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Neuro Final > Neuroplasticity & Neurorehabilitation > Flashcards

Neuroplasticity & Neurorehabilitation Flashcards

1
Q

Neuroplasticity =

A

ability of the nervous system to adapt and reorganize, often as a result of injury, learning, and/or experience

involves the sum of molecular, structural, and physiological neuronal changes

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2
Q

Molecular: changes

A

in gene transcription, protein regulation, and/or neurotransmitter release (amount, type)

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3
Q

Structural: changes

A

E.g., growth of dendritic spines

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4
Q

Physiological: changes

A

in neuronal excitation/inhibition; increased functional complexity of motor neurons

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5
Q

Newly learned information =

A

encoded as new dendrites sprout to connect neurons to specific sites, producing a new pathway that represents the experience

There can be adaptive (e.g., increased motor output) and maladaptive (e.g., neuropathic pain) neuroplastic changes

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6
Q

Neuroplasticity Types:

A

developmental

habituation

learning and memory

recovery from central nervous system (CNS) injury

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7
Q

Developmental =

A

Different regions of the brain become heavily myelinated during pre-programmed sensitive periods, which opens up windows of opportunity for developing specific skills or competencies

After a region is myelinated, a performance permanence sets in

ex)nLanguage-learning

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8
Q

Amount of neurons at age 2-3 is about 2X adult brain:

A

as we age, the old connections are deleted through synaptic pruning, which is the process of removing weakened or ineffective connections

Stronger connections are kept and strengthened

What synapses are kept is determined by experience – most frequently activated are preserved

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9
Q

You develop what you do or know by:

A

repetition and stimulating the areas of the brain for those specific functions; initially use large part of brain, then less as refine behavior (e.g., athletes, musicians)

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10
Q

Neurons MUST have a purpose or:

A

they die (apoptosis – programmed cell death)

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11
Q

developmental NEUROREHAB IMPLICATION:

A

Neuroplasticity = clear age-dependent component

Certain types of plasticity are more prevalent during different periods of life (e.g., babies working on motor control versus speech development)

Training-induced plasticity also occurs more easily in younger brains

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12
Q

Habituation =

A

Decrease in response to a repeated, benign stimulus reflecting a decrease in synaptic activity and/or reduced amplitude of synaptic potentials

With prolonged stimulus repetition, more permanent structural changes occur (e.g., decreased number of synaptic connections)

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13
Q

Habituation NEUROREHAB IMPLICATION:

A

Applied to therapeutic approaches that are intended to decrease the neural response to a stimulus

In vestibular rehabilitation patients are asked to move repeatedly in fashions that typically make them dizzy or nauseous

Also used for tactile defensiveness (i.e. extreme response to cutaneous stimulation) and sensory integration problems with kids, and for helping with phantom limb pain

Start with gentle tactile stimulation, then gradually increase the intensity in an effort to achieve habituation

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14
Q

Learning and Memory =

A

Learning involves the ability of the brain to acquire new knowledge through instruction or experience

memory is the process by which that knowledge is retained over time

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15
Q

During initial stages of motor learning:

A

large and diffuse brain regions show synaptic activity

eventually, once a task is learned, only small, distinct brain regions show increased activity with performance of the task

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16
Q

Forms of synaptic plasticity that contribute to learning and memory:

A

Long-term potentiation (LTP) or facilitation

Long-term depression (LTD)

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17
Q

Long-term potentiation (LTP) or facilitation–

A

a progressive and persistent increase in synaptic strength that occurs with repeat stimulation (can lead to enhanced motor output)

produces long-lasting changes in signal transmission (e.g., greater neurotransmitter release, increase in number of synapses and dendritic connections) associated with learning, makes neurons more “sensitive” to each other

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18
Q

Long-term depression (LTD)–

A

a reduction in the efficacy of synaptic transmission

Serves to selectively weaken certain synapses, as well as recalibrate their set point for further excitation

Also protects synapses from overexcitation by making them less sensitive to an ongoing stimulus

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19
Q

Need both LTD and LTP –

A

if not, eventually synapses would reach some level of maximum efficacy, making it difficult to encode new information

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20
Q

Learning and Memory NEUROREHAB IMPLICATION:

A

Essential component of motor learning, which is a main focus of neurorehabilitation

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21
Q

Recovery from CNS Injury =

A

involves both spontaneous and activity-dependent plasticity

Neurologic recovery occurs through complex combination of spontaneous and learning-dependent processes.

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22
Q

Spontaneous plasticity =

A

entails the variable, spontaneous recovery during the first few months (typically 3 months) post-injury as a result of endogenous biological processes rather than behavioral, pharmacological, or neuromodulatory interventions

Resolution of reversible injuries to neurons and glia (such as alterations in membrane potentials, axon conduction), reversal of diaschisis, activation of cell repair, etc. occur during this timeframe

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23
Q

Spontaneous plasticity - processes include:

A

resolution of inflammation/decreased edema

molecular and cellular changes (e.g., gene expression changes important for neuronal growth activation of growth factors)

structural changes (e.g., axonal sprouting)

electrophysiological changes (e.g., alteration of excitatory/inhibitory balance, particularly in the peri-infarct cortex post-stroke)

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24
Q

Activity-dependent (or training-induced) plasticity:

A

involves functional training to direct and enhance plasticity to restore function

Treatment factors to consider include task complexity, specificity, difficulty, intensity

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25
Q

Recovery from CNS Injury NEUROREHAB IMPLICATION:

A

Training-induced plasticity and recovery is what we focus on in neurorehabilitation

We utilize neuroscience and neuroplasticity principles to develop and/or direct more evidence-based diagnostics and treatments to enhance motor output and recovery in our patients

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26
Q

Neuroplastic Changes and Motor Impairment/ Recovery After Stroke:

A

Injury to the motor cortex leads to the recruitment of motor areas that were not making significant contribution to the lost motor function before injury

1) Changes to existing neuronal pathways

2) Formation of new neuronal connections

3) Overactivation of primary and association motor areas (perilesional and contralesional)

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27
Q

Changes to existing neuronal pathways =

A

Wallerian degeneration

Alterations in white matter

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28
Q

Wallerian degeneration -

A

characterized by anterograde degeneration of the distal portion of axons after injury to the cell body/proximal nerve

Detected as early as 2 weeks post-stroke

Followed by progressive myelin degeneration and eventually fibrosis and atrophy of fiber tracts

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29
Q

Alterations in white matter -

A

microstructural integrity

Occurs not only in the lesioned area but also in brain regions and motor tracts beyond the infarction site (diaschisis)

Such alterations can contribute to behavioral deficits

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30
Q

Formation of new neuronal connections =

A

Cortical remapping – reorganization of movement representations within the motor cortex

Can entail perilesional reorganization, secondary motor area contributions, changes in neuronal activation patterns (e.g., unmasking of latent motor pathways)

Alternative and/or newly formed connections can compensate for loss of original connections

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31
Q

Overactivation of primary and association motor areas (perilesional and contralesional) =

A

In patients who demonstrate more favorable recovery, overactivations tend to diminish over time as learning occurs and it takes fewer brain regions to complete a task

Research has shown that the contralesional hemisphere undergoes neuroplastic changes after stroke, but its role in motor recovery is unclear (e.g., it may play a greater role in the presence of large ischemic infarcts)

Persistent recruitment of contralesional motor areas often appears in patients with poorer functional outcomes

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32
Q

Task-specific training leads to:

A

an increase in the area of motor cortex that controls the muscles used during the task

Therapeutic modulation of neural networks has also been shown to occur following high-intensity exercise/gait training and non-invasive brain stimulation [repetitive transcranial magnetic stimulation (rTMS), transcranial direct current stimulation (tDCS)]

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33
Q

Various events depress motor function after SCI:

A

Direct damage to the spinal cord (severed, bruising)

spinal shock

inflammation

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34
Q

Spinal shock =

A

state of transient physiological (rather than anatomical) reflex depression of cord function below the level of injury with associated loss of all sensorimotor functions

reflects the decreased activity of spinal circuits suddenly deprived of input from the motor cortex and brainstem

Areflexia and flaccid paralysis, including of the bowel and bladder, is observed

May last hours or up to several weeks

Early resolution is a positive sign

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35
Q

Inflammation =

A

entails both local swelling that compresses spinal tracts (impairing neural conduction) and intradural pressure (pressure created by edema and hemorrhage inside the spinal cord, which then expands against the dura)

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36
Q

Neuroplastic changes occur throughout the ___ following SCI

A

neuraxis (spinal cord, brainstem, cortex)

37
Q

Neuronal dysfunction below the lesion primarily occurs due to:

A

immobility and decreases in appropriate afferent input, resulting in a loss of activity in neuronal circuitries below the level of injury, an imbalance in inhibitory and excitatory activity, and a change in spinal reflex behavior

38
Q

Cortical reorganization occurs due to:

A

decreased afferent-related cortical excitation due to direct damage to ascending pathways along with decreased movement-related afferent input

39
Q

More specific neuroplastic changes include:

A

Impaired function of spinal inhibitory pathways

Altered excitability of alpha motor neurons due to loss or reduction in brainstem-derived serotonin and norepinephrine.

Lack of soleus H-reflex depression during the swing phase of walking; disruption of sustained reflex excitability during stance.

40
Q

Impaired function of spinal inhibitory pathways:

A

can lead to increased muscle tone, stretch reflex hyperexcitability, and muscle co-contractions (commonly observed in persons with incomplete SCI)

Spastic muscle tone, however, can compensate in part for the SCI-induced loss of supraspinal drive

Secondary changes in muscle fibers lead to a regulation of muscle tone during functional movements at a simpler level, i.e. without modulated muscle activation

41
Q

In general, movement disorders after SCI are due to:

A

defective utilization of afferent input, reduction in cortical input, and depressed functional state of spinal locomotor circuitries

42
Q

Spontaneous plasticity involves:

A

resolution of neuropraxia (transient nerve conduction block)

changes in neuronal properties (e.g., collateral sprouting, remyelination of spared axons)

changes in cortical and spinal neuronal networks (e.g., modifications of synaptic strength, synaptic rearrangements, reflex adaptations)

43
Q

Training-induced plasticity and recovery:

A

The repetitive activation of particular sensorimotor pathways by task-specific training can reinforce circuits and synapses used to successfully perform the practiced movement

44
Q

Activity-dependent learning/plasticity occurs even in ____

A

Isolated spinal circuits

45
Q

Mechanisms of training-induced recovery include:

A

up-regulation of growth and neurotrophic factors (e.g., BDNF), changes in neuronal excitability, and adaptations within spinal networks

As persons with SCI likely cannot reactivate their normal motor patterns, they may engage new motor patterns of muscle activity to perform as task

46
Q

Neurorehabilitation =

A

interface between rehabilitation medicine and neurology

an active and dynamic process designed to help patients with neurological injury or disease increase their level of function (both at home and in the community), prevent secondary deterioration, facilitate psychological adaptation, and enhance their quality of life

47
Q

Neurorehabilitation involves a multidisciplinary team with structured organization:

A

organized multidisciplinary rehabilitation has been shown to be associated with:

reduced odds for death

institutionalization

dependency compared to other non-specific, general rehabilitation approaches

48
Q

Neurorehabilitation Strategies to Enhance Neural Plasticity and Recovery:

A

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

49
Q

use it or lose it =

A

failure to drive specific brain functions can lead to functional degradation

50
Q

use it and improve it =

A

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

51
Q

specificity =

A

nature of the training experience dictates the nature of the plasticity

52
Q

repetition matters =

A

induction of plasticity requires sufficient repetition

53
Q

intensity matters =

A

induction of plasticity requires sufficient training intensity

54
Q

time matters =

A

different forms of plasticity occur at different times during training

55
Q

salience matters =

A

training experience must be sufficiently salient to induce plasticity

56
Q

age matters =

A

training-induced plasticity occurs more readily in younger brains

57
Q

transference =

A

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

58
Q

interference =

A

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

59
Q

When taking part in motor practice and training, patients need to be an active participant =

A

The task has to be challenging enough, and at a high enough training intensity, to induce adaptive neuroplastic changes

t is important to allow for error feedback/adjustment, so the patient learns how to monitor and adjust motor output

60
Q

Cortical maps are very dynamic:

A

We can form new routes after injury, and new connections with practice (i.e. neurorehabilitation)

61
Q

Strategies to enhance neural plasticity include:

A

Experience, especially enriched environments

Skill training (vs. strength training)

Cortical stimulation – E.g., TMS and tDCS. Can be used to “prime” the motor cortex for subsequent behavior-induced plasticity

Combinatorial therapies

62
Q

Combinatorial therapies –

A

can be used to amplify the effects of single interventions (e.g., cortical stimulation or pharmacological agent + task-specific training)

Augmenting motor practice with stimulation can increase the responsiveness of the nervous system to modulatory influences that occur through motor practice and training (i.e. increased neural excitability), promoting adaptive neuroplasticity and functional recovery

63
Q

Rehabilitation training and pharmacological interventions can enhance ___ processes following CNS injury

A

spontaneous internal neuroplastic

64
Q

Stroke induces various cortical changes and reorganization on the anatomical and molecular level, yet the ____ remains unclear

A

optimal timing, intensity, and type of rehabilitation training to further enhance plasticity

65
Q

Optimal therapeutic approaches can only be designed with:

A

greater understanding of the neurobiology of spontaneous and training-induced recovery

66
Q

presence of critical time windows post-stroke =

A

(i.e. when the brain is most responsive)

for plasticity-promoting agents and training, combined with the heterogeneity of stroke

suggests that appropriate treatment onset times and individually tailored interventions are essential

67
Q

3 step model for rehab schedules:

A

1) determine the metabolic and plastic status of the brain = state of the art imaging and biomarkers

2) enhancement of plastic status of the brain and spinal cord = applications of growth and plasticity promoting factors

3) selection and stabilization of newly formed functional connections = rehabilitative training

68
Q

Motor Recovery vs Motor Compensation

A

Return of motor capacity following neurologic injury or in patients with neurologic disease is often a combination of recovery and compensatory mechanisms

happens at 3 levels

69
Q

Motor recovery - ICF: health condition (neuronal)

A

restoring function in neural tissue that was initially lost after injury

may be seen as reactivation in brain areas previously inactivated by the circulatory event

although this is not expected to occur in the area of the primary brain lesion, it may occur in areas surrounding the lesion (penumbra) and in the diaschisis

70
Q

Motor recovery - ICF: Body functions/Structure (performance)

A

restoring the ability to perform a movement in the same manner as it was performed before injury

may occur through the reappearance of premorbid movement patterns during task accomplishment (voluntary joint range of motion, temporal and spatial interjoint coordination, etc.)

71
Q

Motor recovery - ICF: Activity (functional)

A

successful task accomplishment using limbs or end effectors typically used by nondisabled individuals

72
Q

Motor compensation - ICF: health condition (neuronal)

A

neural tissue acquired a function that it did not have prior to injury

may be seen as activation in alternative brain areas not normally observed in nondisabled individuals

73
Q

Motor compensation - ICF: Body functions/Structure (performance)

A

performing an old movement in a new manner

may be seen as the appearance of alternative movement patterns (recruitment of additional or different degrees of freedom, changes in muscle activation patterns such as increased agonist/antagonist coactivation, delays in timing between movements of adjacent joints) during the accomplishment of a task

74
Q

Motor compensation - ICF: Activity (functional)

A

successful task accomplishments using alternate limbs or end effectors

ex) opening a package of chips using 1 hand and the mouth instead of 2 hands

75
Q

Compensation can be adaptive =

A

characterized by the use of alternate movement patterns, or substitutive, which is characterized by the use of different effectors or assistive devices to replace lost motor components

76
Q

Use of Biomarkers to Guide Neurorehabilitation

A

(e.g., neural markers via TMS or MRI, blood markers) may be used to predict motor recovery and response to therapy after stroke

Improve accuracy of functional motor recovery prognosis

Target therapeutic interventions (personalized medicine)

Optimize patient resources/inform discharge planning

77
Q

Both clinical measures, neural and physiological mechanisms have been shown to be associated with different stroke outcomes (e.g., independence and disability, upper extremity recovery), and several ____ have been developed for these outcomes

A

prediction tools

78
Q

use of prediction tools in healthcare:

A

can assist rehabilitation and goal setting and increase equity of access to therapeutic services

79
Q

For prediction tools to be useful, they must:

A

1) be used at the beginning of recovery

2) make a prediction for a specific timepoint (rather than an outcome at discharge)

3) should be meaningful to patients (e.g., like being able to predict likelihood of achieving specific level of function

4) should combine a small number of variables in an easy way (decision tree, app) for easy use by clinicians

80
Q

online calculator:

A

predictors: age, sex, time to admission, motor FIM score, cognitive FIM score, unilateral neglect

time point: discharge from inpatient rehab

outcome: probability of a motor FIM score > 61 points

externally validated

81
Q

scores and tables:

A

predictors: age, NIHSS, diabetes, previous stroke, atrial fibrillation

time point: discharge from inpatient rehab

outcome: probability of each of 5 categories based on Barthel Index score

not externally validated

82
Q

graphical recovery curves for each predictor:

A

predictors: age, sex, glasgow coma sclae, NIHSS, stroke type

time point: any week up to 1 yrs poststroke

outcome: Barthel Index Score

externally validated

83
Q

PREP2 prediction categories:

A

excellent

good

limited

poor

83
Q

PREP2 - good

A

34-48

potential to be using the affected hand and arm for most activities of daily living within 3 months, though with some weakness, slowness, or clumsiness

promote normal funciton of the affected hand and arm by improving strength, coordination

minimize compensation with other hand and arm and trunk

83
Q

PREP2 - limited

A

13-31

potential to regain some movement in the affected hand and arm within 3 months, but daily activites are likely to require significant modification

unlikely to regain dextrous hand function

promote adaptation in daily activities, incorporating the affected upper limb wherever safely possible

84
Q

PREP2 - poor

A

0-9

unlikely to regain useful hand and arm function within 3 months

may be able to use the affected hand and arm as a stabilizer in bimanual tasks

prevent secondary complications such as pain, spasticity, and shoulder instability

reduce disability by learning to complete daily activities with the stronger hand and arm

84
Q

Future work is needed to investigate the potential role of neural ___ and blood ___ biomarkers in walking recovery post-stroke, and to differentiate between different levels of walking ability.

A

(e.g., TMS/MRI measures)

(e.g., serum levels of BDNF, other markers associated with immune response)

84
Q

Selecting optimal treatment strategies for individual patients based not only on their clinical evaluation, but also on:

A

their neural, blood, and genetic makeup will help tailor treatment strategies to maximize therapeutic effects, helping to optimize function and quality of live in persons with stroke

Neuro Final (10 decks)

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