skill acquisiton Flashcards

1
Q

what is skill aquisition

A

ability to reliably deliver accurate execution

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2
Q

What occurs during skill aquisition

A

there is a speed-accuracy trade-off and slow learning
there are cellular changes ie neuroplasticity
and can be system level changes

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3
Q

what are system levels for skill acquisition

A

move from cortical to sub-cortical
automatisation
decreased cognitive effect

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4
Q

what are the four mechanisms of motor learning

A

Instructive
reinforcement
use-dependent
sensorimotor adaptation

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5
Q

what is instructive motor learning?

A

strategy based, explicit
primary driver = performance-based external feedback
primary neural substrate involved is prefrontal cortex
cognitive load = high

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6
Q

what is reinforcement motor learning

A

Reward-based
Primary driver: outcome-based external feedback
primary neural substrate involved: basal ganglia
Medium cognitive load

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7
Q

What is use-dependent cognitive learning

A

Repetition based
Primary driver: task-specific massed practice
Primary neural substrate involved: motor cortex, spinal cortex
Medium cognitive load

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8
Q

What is sensorimotor adaptation

A

recalibration, implicit
Primary driver: sensorimotor prediction errors
Primary neural substrate: cerebellum
Low cognitive load

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9
Q

what is the process of long-term potentiation

A

Voltage-gated NMDA receptors in membrane at a new synapse site
Ca2+ influxes only when there is coactivation of pre and post-synaptic membranes
Ca”+ influx stimulates insertion of non-voltage gated AMPA receptors into membrane

AMPA receptors can’t figure out useful connection till both fire at same time so initially connection is weak

There is a resultant increase in post-synaptic neuron receptors
Originally nerve 1 cant make nerve 2 work but after time body realises possible useful connection and AMPA receptors easier for nerve to carry signal

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10
Q

what is long-term potentiation

A

a cellular mechanism of memory formationin the brain
persistent strengthening of synpases based on recent patterns of acivity

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11
Q

what is the process of long term depression?

A

if connection isn’t being used or is unhelpful the connection can be removed
this stops nerve 1 directly impacting on nerve 2
opposite process to potentiation
decrease post-synaptic Ca2+ results in reduction of AMPA receptor initially
followed by deletion of synapses if continued failure to coactivate
may completely lose synapse

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12
Q

what are the 10 principles of experience-dependent plasticity

A

use it or lose it
use it and improve it
specificity
repetition matters
intensity matters
time matters
salience matters
age matters
transference
interference

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13
Q

what is the use it or lost it principle

A

failure to drive specific brain functions can lead to functional degradation

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14
Q

what is the use it and improve it principle

A

training that drives a specific brain function can lead to an enhancement of that function

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15
Q

what is the specificity principle

A

nature of the training experience dictates the nature of the plasticity

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16
Q

what is the repetition matters principle?

A

induction of plasticity requires sufficient repetition

17
Q

what is the intensity matters principle

A

induction of plasticity requires sufficient training intensity

18
Q

what is the time matters principle

A

different forms of plasticity occur at different times during training

19
Q

what is the salience prinicple

A

the training experience must be suffiently salient to induce plasticity

20
Q

what is the age matters principle

A

training-induced plasticity occurs more readily in younger brains

21
Q

what is the transference principle

A

plasticity in response to one training experience can enhance the acquisition of similar behaviours

22
Q

what is the interference principle

A

plasticity in response to one experience can interfere with the acquisition of other behaviours

23
Q

what are possible post-lesional physiological changes

A

oedema
diaschisis
excitotoxicity
apoptosis

24
Q

what is excitotoxicity

A

cells die releasing neurotransmitters increasing area of issue

25
Q

what is apoptosis

A

oedema resolves spontaneous recovery occurs
larger area affected by stroke
loss of ability to communicate
as oedema reduces should regain these cells

26
Q

what are the mechanisms for injury induced plasticity

A

denervation hypersensitivity
synaptic hypereffectiveness
unmasking silent synapses
regenerative synaptogenesis
reactive synaptogenesis

27
Q

what is denervation hypersensitivity

A

where nerves lost connections are easier to generate reaction potential due to reduced polarity

28
Q

what is synaptic hypereffectiveness

A

at synpase point takes smaller amount of neurotransmitter and fewer connections

29
Q

what is unmasking silent synapses

A

no longer live connections in these areas but are able to make better use of these

30
Q

what is regenerative synaptogenesis

A

reestablishing synapse so where one synapse connected try and maximise connections and find pathways to regain function

31
Q

when may motor learning through plasticity have constraints

A

process of automatisation can be harder with parkinson’s disease
cognitive impairment may prevent use explicit learning mechanisms
cerebellar impairment may prevent use of sensorimotor adaptation