Psyc2020 - Motor Control And Action

There are parallel circuits that flow up and down through the system (it is hierarchical)

Sensory feedback and feedforward are crucial for modulating the output of the motor system

Consists of Muscle, neuromuscular junction

It is the lowest level of hierarchy = motor unit = where motor neurone and muscle fibres it innervates.

Ach is the neurotransmitter

Muscle fibres with membrane attach to tendon, which pulls the bone

Point of Innervation

Signals descend to muscles through pairs of Dorsolateral Tracts and pairs of Ventromedial Tracts in spinal cord

Terminate in contralateral half of one spinal cord segment and sometimes directly on motor neurone

Two Types: Corticospinal and Corticorubrospinal

Important for movements of limbs and independent movement for fine tune

Direct Tracts in Dorsolateral System that go from motor cortex and go straight to distal limb muscles

- they cross over at the medullary pyrmaid

Indirect Tracts in Dorsolateral System that go through red nucleus (where they cross over), some leave to control controlateral facial muscles, via the nuclei of cranial nerve, others go to distal limbs

After transecting dorsolateral corticospinal tracts in medullary pyramids monkeys could stand, walk and climb but could not use limbs for activities i.e. reaching for objects

More diffuse with axons innervating interneurones in several segments of spinal cord

Two Types: Ventromedial Corticospinal and Cortico-brainstem-spinal

Direct tracts in Ventromedial system: from primary motor cortex they are ipsilateral and diffusion doesn't occur until the spinal cord

They activate proximal (close muscles) like thighs

Important for posture and whole-body movements

Indirect tracts in Ventromedial system, they stop at the tectum (reticular formation) where they diffuse and have bilateral representation

After transecting ventromedial tracts, monkeys had postural abnormalities and impaired walking/sitting.

Important for sequencing, orientation, and navigation, fine tune movement, balance and learning functions

Takes input from primary and secondary motor cortex

Feedbacks from motor responses from somatosensory and vestibular systems

Fine tune walking is destroyed - more shaky for fine tune movement rather than when not moving.

Complex heterogeneous interconnect nuclei - this makes it a highly interconnected with nuclei that work together in own individual way

Modulates movement and cognitive functions including habitual responses and implicit learning

It is an ongoing feedback/feedforward loop that has two pathways

Direct: Selection of actions that goes straight to the thalamus (just excitation)

Indirect: Inhibition of actions, that has multiple pit stops, so many nuclei are involved (has a balanced system of excitation and inhibition)

Basal Ganglia > Thalamus > Supplementary Motor Area > Primary Motor cortexs

Putamen receives signals from Substantia Nigra, which produces dopamine

Putamen has two dopamine receptors

D1 = excitation = Direct

D2 = inhibition = Indirect

Imbalance between the activation of nuclei in the intact system of basal ganglia which leads to extra or reduce movements

Loss of Neurones and Pigmentation

The output of one nucleus either excites (enhances) or inhibits (suppresses) the output of the next nucleus in the system

Symptoms that you see that shouldn't be there

Tremor at resting - disappears when use limb

Rigidity - resistance to passive movement = postural problems

Rigidity + Tremor = cogwheel

Forward/Backward Leaning

Postural Hypotension = many falls

Hypokinesia: Reduction in spontaneous movement

Akinesia: Slow initiation of movement

Progressive slowing or freezing during movement

Reduction of range and scale of movement

Dull weak voice with no inflections (hypophonia)

Unemotional Expression

Disorientation

Affect

Auditory/Vision Hallucinations

Poor working memory

Paradoxical Movement Problems

Dyskinesias at peak dose

End -of-dose dysfunction

On-off cycles

Freezing

Eventual drug failure

Hereditary Nature: Autosomal dominant with complete lifetime penetrance, chromosome 4

Manifestation in Adulthood

Tendency to 'insanity and suicide'

Destruction of GABAergic/cholinergic within caudate and putamen

Progressive striatal atrophy

Defective Metabolism precedes loss of tissue

First: Depression, anxiety, irritability, impulsivity and aggression

Then:

Restlesness/poor coordination

Altered Speech

Bradyphrenia and Bradykinesia

Poor motor/reduced speed

Athetosis, Chorea

Often appear to be fragments of normal behaviour, that look voluntary but are actually involuntary

Increase with stress and voluntary movements

Quasi-undulating character is idiosyncratic to individuals

The caudate nucleus shrinks to a sharp thin strip, below the ventricle; there is ventricular enlargement

Affects: Motor and Verbal, otherwise normal sensory and cognition

Effects: Echolalia, Coprolalia, involuntary (worse under stress), partly suppressible, sleep deprivation increases, premonitory sensory phenomena

Causes: Genes and environment

Imbalance of GABA in basal ganglia

Management when severe

Before tic onset: mesial and lateral pre-motor activation

At tic onset: sensorimotor including superior parietal lobe activation

Plus basal ganglia

Located: Precentral Gyrus of Frontal Lobe

Major hub of convergence of cortical motor signals and outgoing point of signals

Mapped by homunculus

Damage to Primary Motor Cortex

Results in weakness (loss of power) in the body part represented by that site on body map

Input from association cortex

Output to primary motor cortex

Consists of:

preSMA
SMA - supplementary motor area

Dorsal and Ventral Premotor

3 x cingulate motor areas

Programming of specific patterns of movement

Posterior Parietal Lobe

Input from more than one sensory system: integrations knowledge of position of objects, position of body parts and direct attention

Damage: results in ataxia and impaired body representation

Posterior Parietal Lobe

Output to Dorsolateral prefrontal association cortex, secondary motor cortex and frontal eye fields

Damage: results in apraxia and contralateral neglect

Involved in decision to make an action - not the action itself and not processing the target

Input: Posterior parietal cortex

Output: Secondary motor, primary motor, and frontal eye fields

Inability to use visual information

Deficit is more severe in periphery of visual field

Visual fixation preserved

Results in: Awkward or incorrect movements and errors in accuracy

Had a stroke

Had to reach out to dots whilst fixating on centre dot

Deficit more severe in periphery of visual field and often over/undershot

Inability to act in a meaningful/purposeful way

A disorder of skilled movement resulting from neurological dysfunction

Knowing what our own body parts are doing is essential when a body part is obscured from vision during planning and execution of movement

Patient had head injury and had cyst enroaching on cortex - there was no visual neglect or extinction - on left superior parietal lobe

Complaint: perceives her right arm and leg to drift and fade unless she is able to see them

So in bed - loss of limb position knowledge

Conclusions: Superior Parietal Lobe is critical for sensorimotor integration by maintaining an internal representation of body's state

Controllers (perception of goal to movement

Links to motor commands and predictors (efference copy)

Predictors of movement to perception

Links to predicted state

Because of the efference copier, you know you are about to touch yourself so you are prepared for it

Can't suppress the actions of the hand

There is no connection between goal and affordances, so there is no efference copy to go to parietal lobe (it is unexpected)

Activation of actions by irrelevant affordances which are not suppressed by intended actions

A basis for action comprehension and action imitation

The action observation system

William James - every mental representation of a movement awakens to some degree the actual movement which it is object

They respond to sight of only goal-directed actions, as long as the goal is achieved (even out of sight), to sound of an action and when action is performed by hands but not tools

Premotor and Parietal Cortices activated by perception and greater activation when replicating movement

Allows for understanding and planning of actions

Did not occur when used pliers

Delayed execution

Activated when sees the action even when behind screen, but not when there is no object there

If you give people time to learn about pliers/robots then people can learn/elicit the action

context matters

experience matters

indivudal differences matter

Hearing - doing system that is highly dependent on the individuals motor repertoire

Used trained (knew how to play) and untrained music sequences

Frontoparietal motor regions were observed in trained but not when untrained

Activation was more active during listening of trained music than untrained

Experience-Specific - movements are not goal-directed but they are meaningful

e.g. dances have meaning of the final body position of the people doing the moves

Humans can respond to 'robotic' stimuli as well as other humans if we have experience with those stimuli