Neuro Day 1

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Neuroplasticity, role of neuro physio, Clinical reasoning, rehab program & stroke

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170 Terms

1
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What is the primary role of a Neurological Physiotherapist?

They manage people with movement disorders resulting from injuries and disease of the brain, spinal cord, and the broader neuromuscular system.

2
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Which client populations do Neurological Physiotherapists work with?

Those with disorders or damage, degenerative conditions and those with movement disorders, all arising from the brain, spinal cord or neuromuscular or sensory/motor system/s

3
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List the acute care settings where Neurological Physiotherapists work.

Acute wards, stroke units, and neurological wards.

4
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List the rehabilitation and community settings where Neurological Physiotherapists work.

Rehab units (inpatient/outpatient), private practice rehab, rehab in the home/community (e.g., transition care programs) and outreach services.

5
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What are the six key areas of knowledge and scientific evidence applied by Neurological Physiotherapists?

Neuroanatomy; neural plasticity; motor control; motor learning & skill acquisition; biomechanics of normal movement; and principles of effective coaching.

6
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What are the primary guiding principles related to client engagement?

Knowledge & scientific evidence, Fostering active participation and self-management, and being patient centred, family centred, ongoing use of clinical reasoning processes, delivered with ICF framwrok, based on EBP

7
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What actions must clients and family/carers be empowered to take following diagnosis?

Take responsibility for health/lifestyle issues; work with the carer/spouse/fam as early as practical; and the client must take an active role rather than be a passive recipient of therapy.

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How is client autonomy respected within the patient-centred model?

Encourage and respect the client's autonomy, control & choice; respect values, priorities & perspectives; and always involve the client/family in goals & decision.

9
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Which framework is used for service delivery?

The ICF framework (International Classification of Functioning, Disability and Health).

10
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List the core components of the ICF framework.

Health condition; Body functions & structures (body level impairments); Activity (behaviour/person level); and Participation (Societal level/roles).

11
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List the six specialized physiotherapy approaches

Neurodevelopmental, Motor learning, Proprioceptive Neuromuscular facilitation, Bobath, Brunnstrom, and Feldenkrais

12
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What is Neuroplasticity?

The capacity of the CNS to reorganise itself by forming, modifying & strengthening neural connections to both internal experiences & external stimuli.

13
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What types of changes does Neuroplasticity include?

Neurostructural, neuroreceptive & neurochemical changes.

14
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Name the two types of Neural Reorganisation.

Function-enabling plasticity and function-disabling plasticity.

15
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List examples of Function-Disabling plasticity.

Depression, anxiety, addiction, chronic pain, and chronic dizziness.

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List examples of Function-Enabling plasticity.

Learning, including language, skills, sports, and knowledge.

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What factors determine neural reorganisation post-lesion?

It depends largely on inputs received and outputs demanded post-lesion.

18
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Define Synaptic Plasticity.

Change that occurs at synapses, which is the junction between neurons.

19
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What does Synaptic Plasticity control? And is fundamental to which cognitive processes?

How effectively two neurons communicate with each other. Involved in learning & memory

20
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Define Long Term Potentiation (LTP).

Enhances synaptic efficacy by increasing receptor density & neurotransmitter release.

21
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Define Long Term Depression (LTD).

Reduces synaptic efficacy & refines synaptic networks.

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What is the benefit of Long term depression?

Good at refining synaptic networks (progressing from challenging to automatic processes).

23
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Define structural plasticity

the brain's ability to physically change its anatomical structure, including creating new neurons and altering existing neural connections

24
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Define Synaptogenesis (Structural Plasticity).

The formation of new synapses.

25
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Define Dendritic branching (Structural Plasticity).

Dendrites grow as cells adapt & respond to new information.

26
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Define Synaptic pruning.

The process of synapse removal.

27
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What is the purpose of Synaptic pruning?

Helps refine neural networks & increase efficiency.

28
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When does Synaptic pruning occur?

As part of brain maturation.

29
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Why is Structural Plasticity vital after injury?

It is vital for re-establishing function post injury.

30
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Which brain area undergoes more physical changes post-injury?

The area around the stroke/injury.

31
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Define Neurogenesis.

Refers to the generation of new neurons.

32
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Where does Neurogenesis predominantly occur?

In the hippocampus & subventricular zone.

33
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Neurogenesis is integral in which processes?

Learning, memory, emotional regulation & cognitive flexibility.

34
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How does age affect Neurogenesis?

It declines with age.

35
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What is associated with raised BDNF in the hippocampus?

Neurogenesis.

36
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What is BDNF?

Brain-derived neurotrophic factor; a protein crucial for the survival, growth, and function of neurons. It is vital for synaptic plasticity, learning, and memory, and plays a key role in maintaining brain health

37
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Define Intrinsic Neuronal Plasticity (INP).

changes in electrophysiological properties of individual neurons due to it's own activity through ion channel regulation & excitability

38
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What specific modifications define Intrinsic Neuronal Plasticity?

Modification in ion channel expression, metabolic activity, neurotransmitter density. Can occur instantaneously

39
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What effect does intrinsic neuronal plasticity have on neurons?

Can increase or decrease neuronal excitability and enhance responsiveness to incoming stimuli.

40
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Define Network level plasticity.

large scale reorganisation of neural circuits & connectivity patterns.Functional connectivity

41
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What specific shifts occur in Network level plasticity? Allowing what? Why is this important post injury?

Shifts in functional connectivity between brain regions. Allows for adaptations to new experiences and learning, and compensatory mechanisms after injury

42
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Provide an example of compensation after brain injury.

Adjacent cortical regions & contralateral motor networks are recruited to assume lost function.

43
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Does Network level plasticity produce changes quickly or slowly?

It takes longer than INP to produce long-term changes.

44
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How does the general process of neural plasticity change after a brain injury?

It stays the same (i.e., behaviours demands still drive neural plasticity).

45
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What physical issues significantly impair neuronal function after injury?

Oedema, inflammation & altered neuronal excitability. Structures that were not designed to perform specific functions may need to compensate.

46
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What specific structures are damaged post-stroke?

Damage to grey matter AND ascending & descending white matter tracts (axons) and white matter connections between cortical & subcortical structures.

47
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Describe the role of white matter tracts?

They are the "highways of the brain" – the message cannot get through if the pathway isn't there.

48
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List the mechanisms of Grey Matter neuroplasticity.

Synaptogenesis (creation of new connections); Synaptic plasticity / remodelling; Neurogenesis; Intrinsic neuronal plasticity, ion channel regulation & excitability; and Reorganisation of neural networks.

49
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When does Synaptic plasticity occur with motor learning?

Not with repetitive practice alone, but relies on intensity, challenge, variability of practice, motivation & salience.

50
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List the mechanisms of White matter plasticity.

Remyelination of axons; Axonal sprouting (expansion of new axonal branches from presenting neurons); Axonal remodelling; and Connectivity reorganisation (altered long range connection between regions).

51
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What is the requirement for White matter plasticity to occur?

It is use dependent; activity = increased axonal firing = proliferation of oligodendrocytes.

52
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What are oligodendrocytes responsible for?

Remyelination of axons, axonal sprouting & synaptogenesis.

53
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Define Spontaneous Recovery / restoration.

Returning function to a brain area where the neurons were not lost but became dysfunctional following injury.

54
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List the mechanisms of Spontaneous Recovery.

Resolution of local oedema, Improvement of local circulation, Recovery of partially damaged ischaemic neurons, and Resorption of local toxins.

55
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Define Recruitment (in structural recovery).

Increasing the involvement of a brain area to perform a function that was lost after injury.

56
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Define Retraining (in structural recovery).

Adapting a brain area to perform a completely novel function.

57
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Describe the activity of the bilateral motor cortex post-stroke.

There is a greater degree of bilateral motor cortex activity (the other side kicks in & takes over).

58
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When does this increased bilateral activity occur and diminish?

Particularly in the acute period; it diminishes within months of the stroke onset.

59
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Which secondary cortical areas are increasingly recruited in the affected hemisphere?

Premotor cortex especially, and the Supplementary cortical area.

60
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List what changes occur to the cortical reorganisation of motor skills

Greater degree of bilateral motor cortex activity, increased recruitment of secondary cortical areas in affected hemisphere, increase in ipsilateral cortical involvement early on, brain is most sensitive to neuroplastic changes <3 months post stroke

61
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Ischemia triggers post stroke

Upregulation of genes responsible for neuronal growth, increases in long term potentiation, enabling strengthening of synapses & improved neurotransmission. Alterations in excitation & inhibition via neurotransmitters. Axonal sprouting around infarct site

62
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KEY POINT: How should rehabilitation for patients be approached?

It should be holistic to ensure optimal chance of change & progression.

63
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Define Diaschisis.

Change of function in a portion of the brain connected to a distant but damaged brain area.

64
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How does an area affected by Diaschisis recover?

It goes quiet after communication is stopped with the damaged area, regains confidence & re-commences usual processes.

65
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List the 10 Principles of Experience-Dependent Plasticity.

Use it or lose it; Use it & improve it; Specificity; Repetitions; Intensity; (Difficulty); Time sensitive; Salience, Motivation, Attention; Age matters; Transference; Interference.

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PRINCIPLE: Use it or lose it.

Failure to drive specific brain functions can lead to functional degradation.

67
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PRINCIPLE: Use it & improve it.

Training that drives a specific brain function can lead to enhancement of that function.

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PRINCIPLE: Specificity (definition).

The nature of training the experience dictates the nature of plasticity.

69
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What neuroplastic changes result from Skill training?

Synaptogenesis & changes in cortical motor maps.

70
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What neuroplastic changes result from Aerobic training?

Primarily angiogenesis in the motor cortex, increases blood flow, increases cortical excitability & increases levels of BDNF.

71
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What is the functional benefit of Aerobic training?

It is good for priming the brain to learn.

72
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What neuroplastic changes result from Strength training?

Primarily synaptogenesis in the spinal cord and increases cortical excitability.

73
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Why is Task specificity important?

Patients require task-specific training (skilled) in order to drive neural plastic changes.

74
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What type of practice does not cause significant changes in the brain?

Unskilled repetition of existing motor movements.

75
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What does Timing specificity promote?

The normal timing of muscle activity. We learn new motor skills by coordiating movements in time. Neurons that fire together wire together (tend to strengthen their connections between one another).

76
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PRINCIPLE: Repetition Matters.

Repetition is required to drive neural plasticity (total number of stimuli provided).

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PRINCIPLE: Intensity matters (definition).

Total number of stimuli per unit time; "lots and lots".

78
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Which practice schedule creates more permanent neural changes?

Short regular intervals of practice, rather than the 'one off' longer sessions.

79
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PRINCIPLE: (Difficulty).

Induction of plasticity requires an appropriate level of difficulty (Not too hard/not too easy) To drive maximal changes in behaviour.

80
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PRINCIPLE: Time Sensitive.

Neural restructuring should work anytime, but there is a time window after brain damage when it is particularly effective.

81
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What is this effective time window called?

Lesion-induced reactive plasticity.

82
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When is the ideal time and when is rehabilitation shown to be less effective post-stroke?

Ideal 24-48 hours post stroke. If initiated more than 30 days post stroke (in promoting cortical reorganisation & improving function).

83
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PRINCIPLE: Salience, Motivation, Attention (requirement).

The task learnt must be important to the individual.

84
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How does Salience promote plasticity?

Salience = increased attention = increased neural plasticity.

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PRINCIPLE: Age matters (effects of aging).

Reactive neuronal synaptogenesis declines, sprouting responses are less robust, and synaptic replacement rates diminish as animals age. Younger stroke patients demonstrate slightly faster functional recovery.

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PRINCIPLE: Transference.

Plasticity in response to one training experience can enhance the acquisition of similar behaviours (learning from one skill can be transferred to another).

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PRINCIPLE: Interference.

Plasticity in response to one training experience can interfere with the acquisition of other behaviours (learning of one skill can interfere with the learning of another).

88
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List the Stimulation-based (non-invasive) priming techniques.

Periphery electrical stimulation (TENS & NMES), Transcranial direct current stimulation (tDCS), and Repetitive transcranial magnetic stimulation (rTMS).

89
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What is the effect of TENS (sensory) & NMES (muscle stim)?

They induce changes in cortical stimulation.

90
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How do different frequencies of sensory electrical stim affect motor responses?

High frequency decreases/inhibits response; Low frequency is excitatory.

91
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What significantly increases cortical excitability involving voluntary movement?

Pairing voluntary movement & electrical muscle stimulation.

92
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Define Transcranial direct current stimulation (tDCS).

Application of a weak direct current to the brain using 2 surface electrodes.

93
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How does tDCS work internally?

The current penetrates the cranium and alters resting membrane potentials in underlying neural tissue.

94
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What is the general effect of tDCS on the cortex?

It can increase or decrease cortical excitability.

95
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What is the benefit of combining tDCS with physio?

Can improve excitability of the motor cortex, physical performance & motor learning.

96
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Define Repetitive transcranial magnetic stimulation (rTMS).

Passes a magnetic field through the skull & elicits electrical currents in the underlying neural tissue.

97
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How does rTMS affect the cortex?

Depending on the frequency of the pulse, it can increase or decrease cortical excitability.

98
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List the Non-stimulation based priming methods.

Motor imagery, Action observation, Mirror therapy, Movement based priming, and Aerobic exercise.

99
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Define Motor imagery.

Mental rehearsal of a goal directed action.

100
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What benefits does Motor imagery provide?

Can promote brain reorganisation & increase blood flow to the motor area responsible for the desired action.