactions of joint action → H, K & A

Minimise drop in CoG ○

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Lateral pelvic tilt

Minimise lateral movement of CoG ○

Valgus @ knees ↓ width of BoS

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Trunk motion

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Upper extremity motion

Gait Analysis Ten elements of assessment

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1. Step length asymmetry 2. Ankle at contact 3. Knee at contact 4. Stance phase knee flexion 5. Duration of single-limb support 6. Ankle and foot angles during push-off 7. Swing phase knee flexion 8. Trunk angle 9. Frontal plane: excess hip drop (Trendelenburg sign) 10. Transverse plane: posture

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Factors for normal walking ○

each leg in turn must be able to support the body weight without collapsing

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balance must be maintained (statically or dynamically) during single limb stance

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the swinging leg must be able to advance to a position where it can take over the supporting role

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sufficient power must be provided to make the necessary limb movements and to advance the trunk

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Factors for abnormal walking → does not meet one of these criteria = unable to walk ○

can result from a disorder in any part of the body’s system

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can also result from the presence of pain

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because the end result is a complicated process, several different original problems may manifest themselves in the same gait abnormality

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person has no choice, the movement being “forced” on them by weakness, spasticity or deformity

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OR

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movement is a compensation, which the subject is using to correct for some other problem, which therefore needs to be identified

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Affecting factors

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Age, injury, clothing, footwear, environment, disease & fitness

Stroke → hemiplegic gait analysis ●

R hemisphere stroke

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L hemiplegia

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Asymmetry in pressure distribution (L&R) ○

In stance phases between legs

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Slow gait, short stride

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Short LT step

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LT ankle limited DF

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LT knee limited F

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LT hip hiking

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LT arm in fixed F

WEEK 5 Recap: Kinetics of Gait ●

Kinetics = forces & torques → forces exerted against ground

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Gait = balance of ext v int forces ○

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CoM moves over pivot point ○

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All about energy (potential & kinetic)

Inverted pendulum (stance)

Stance phase: ○

mid stance → high P.E & low K.E

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Toe off → low P.E & high K.E

Swing phase (conventional pendulum) ○

Mid → high P.E & low K.E

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Low → low P.E & high K.E

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Gait natural frequency dictated by leg

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Torque = force x moment arm

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Ant directed, post directed

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Centre of pressure = important (pathology)

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P = m x Ω (watts) ○

P(j) = power @ a joint

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M(j) = moment @ a joint

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Ω(j) = angular velocity @ a joint

● ↓ dependance on muscle activation (bipedal benefit) Neural Control of Gait (neuromuscular) ●

Retained & discharged parts through evolution

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Produce essential locomotion w/out brain (cortex)

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Spinal cord → produce rhythmic contractions

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Sucrose blocks / removes communication between levels ○

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Phase shifting (need to communicate to maintain funcion)

CPG = central pattern generator

Replicating Human Gait ●

Humanoid robots → not as effective as human gait

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Exoskeleton development

TUTORIAL NOT

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