MIDTERM #1 Flashcards

1
Q

Motor control is defined as?

A

the ability to regulate or monitor and direct and intiate the mechanisms essential to movement

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2
Q

What does motor control address?

A

How the CNS organizes individual muscles and joints into coordinated movements

How sensory information is used to select and control movement

How perception influences movement

How movement problems can be treated

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3
Q

How is movement generated?

A

Movement is generated by an individual to meet the demands of a specific task that is being performed in a specific environment

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4
Q

Factors that influence motor control?

A

Task
Individual
Environment

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5
Q

What is individual factors?

A

The interaction of structural (anatomy) and functional (physiology) processes within the individual influences the control of movement

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6
Q

What are the components of individual factors?

A

Perception (sensory): somatosensory, vestibular, visual

Cognition: problem solving, planning, attention

Action (motor): neuromuscular, biomechanical

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7
Q

“Perception” factors influence how?

A

how the individual integrates sensory information to regulate movement

e.g., body position, features of the environment

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8
Q

“Cognition” factors influence how?

A

how the individual establishes the intent or goals of movement

e.g., planning, problem-solving, motivation

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9
Q

“Action” factors influence how?

A

how the individual generates a motor output sent from CNS to muscles

e.g., size, strength, neural pathways

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10
Q

What is task factors?

A

The nature of the task regulates the neural mechanisms controlling movement

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11
Q

What are the components of task factors?

A

Discrete vs Continuous tasks

Closed vs Open tasks

Body Stability vs Transport/Mobility tasks

Object Manipulation tasks

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12
Q

Important to consider task factors when?

A

determining what tasks should be taught, in what order, and at what time

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13
Q

Important to consider task factors when?

A

determining what tasks should be taught, in what order, and at what time

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14
Q

How would you progress to moving out of bed into a chair for this hip surgery patient?

A

Move from supine to sitting, pivot legs, move to edge of bed and back, sit to stand, stand to sit

Recognize that this is a mobility task – gradually increase the mobility challenge

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15
Q

What are environmental factors?

A

The features of the environment regulate the neural mechanisms controlling movement

Regulatory features

Non-regulatory features

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16
Q

What are Regulatory features?

A

aspects of the environment that directly shape a movement (e.g., characteristics of a walking surface, size of an object)

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17
Q

What are Non-regulatory features?

A

aspects of the environment that may affect the performance of a movement (e.g., ambient light, distractions)

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18
Q

What are Theories of Motor Control?

A

A theory of motor control is a group of abstract ideas about how movement is controlled.

Ex. A pile of bricks alone is not of use, putting them together can create an organized and structured theory.

Many theories exist, each attempting to explain and interpret what is known about motor control processes

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19
Q

Motor control theories tend to vary based on?

A

The relative importance placed on various neural components (e.g., central, peripheral, supraspinal)

The relative importance of the environment in controlling movement

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20
Q

Generally, the theories are developed to try to solve the ?

A

“degrees of freedom problem”

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21
Q

What is the reflex theory?

A

Complex behaviour can be explained through the combined actions of individual reflexes

Each reflex in the chain is a consistent output in response to a specific stimulus

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22
Q

What is the limitations of the reflex theory?

A

Novel movements

Movements without a sensory stimulus

Rapid movements (processing time)

Same stimulus, different response (ability to override reflexes)

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23
Q

What is the hierarchical theory?

A

Motor control is organized such that higher centres (e.g., cerebral cortex) exert control over lower centres (e.g., spinal cord) – “top-down”

Maturation of reflexes is the basis of motor development and control

Reflexes controlled by lower centres are inhibited as higher centres emerge

Pathology in higher centres can lead to persistence or emergence of “primitive reflexes”

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24
Q

What is the limitations of the hierarchical theory?

A

Not all low-level behaviours are primitive (pain withdrawal), and not all high-level behaviours are mature

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25
Q

What is the motor programs theories?

A

Patterned motor responses (“motor programs”) can be initiated either by central processes (i.e., voluntary) or in response to a stimulus (i.e., a reflex)

Higher level motor programs that contain “rules” (i.e., schema) for accomplishing a task that can be applied in different circumstances

Central pattern generators (CPGs, spinal cord neural networks) that produce locomotor patterns in cats in the absence of sensory or descending input

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26
Q

What is the limitations of the motor programs theories?

A

Does not account for other factors that are used to plan and initiate movements (e.g., body position, fatigue, environment)

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27
Q

What is the systems theories?

A

The control of integrated movement is distributed among many interacting systems that work together to move a mechanical system (i.e., the body)

Focus on biomechanics – engineer’s perspective

Synergies represent muscles that act as a unit, higher control centres turn up and down activation of a synergy according to demands

Dynamical systems theory suggests that individual elements within a complex system “self-organize”

No need for an external command (i.e., motor program)

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28
Q

What is the limitations of the systems theories?

A

Presumption that the nervous system has a minimal role

Difficult application

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29
Q

Motor Program vs Systems Theories?

A

Opposing views on movement variability

Motor program theories – variability represents error

Systems theories – variability is a normal part of movement, allows adaptation to environmental changes

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30
Q

What is the ecological theory?

A

Emphasizes the importance of determining how an individual detects and uses information from the environment

Shift from sensory-motor system to perception-action system

The perception of environmental information is most important to supporting the actions needed to accomplish the task

Considers the role of the environment from a psychological, rather than physical (i.e., systems), perspective

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31
Q

What is the limitations of the ecological theory?

A

Downplays the importance of the organization of the various components of the nervous system

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32
Q

Scientific theory and clinical practice: Neurofacilitation approaches?

A

Informed by reflex and hierarchical theory

Reflex chains are under top-down control – cortex -> brainstem -> spinal cord

Sensory input stimulates normal movement patterns

Cortical damage release abnormal reflexes, need to restore cortical control

Neurologic recovery similar to development

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33
Q

Steps to Neurofacilitation approaches?

A

1) Inhibit “abnormal” movement patterns, facilitate “normal” movement patterns

2) Repeat normal movement patterns until they transfer to functional tasks

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34
Q

What are task-oriented approaches?

A

Informed by elements of all theories discussed

Movement emerges as an interaction among many different systems

Movement is organized around a behavioural goal and is constrained by the environment

Predictive and adaptive control in response to sensory feedback

Behaviour is a result of the neural damage and the function of the remaining systems

Functional task training, not basic movement patterns

Need to solve the problem – many solutions

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35
Q

Motor learning is defined as?

A

a relatively permanent change in the capacity to perform a motor skill

Learning is something that sticks. (Not lucky performance)
Capacity – learning is a construct, you have capacity to perform skill but it doesn’t mean you will perform well every time.

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36
Q

Another definition of Motor learning is defined as?

A

the (re)acquisition and/or modification of movement skills under “normal” circumstances (motor learning) or following injury (recovery of function) that leads to improved motor performance

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37
Q

Key points about motor learning?

A

Learning is a process (takes time)

Depends on interaction between motor, sensory/perceptual and cognitive processes

Occurs through experience or practice, as the individual, task and environment interact

Cannot be measured directly

Inferred from retention/transfer tests

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38
Q

What is performance?

A

observable behaviour, execution of a skill at a specific time and in a specific situation

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39
Q

What is learning?

A

Cannot be directly observed, must be infered by observing performance

Changes in performance during practice do not necessarily reflect learning

2nd definition: the (re)acquisition and/or modification of movement skills…”

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40
Q

What are performance variables?

A

factors that affect a person’s performance but not necessarily the learning of the task (e.g., alertness, anxiety, fatigue)

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41
Q

What is Motor sequence learning?

A

incremental acquisition of sequential movements into a well-articulated behaviour

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42
Q

What is Motor adaptation?

A

capacity to compensate for environmental changes

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43
Q

What is the process that modifies a behaviour?

A

Learning

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44
Q

What is memory?

A

The ability to remember past experiences

Allows you to store and retrieve the information that you learn

The “record” left by a learning process

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45
Q

What is explicit memory?

A

conscious ability to recall information and previous experiences (i.e., facts, events)

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46
Q

What is implicit memory?

A

unconscious changes in behaviour that occur as a result of prior experiences

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47
Q

What is explicit learning?

A

The formation of explicit memories requires conscious awareness and attention

Explicit learning is most effective when the individual is motivated and attentive

In early skill learning, athletes may depend on explicit memory, but in later stages skills are typically drawn from implicit memory

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48
Q

What is Implicit, non-associative learning?

A

Occurs when you encounter a single stimulus repeatedly

Habituation and sensitization

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49
Q

What is habituation?

A

decrease in responsiveness that occurs with repeated exposure to a non-painful stimulus (e.g., treating dizziness or vestibular dysfunction)

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50
Q

What is sensitization?

A

increase in responsiveness to a threatening or painful stimulus (ex. you previously injured self and act ina way to avoid that stimulus again)

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51
Q

What is Implicit, associative learning?

A

The development of an association between two stimuli (classical), or an association between a behaviour and a consequence (operant)

Classical conditioning

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52
Q

What is classical conditioning?

A

Unconditioned stimulus = physical cue
Conditioned stimulus = Verbal cue
Response = Walk

Now imagine going back to one but replacing physical cue with verbal cue – now the person gives their own cue and tries to have it e replaced with some intrinsic cue that they are walking.

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53
Q

What is operant conditioning?

A

A behaviour becomes associated with a particular consequence, producing either a tendency to repeat (reinforcement) or not to repeat (punishment) – the “law of effect”

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54
Q

What is operant conditioning?

A

A behaviour becomes associated with a particular consequence, producing either a tendency to repeat (reinforcement) or not to repeat (punishment) – the “law of effect”

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55
Q

What is Implicit, procedural learning?

A

The development of an ability to perform a task without attention or conscious thought following repetition of the task (e.g., practice)

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56
Q

What are Theories of Motor Learning?

A

Several theories of motor learning that:

Attempt to explain and interpret what is known about motor learning processes

Provide a framework for clinical practice that influences clinical decision-making

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56
Q

What are Theories of Motor Learning?

A

Several theories of motor learning that:

Attempt to explain and interpret what is known about motor learning processes

Provide a framework for clinical practice that influences clinical decision-making

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57
Q

What are the Motor learning processes?

A

Schema theory

Ecological theory

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58
Q

What are the Motor learning stages?

A

3-stage Fitts and Posner model

3-stage Systems model

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59
Q

What is the Schmidt’s Schema Theory?

A

1) Identify task and “class of actions”

2) Retrieve the appropriate Generalized Motor Program (GMP)

3) Add the Movement-specific parameters to the GMP depending on performance characteristics

Ex. Class of action ex. kicking, throwing, walking, etc.

Movement-specific parameters ex. see that you’re holding a golf club and not a baseball bat.

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60
Q

What is a schema in terms of the CNS?

A

Schema are the rules used by the CNS to make decisions regarding which movement-specific parameters to apply.

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61
Q

What is the recall schema?

A

Used to select a response

Relates the initial conditions (e.g., weight of an object) and movement parameters (e.g., force used) with a desired movement outcome

Learn from your outcome to do better next time

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62
Q

What is the recognition schema?

A

Used to evaluate a response

Compares the expected outcome and sensory consequences of the movement with the actual outcome and sensory consequences

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63
Q

What is something learning involves?

A

Learning involves constantly updating recall and recognition schema (remember inverse models?)

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64
Q

What is the ecological theory in terms of motor learning?

A

Related to systems and ecological theories of motor control

Focuses on:

The interaction between the perceptual and motor systems

Practice involves the search for optimal strategies – finding the most appropriate motor response and perceptual cues

task-relevant mapping of perception and action

Augmented feedback can facilitate the search

Emphasizes the exploration of the “perceptual-motor workspace” – Discovery-based learning

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65
Q

Both Schema and Ecological Theories of motor learning suggest that practice variability is important for skill learning. How?

A

Schema theory – variable practice promotes formation of accurate recall and recognition schema across contexts

Ecological theory – variable practice promotes linking of perceptual cues with the appropriate motor response

Beer Example*
Regulatory- how much beer is in glass
Non-regulatory- colour of beer

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66
Q

Motor learning slide 31

A

Memorize chart

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67
Q

What stages are involved in the 3-stage Systems Model?

A

Novice:

Movement simplified by reducing degrees of freedom (e.g., constraining multiple joints by co-activating muscles)

Makes task easier to perform, but not efficient or adaptable

Advanced stage:
Increase in degrees of freedom (e.g., allow movements at additional joints)

Improvement in coordination, efficiency, adaptability

Expert stage:

Exploiting the mechanical and inertial properties of the moving segments
Continued improvements in coordination and efficiency

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68
Q

Rehabilitation = ?

A

Re-learning

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68
Q

Recovery vs Compensation?

A

Recovery – restoration of an original movement strategy to accomplish a task

Compensation – implementation of an alternative movement strategy to accomplish a task

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69
Q

What is Constraint-induced movement therapy (CIMT)?

A

“Use it or lose it”

Used to overcome “learned non-use” of an affected limb due to neurologic damage

The unaffected limb is constrained while the individual takes part in an intense and repetitive training regimen over a relatively short period of time

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70
Q

What is the constraint-induced movement therapy (CIMT)’s links with motor learning principles?

A

Promotes explicit recognition that the limb can be used

Develop associations between its use and success

Relearning of skills-sequences and adaptation

Redevelopment of schema

Searching for solution

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71
Q

What is Neuroplasticity?

A

to change and re-organize in response to experience or environmental constraints

the capacity of the central nervous system

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72
Q

2 components of Neuroplasticity?

A

1: Chemical changes (e.g., neurotransmitters, neurotrophins, neuropeptides) -> fast -

2: Structural changes (e.g., dendritic branching, synaptogenesis) -> slow – takes time

Refer to snowboarding example Physiology of Motor Learning slide 5

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73
Q

What is long-term potentiation?

A

Activity-dependent increase in synaptic efficacy

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74
Q

What is synaptic efficacy?

A

the strength of connections between neurons

Did something for a long time and there was an increase in the strength of neurons

Everytime you perform a skill you’re activating those pathways and eventually they get stronger and it becomes easier.

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75
Q

What is long-term depression?

A

Activity-dependent decrease in synaptic efficacy

When it isn’t activated it starts the whither away

Ex. you don’t practice a skill for a while and stop being as good at skill

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76
Q

What is the direction of the neural correlates of explicit memory?

A

Association areas – e.g., posterior parietal cortex -> Medial temporal lobe areas – rhinal cortex, amygdala -> Hippocampus -> Prefrontal cortex

2 pathways:
Prefrontal cortex -> Medial temporal lobe areas – rhinal cortex, amygdala
OR
Prefrontal cortex -> thalamus -> hippocampus

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77
Q

Difference between hippocampus and pre frontal cortex?

A

Hippocampus has the info

Prefrontal cortex guides you onto the right tracks

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78
Q

What did Wilder Penfield discover?

A

Performing medial temporal lobe surgery in patients with epilepsy

Stimulated temporal lobes of conscious patients

Patients experienced memories as though they were happening again!

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79
Q

What is Non-associative learning?

A

An increase (sensitization) or decrease (habituation) in the responsiveness to a particular stimulus following repeated exposure to the stimulus

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80
Q

What is the effect of Sensitization?

A

Increased responsiveness

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81
Q

What is the effect of Habituation?

A

Decreased responsiveness

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82
Q

What is the Short-Term Mechanisms
(Functional/Physiological) of Sensitization?

A

Increased EPSP amplitude

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83
Q

What is the Short-Term Mechanisms
(Functional/Physiological) of Habituation?

A

Decreased EPSP amplitude

84
Q

What is the Long-Term Mechanisms
(Structural/Anatomical) of Sensitization?

A

Increased number of synaptic connections

85
Q

What is the Long-Term Mechanisms
(Structural/Anatomical) of Habituation?

A

Decreased number of synaptic connections

86
Q

What is habituation Short-term changes?

A

transient decrease in the synaptic effectiveness of neurons in the vestibular pathway (reduced symptoms during a therapy session)

87
Q

What is habituation long-term changes?

A

relatively permanent decrease in the number of synaptic connections involving neurons in the vestibular pathway (reduced symptoms outside of therapy)

88
Q

What is associative learning?

A

The development of an association between two stimuli, or between a behaviour (response) and a consequence (stimulus)

89
Q

Components of associative learning?

A

Classical and Operant conditioning

90
Q

Something to note about associative learning?

A

for classical conditioning to occur, the conditioned stimulus must be applied just prior to the unconditioned stimulus (that produces the response)

91
Q

Example of associative learning?

A

Unconditioned Stimulus – Physical cue

Conditioned Stimulus – Verbal cue

Response – Walk with activation of specific muscle group

92
Q

What is Motor adaptation?

A

Motor adaptation refers to the capacity to modify motor skills to account for environmental changes

In some instances it may be considered a form of operant conditioning

Seen as an error signal, you don’t want that to happen again- create a pathway for it to not happen again as the errors keep occuring

93
Q

What are Mossy fibers?

A

ongoing movements (continuous)

94
Q

What are Climbing fibers?

A

movement errors (occasional)

95
Q

What part of the brain is involved in Motor adaptation?

A

Cerebellum is highly involved in this form of learning

96
Q

Steps of motor adaption in brain?

A

1: Proprioceptive information up the spinal cord, pons, into cerebellar cortex

2: Purkinje cells in cerebellar cortex inhibit the cerebellar nuclei

3: Tonic excitatory drive to M1

97
Q

What is procedural learning?

A

The development of the ability to perform a task without attention or conscious thought following repetition of the task (e.g., practice)

Cortico-striatal (i.e., basal ganglia) loops

98
Q

What is the Role of Somatosensory Cortex?

A

During learning, activity in the somatosensory cortex may promote LTP in pathways in the motor cortex

Once a skill is learned, a lack of somatosensory input does not markedly impact performance of the skill

Use feedback and adapt

Need somatosensory cortex to learn a skill but if you have learned the skill and then removed the somatosensory cortex, you can still perform the skill

98
Q

What is the Role of Somatosensory Cortex?

A

During learning, activity in the somatosensory cortex may promote LTP in pathways in the motor cortex

Once a skill is learned, a lack of somatosensory input does not markedly impact performance of the skill

99
Q

What does the Removal of left somatosensory cortex do to the brain?

A

Right side: unable to learn the task

Left side: able to learn the task

100
Q

What does the Removal of right somatosensory cortex do to the brain?

A

Left side: still able to perform the task

101
Q

What is the Role of Motor Cortex?

A

When learning a skill, the area of the motor cortex activated is gradually increased

Once a skill is learned, motor cortex activation decreases

102
Q

Explain Neuroplasticity and recovery of function?

A

Growth and reorganization of neural pathways can occur in the adult CNS following neurological pathology

103
Q

What is Restorative (direct) changes?

A

repair/recovery of the injured neural tissue

getting back to normal, restoring

104
Q

What is Compensatory (indirect) changes?

A

recovery of function via compensatory neuronal reorganization (e.g., networks, pathways)

finding new ways

105
Q

What are the Mechanisms of neuronal injury?

A

Neuronal damage can occur as a result of a direct insult (e.g., severed axon) or secondary to another injury (e.g., edema, blood flow)

Breaking of neuronal cells

Those connections die and there is degeneration

Swelling can push on neuron causing neural shock –n acute care would want to get swelling down to see what long term damage has occurred

106
Q

What are the Intercellular responses to injury?

A

Denervation supersensitivity

Silent synapse unmasking

Neural regeneration

Collateral sprouting

107
Q

What is Denervation supersensitivity?

A

post-synaptic membrane becomes hypersensitive to the NT previously released by a damaged pre-synaptic neuron (e.g., increased number of post-synaptic NT receptors)

De innervated – less input – becomes hypersensitive – even though damaged, can still perform activities

108
Q

What is Silent synapse unmasking?

A

activation of a previously dormant or suppressed synaptic connection

109
Q

What is Neural regeneration?

A

regrowth of a damaged axon

110
Q

What is Collateral sprouting?

A

sprouting of new dendritic spines or collateral axons to innervate synaptic sites previously innervated by a damaged neuron

111
Q

What happens during Cortical reorganization following injury?

A

Reorganization of neural pathways can occur after injury due to:

strengthening of pre-existing synaptic connections (localized reorganization)

creation of new synaptic connections (more widespread reorganization)

112
Q

Strategies to enhance neuroplasticity?

A

Plasticity that supports motor learning and functional recovery after injury takes time

Great interest in approaches that might facilitate the process

Some important points:

Use it or lose it – plasticity goes both ways

Use it and improve it – training can improve function

Specificity – nature of training impacts nature of plasticity

Repetition – more repetitions the better

Age matters – younger brains more malleable

Interference – plasticity related to one skill can interfere with another

113
Q

What can be used for brain stimulation?

A

TMS can be used to alter excitability of brain regions and bias them towards plasticity

EXAMPLE:

Participants with chronic stroke received repetitive TMS over the primary somatosensory cortex immediately before practice of a motor skill on 5 consecutive days

Participants receiving stimulation improved more than those receiving sham stimulation

114
Q

Besides TMS, what can be used for brain stimulation?

A

Transcranial direct current stimulation (tDCS) can be used in a similar way to TMS but delivered during motor practice

115
Q

About TMS and tDCS?

A

Generally, these approaches attempt to alter the resting membrane potential of neurons such that they are more (or less) likely to transmit an action potential, and ultimately undergo LTP or LTD

116
Q

About TMS and tDCS?

A

Generally, these approaches attempt to alter the resting membrane potential of neurons such that they are more (or less) likely to transmit an action potential, and ultimately undergo LTP or LTD

117
Q

Cardiorespiratory exercise promotes production of?

A

several neurochemicals that can enhance LTP (e.g., brain-derived neurotrophic factor)

118
Q

Regular exercise training is associated with increased volume of what part of the brain?

A

hippocampus

119
Q

Cardiorespiratory exercise immediately before or after practice of a skilled task can what?

A

may speed up and/or enhance learning of the skill

Increasing evidence that the brain is more ‘plastic’ in the hour after cardiorespiratory exercise than in a resting state

120
Q

Which of the following is an example of a restorative change in the nervous system that may occur after neurologic damage?

Collateral sprouting
Neural regeneration
Silent synapse masking
None of the above.

A

Neural regeneration

121
Q

Which of the following is an example of a restorative change in the nervous system that may occur after neurologic damage?

A
122
Q

What is tone?

A

residual (left over) muscle tension or continuous and passive partial contraction of muscles (don’t have to be tensed up, its always there)

– ex. after studying for a while your shoulders may be hunched over from being in same position.

123
Q

What is hypertonia?

A

increased muscle tension - spasticity, rigidity

124
Q

What is hypotonia?

A

decreased muscle tension, flaccidity

125
Q

What is hypotonia?

A

decreased muscle tension, flaccidity

126
Q

Movement = ?

A

kinesia

127
Q

Hyper and hypotonia are distinct from?

A

strength/weakness, which refers to active movement

i.e., hypotonia ≠ weakness

128
Q

What is hyperkinesia?

A

Movement

excessive abnormal movement

129
Q

What is hypokinesia?

A

Movement

decreased ability to produce movement

130
Q

What is bradykinesia?

A

Movement

slowness of movement

131
Q

What is akinesia?

A

Movement

loss of ability to move voluntarily

132
Q

What is Abnormal synergies?

A

Movement

sequencing of muscle activation for functional tasks

refers to an abnormal coupling of muscles during functional movements

Inability to selectively recruit a limited number of muscles

Emergence and disappearance of abnormal synergies is characteristic of the recovery process after stroke (hierarchical theory, neurofacilitation approaches)

133
Q

What is coactivation?

A

Movement

simultaneous activation of agonists and antagonists during functional movement

134
Q

What is ataxia?

A

Coordination

lack of voluntary coordination of movement (e.g., gait abnormality)

Greek translation – “a lack of order”

People who have cerebellar damage

135
Q

What is a Resting tremor?

A

Involuntary movement

occurs when body part is not voluntarily active

136
Q

What is a Intention tremor?

A

Involuntary movement

occurs during the performance of a voluntary movement

137
Q

What is Chorea?

A

Involuntary movement

repetitive, brief, irregular and rapid involuntary movements that move between body parts

138
Q

What is Athetosis?

A

Involuntary movement

continuous stream of slow, flowing, writhing involuntary movements

139
Q

What is Dystonia?

A

Involuntary movement

uncontrollable muscle tension leading to diverse, uncontrolled movement

140
Q

When a post-synaptic membrane becomes hypersensitive to the neuron previously released by a damaged pre-synaptic neuron, it is termed?

A

Denervation supersensitivity

141
Q

Motor Cortex Pathology components?

A

Motor weakness

Hypertonia (spasticity)

Abnormal synergies

Co-activation

142
Q

Strength refers to?

A

the ability to generate sufficient tension in a muscle for posture and movement

143
Q

Weakness refers to?

A

an inability to generate normal levels of force

144
Q

Motor weakness depends on?

A

Musculoskeletal properties of the muscle

Neural activation

145
Q

What is neural activation?

A

of units recruited, type of units recruited, discharge rate/frequency of units recruited

(ex. just a twitch or is it a whole movement?)

146
Q

What happens if there is a upper motor neuron lesion?

A

UMN lesion → decreased descending excitatory/facilitatory input to LMNs → decreased motor unit recruitment → motor weakness

147
Q

Lesion size and location influences what?

A

Severity (paresis to

paralysis/plegia)
Pattern of weakness

Examples – stroke, cerebral palsy

Note – unilateral lesions can also cause bilateral weakness

148
Q

What is Hemiparesis/hemiplegia?

A

one side of the body

149
Q

What is Paraparesis/paraplegia?

A

lower limbs only

150
Q

What is Quadri (tetra) paresis/quadri (tetra) plegia?

A

all four limbs

151
Q

What are the treatmeant approaches for motor weakness?

A

Strength training (progressive resistance)

Bilateral training

Functional electrical stimulation

152
Q

What is Bilateral training?

A

Cross-education – increase in strength of untrained limb following training of opposite limb

153
Q

What is Functional electrical stimulation?

A

Uses electrical current to generate movement in otherwise paretic muscles

154
Q

What is spasticity?

A

Increased muscle tone (i.e., type of hypertonia) that is velocity-dependant (↑ stretch velocity and ↑ resistance to stretch)

UMN lesion -> decreased descending inhibitory (ex. flaccidity)
Input to LMNs -> increased LMN stretch reflex excitability -> increased passive resistance to stretch

Lack of descending excitatory drive can also lead to ‘denervation supersensitivity’ in lower motor neuron and enhance the stretch reflex too

155
Q

Continuous high muscle tone can lead to?

A

stiffness, muscle shortening and bone and joint deformities

156
Q

There are common patterns of spasticity that tend to occur in the upper and lower limbs after motor cortex lesions. What are they?

A

Upper-limb – adducted, internally rotated shoulder, flexed wrist

Lower limb – equinovarus foot (points down and in)

157
Q

What is a contracture?

A

when bone joint cannot be opened fully

158
Q

Role of spasticity in limiting functional motor performance has been debated. What is incorrrect and what is correct?

A

INCORRECT:
*Spasticity could limit the ability to move quickly
*Excessive stretch reflex in antagonist could interfere with agonist contraction

CORRECT:

*Inadequate recruitment in agonist is the main issue (not increased activity in antagonist)
*Abnormal reciprocal inhibition is more problematic
*Spasticity could be protective against disuse atrophy

**Science-based recommendation: Focus less on the spasticity and more on the paresis

159
Q

Treatment approaches for spasticity?

A

Pharmacological

Surgical

Prolonged stretching

160
Q

What is Pharmacological approach for spasticity?

A

(must consider potential side effects – e.g., toxicity)

Baclofen, Botox

161
Q

What is Surgical approach for spasticity?

A

(e.g., brain, spinal cord, peripheral nerves, muscles)

Sever afferent pathways, lengthen tendons

162
Q

What is Prolonged stretching approach for spasticity?

A

(e.g., manual therapy, splints, orthoses)

163
Q

Strength training in limbs with spasticity was previously avoided but now…

A

now there is clear evidence that strength and spasticity are unrelated

164
Q

Co-activation may represent a?

A

Loss of normal reciprocal inhibition mechanisms

Normal early form of inter-joint coordination (i.e., freezing of degrees of freedom in early motor learning)

165
Q

Treatment approaches for abnormal synergies and co-activation?

A

Muscle patterning practice

Cueing

Mental practice

Biofeedback

166
Q

What is Muscle patterning practice?

A

Repeat, repeat, repeat

167
Q

What is Cueing?

A

Think of neurofacilitation approaches

Verbal, physical, sensory

168
Q

What is Biofeedback?

A

Visual presentation of EMG

169
Q

Weakness in motor cortex pathologies may be due to?

A

Reduced # of motor units recruited

Reduced frequency of motor unit recruitment

Altered types of motor units recruited

170
Q

Components of Cerebellum Pathology?

A

Hypotonia (spino-cereb.) – low tone

Ataxia (vestibulo, spino, cerebro-cereb.)- loss
of coordination

Intention tremor

171
Q

What does Vestibulocerebellum control?

A

postural stability, eye movements

172
Q

What does Spinocerebellum control?

A

movement correction, muscle tone

173
Q

What does Cerebrocerebellum control?

A

planning, coordinating, timing movements

174
Q

Spino-cerebellum maintains tone through?

A

descending drive to gamma-motor neurons

175
Q

Spino-cerebellum maintains tone through?

A

descending drive to gamma-motor neurons

176
Q

Different motor neurons and tone?

A

Alpha – extrafusal

Gamma- intrafusal – coiled around muscle spindles – damage to this means less activation to muscle spindles – less tone

177
Q

Damage to spino-cerebellum disrupts what?

A

the drive down to the gamma motor neuron and reduces tone

178
Q

Gamma motor neuron drive controls what?

A

muscle spindle sensitivity

When disrupted, stretch reflex response decreased and tone becomes low

179
Q

Hypotonia treatment approaches?

A

No established treatment approach

Strength training (progressive resistance)

Sensory stimulation

Functional electrical stimulation

Alignment

180
Q

Hypotonia treatment approaches?

A

No established treatment approach

Strength training (progressive resistance)

Sensory stimulation

Functional electrical stimulation

Alignment

181
Q

Ataxia typically affects movements that involve?

A

multiple joints or specific sequencing/timing

182
Q

Damage to any area of the cerebellum (spino, vestibulo, cerebro) can result in ________ but it manifests in what different ways?

A

Ataxia

Eye movements

Delayed movement onset/termination

Errors in movement amplitude/direction

Impaired ability to perform alternating rhythmic movements

183
Q

Ataxia
During gait, ataxia can manifest as?

A

postural instability (e.g., wide based stance) and unsteadiness (e.g., staggering gait)

184
Q

Evidence that cerebellar cells are particularly sensitive to alcohol – exposure during development or chronic consumption can cause?

A

cerebellar degeneration

185
Q

Part of cerebellar ataxia may relate to the role of?

A

the spinocerebellum and cerebrocerebellum in error correction

186
Q

Treatment approaches for ataxia?

A

Task-oriented, functional movement practice
Repetition!

Imposing time constraints

Cues (metronome, music, visual)

Sensory stimulation
Neurofacilitation approaches

187
Q

Which of the patients is most likely to have a history of cerebellar stroke?

Patient A
Decreased muscle tone
Intention tremor
Errors in movement amplitude (overshoots/undershoots targets)
Impaired ability to perform alternating rhythmic movements

OR

Patient B
Increased muscle tone (spasticity)
Abnormal resting posture of the upper limbs
Motor weakness
Abnormal upper limb flexor synergy

A

Patient A.

188
Q

Basal Ganglia Pathology includes?

A

Hypokinetic Disorders

Hyperkinetic Disorders

189
Q

What are hypokinetic Disorders?

A

(e.g., Parkinson’s Disease)

Rigidity
Akinesia/Bradykinesia
Resting tremor

190
Q

What are hyperkinetic Disorders?

A

(e.g., Huntington’s)

Hypotonia
Involuntary movements
Athetosis
Chorea
Dystonia

191
Q

What is rigidity?

A

Increased resistance to passive movement of the limb (i.e., tone) that is not velocity-dependent (i.e., stretch velocity does not affect resistance)

192
Q

Akinesia/Bradykinesia loss of ability to?

A

Loss of ability to move voluntarily/slowness of voluntary movement

193
Q

Challenges with initiation of movement with basil ganglia?

A

Think about basal ganglia connections to prefrontal cortex and supplementary motor area

– areas involved in movement planning!

194
Q

Bradykinesia may relate to a suppressed level of?

A

excitability within the motor system

195
Q

Hypokinetic basal ganglia conditions can also lead to reduced what?

A

amplitude of movements.

196
Q

What is a tremor?

A

involuntary, rhythmic muscle contraction

197
Q

Resting tremor occurs in a body part that is?

A

not voluntarily activated and is supported against gravity (i.e., it is completely at rest)

Distinct from ‘intention tremor’ and other ‘action tremors’ (occurs during any voluntary movement)

198
Q

Amplitude of tremor increases during?

A

mental stress or movements of other parts of the body

Electrophysiological recordings of cells in basal ganglia firing at the same frequency as tremor movements – possibly a compensatory mechanism to cope with low dopamine

199
Q

Treatment approaches for Hypokinetic basal ganglia disorder?

A

Pharmacological approaches for rigidity and tremor

Prolonged stretching, and general movement for rigidity

Cueing (auditory) and time-constrained movements for Akinesia/Bradykinesia

200
Q

Hypotonia Basal ganglia may contribute to tone through?

A

long-latency reflexes – damage caused by HD may reduce that output

201
Q

These movements also happen as a side effect of medication (i.e., levodopa) delivered to treat Parkinson’s Disease. Whatv are they?

A

Chorea and Athetosis

202
Q

These movements also happen as a side effect of medication (i.e., levodopa) delivered to treat Parkinson’s Disease. Whatv are they?

A

Chorea and Athetosis

203
Q

What movements can dystonia produce?

A

Movements generated are diverse – slow and rapid

Twisting, repetitive movements and abnormal posture

204
Q

What movements can dystonia produce?

A

Movements generated are diverse – slow and rapid

Twisting, repetitive movements and abnormal posture

205
Q

Treatment approaches for Hyperkinetic basal ganglia disorder?

A

Similar to cerebellar pathology, no established treatment of hypotonia
Strength training, sensory stim, functional electrical stim, alignment

Compensatory strategies used for involuntary movements
Hands in pockets, “using” involuntary movements to perform functional tasks, providing hand holds or fixation points

Weight bearing considered important to increase joint stability (low tone + excessive movement = joint instability)

206
Q

Which of the patients is most likely to have a hypokinetic basal ganglia disorder?

Patient A
Decreased muscle tone
Involuntary sustained contractions causing abnormal postures
Involuntary rapid jerky movements during voluntary movement

OR

Patient B
Increased muscle tone (rigidity)
Resting tremor
Difficulty initiating voluntary movements
Slow execution of voluntary movements

A

Patient B.

207
Q

Which of the patients is most likely to have a hypokinetic basal ganglia disorder?

Patient A
Decreased muscle tone
Involuntary sustained contractions causing abnormal postures
Involuntary rapid jerky movements during voluntary movement

OR

Patient B
Increased muscle tone (rigidity)
Resting tremor
Difficulty initiating voluntary movements
Slow execution of voluntary movements

A

Patient B.