Postural control

What is postural control

Ability to

1) maintain CoM in BoS when standing still when BoS X change

2) regain appropriate body orientation after external stimulus w/ or w/o change in BoS

3) Maintain/ regain stability after self initiated movements

Types of external stimulus of postural control system that postural control system responses to

1) External stimuli: constant environmental forces w.g. gravity

2) occasional environmentally generated forces: ground reaction forces/ being pushed/ support removed

Types of internally generated stimuli that postural control system responses to

1) Rhythmical internally generated forces —> breathing/ gait

2) Occasional internally generated forces —> coughing/ laughing

What systems are used to process the stimuli

Visual: give info about movement + position of self/ environment —> amount of light

Vestibular: give info abt head orientation + movement

Somatosensory: info abt pressure + movement + surface changes + irregularities

—> selected + weighted by CNS based on availability + accuracy + value

What happens when there is lack of proprioceptive info

Sensory ataxia

—> caused by proprioceptive neuropathy

—> X perceive movement + position of legs —> staggers

—> compensation by sight

How to test for postural control

Measure changes in center of mass —> mean position of matter in body —> anterior to S1 vertebrae

—> in quiet erect standing: slightly anterior to acromion p/ close to greater trochanter/ anterior to knee joint + ankle joint

—> normal erect posture: small AP + medial lateral oscillations of body in space bc small changes in muscle activation + connective tissue compliance

—> changes in CoM is reflected in changes in center of pressure

Factors affecting CoP

Increase in age: higher postural sway —> CoP varies more —> changes in sensory info + motor ability in ageing

Unstable surfaces + eyes closed ( limitations of visual input to CNS) —> higher postural sway —> CoP changes much

Features of voluntary motor output of postural control system

1) Cortically driven

2) Self generated/ in response to external stimuli

3) Purposeful activites

4) Complex + coordinated w/ infinite variety

5) Through corticospinal + corticobulbar tracts

Features of anticipatory output of postural control system

1) Postural muscles activated before voluntary movement begins

—> anticipate destabilising forces

2) Cortically driven

3) Memory based —> can adapt w/ repetition + changes w/ circumstances

Features of automatic motor output of postural control system

1) Control: brainstem + cortex

2) External stimuli triggered

3) Slight latency following external stimuli

4) Coordinated + generalised patterns

5) Adaptable to conditions

—> different strategies to automatic motor output

Ankle strategy for automatic output

Application: slow + low aplitude perturbation

Contact surface: Firm + wide + longer than foot

Muscle recruitment: distal to proximal

Head movement: in phase w/ hips

Hip strategy for automatic output

Application: fast + large amplitude perturbation

Contact surface: unstable + narrow/ shorter than feet

Muscle recruitment: proximal to distal —> rapid trunk adjustments

Head movements: out of phase w/ hips

Step strategy for automatic motor output

Applications: fast + large amplitude perturbations —> prevent falls+ when other strategies fail

Alters BoS —> recruitment of many muscles

Reflex motor output of postural control system

Simplest neural circuit

Modifications directly at spinal cord

Regulate local muscle contraction only

Highly stereotypical

What are the mechanisms underlying the changes in movement associated w/ acute pain episode 1

Pain adaptation theory: 

Esp group 3 + 4 afferences activated when there is pain/ damage/ threat of damage in an area  → excite antagonist muscles + increase their muscle activity + inhibit muscle activity of the agonist muscles → overall decrease in amplitude + velocity of  muscle movement 

→ only  when muscle X need to maintain the task 

Mechanisms underlying movement changes associated w/ acute pain episode 2

When muscle needs to maintain the task: surface EMG shows varied activation in induced MSK pain → single unit motor neuron discharge rate is lower during force matched contraction w/ pain ( same amount of force is produced ) – general inhibition of agonist motor neuron pool 

Mechanisms underlying movement changes associated w/ acute pain episode 3

Some single motor neurons are only discharging when there is pain/ other that only discharge in no pain condition → redistribution of motor units that are active during pain vs no pain  → how force is maintained even though motor neuron unit discharge rate is lower 

→ X change in overall surface EMG bc there is both increase + decrease in single motor neuron activity → pain adaptations may be overlooked w/ surface EMG ( summation of all SMU activity )

Reasons for altered motor neuron discharge during pain:

 

1. Input to motor neuron pool from nociceptive stimulation:

2. Changes to descending drive:  central pain → pain inhibitory systems from motor cortex or peripheral nociceptive 

→ small decrease in discharge rate at a group level of single motor units in anticipation of pain + pain → some single motor neurons discharged only in pain/ anticipation of pain → redistribution of motor neurons 

→ mostly likely due to altered descending control

Purpose of altered motor neuron discharge in pain

1. Larger units: protective + faster force production / greater nociceptive input to smaller neurons 

2. Alter load in painful parts( unloading )  → protective → changes biomechanics w/ pain

Effects of different factors on production of force w/ acute pain

Tasks w/ greater degree of freedom: X effect on stress reduction

Neural control of muscle in synergist group: amount of force can be compensated by other muscles in the same group if there is a muscle in pain

Bilateral task: compensation of muscle force production w/ non painful limb

What are the structures that control movement? 

Structures	Function
Cerebral cortex/ motor areas	Planning/ initiation of voluntary movement
Primary motor cortex	Initiation + execution of motor plans by developing program of commands for lower motor neurons
Premotor cortices	Planning + selecting complex movements → postural preparation prior to event + process visual info

Structures controlling movement 2

Supplementary motor area	specifies the sequence + extent of muscle contractions needed for a movement
Posterior parietal cortex	takes sensory info + forms conscious map of body + relationship w/ surroundings
Cerebellum	Sensory motor integration + learning
Brain stem	Basic movement + posture
Spinal cord	Reflexes: involuntary movement

What are the features of a somatotopic map

Plasticity of somatotopic map: 

Once de-innervation of a muscle → the region dedicated to the muscle will be redistributed to other nerves + muscles → deprivation of input from particular muscles cause reduction of representation of muscles in brain

What tools are used to detect active brain areas + how it is used

1.  MRI → determines regions of flow of oxygenated blow flow to active brain regions 

2. intracortical electrical stimulation 

3. Transcranial magnetic stimulation 

How does TMS function + used to investigate control of movement

Mechanism: 

1. Stimulating coil creates magnetic field  → initiates electric current in neurons → travels through upper + alpha motor neurons → movement produced ( recorded as acceleration/ motor evoked potential w/ EMG ) 

Using TMS to provide insight into cortical control of movement: 

1. Effect of voluntary contraction: motor evoked potential of the muscle performing contraction is greater than that of a relaxed hand → Increased corticospinal excitability at spinal + cortical level ( neurons are more excitable at the time of voluntary contraction + more action potentials generated  by same TMS pulse )

Mechanism of use dependent plasticity of the brain: 

1. Cortico-motor pathway is strengthened w/ voluntary contraction → Increased motor evoked potential + movement amplitude for the same stimulus

2. Complex skill training( e.g. matching targets —> increases corticospinal excitability —> ability to match targets increases —> adaptation of corticospinal tract to specific task trained

Can pain alter training induced motor plasticity + why does pain reduce training ability? 

1. Pain training:

→pain reduced ability to learn new motor task ( X increase in cortico-motor excitability ) →  X match target very well in pain condition → X train well under pain

Why X train well in pain : 

Does pain in training alter training induced motor plasticity when task performance is matched → pain in the area that is trained X stop motor plasticity in the experiment 

Is it the distraction of pain rather than direct nociceptor stimulation near trained area influencing motor plasticity → X change in index finger movement direction → when attention is draw away from the area performing the task → motor plasticity is inhibited

How does chronic low back pain affect trunk muscle contraction

delay in transverse abdominis activation relative to anterior deltoid movement → retraining can reduce the delay of activation of the transverse abdominis ( motor behaviour improved )