Neuroplasticity and neurorehabilitation Flashcards

1
Q

define neuroplasticity

A

the ability of the nervous system to adapt and reorganize, often as a result of
injury, learning, and/or experience. It involves the sum of molecular, structural, and
physiological neuronal changes

Newly learned information is 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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2
Q

what are the different types of neuroplasticity

A

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

Structural: E.g., growth of dendritic spines

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

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3
Q

neuroplasticity types

A

Types of neuroplasticity include developmental, habituation, learning and memory, and
recovery from central nervous system (CNS) injury

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4
Q

developmental neuroplasticity

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.
Language-learning is one example.

 Amount of neurons at age 2-3 is about 2X adult brain; 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.

 You develop what you do or know by 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)

 Neurons MUST have a purpose or they die (apoptosis – programmed cell death).

 The whole process is neuroplasticity – like pruning a brush to allow room for stronger
new growth

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5
Q

neuro rehab implication - developmental

A

Neuroplasticity has a 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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6
Q

habituation

A

Habituation is 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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7
Q

neuro rehab implication - habituation

A

Applied to therapeutic approaches that are intended to decrease the neural response to a
stimulus. For example, 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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8
Q

learning and memory

A

Learning involves the ability of the brain to acquire new knowledge through instruction
or experience, while memory is the process by which that knowledge is retained over
time.
 During initial stages of motor learning, 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

Need both LTD and LTP – if not, eventually synapses would reach some level of
maximum efficacy, making it difficult to encode new information

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9
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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10
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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11
Q

neuro rehab implication - recovery from CNS injury

A

Recovery from CNS injury, such as stroke and spinal cord injury, involves both
spontaneous and activity-dependent plasticity

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12
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.
o 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.
o Processes include 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), and
electrophysiological changes (e.g., alteration of excitatory/inhibitory balance,
particularly in the peri-infarct cortex post-stroke)

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13
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.

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

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14
Q

neuro rehab implication - training induced plasticity

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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15
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. Neuroplastic changes
associated with motor impairment and recovery post-stroke can include: changes to existing neuronal pathways, formation of new neuronal connections, overactivation of primary and association motor areas

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15
Q

changes to existing neuronal pathways after stroke

A

Wallerian degeneration - 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.

Alterations in white matter 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

15
Q

formation of new neuronal connections after stroke

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

16
Q

overactivation of primary and association motor areas after stroke

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.

o 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

17
Q

Task-specific training leads to

A

Task-specific training leads to 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)]

18
Q

neuroplastic changes and motor impairment/recovery AFTER SCI

A

Various events depress motor function after SCI. Direct damage to the spinal cord (severed,
bruising), spinal shock, and inflammation.
 Spinal shock is 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.
 Inflammation 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)

19
Q
A

Neuroplastic changes occur throughout the neuraxis (spinal cord, brainstem, cortex) following
SCI. Neuronal dysfunction below the lesion primarily occurs due to 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.
Cortical reorganization occurs due to decreased afferent-related cortical excitation due to direct
damage to ascending pathways along with decreased movement-related afferent input.

20
Q

More specific neuroplastic changes include:

A

 Impaired function of spinal inhibitory pathways, which 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.
 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

21
Q

In general, movement disorders after SCI are due to

A

In general, movement disorders after SCI are due to the defective utilization of afferent input,
reduction in cortical input, and depressed functional state of spinal locomotor circuitries.

22
Q

spontaneous plasticity involves…

A

Spontaneous plasticity involves resolution of neuropraxia (transient nerve conduction block),
changes in neuronal properties (e.g., collateral sprouting, remyelination of spared axons), and
changes in cortical and spinal neuronal networks (e.g., modifications of synaptic strength,
synaptic rearrangements, reflex adaptations).

23
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. Activity-dependent learning/plasticity occurs even in isolated
spinal circuits. Mechanisms of training-induced recovery include 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

24
Q

neurorehab definition

A

Neurorehabilitation is the interface between rehabilitation medicine and neurology, and is 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.

Neurorehabilitation has a sound theoretical and conceptual basis derived from the World
Health Organization’s International Classification of Functioning, Disability, and Health (ICF) (see
figure below, adapted for stroke).2 The ICF model is used to guide assessment in stroke and for
shared goal-setting.

25
Q

neurorehab team and PT role

A

Neurorehabilitation involves a multidisciplinary team with structured
organization, effective communication, and processes to provide multimodal treatment
programs for persons with neurological injury or disease. Physical therapists (or
physiotherapists) are a vital part of these teams, and contribute expertise as movement system
specialists by assessing and designing treatment interventions aimed at improving motor
function, patient independence, and quality of life. Organized multidisciplinary rehabilitation
has been shown to be associated with reduced odds for death, institutionalization, and
dependency compared to other non-specific, general rehabilitation approaches.

26
Q

neurorehab strategies to enhance plasticity and recovery

A

based on 10 principles
1. use it or lose it
2. use it and improve it
3. speccificity
4. repetition matters
5. intensity matters
6. time matters
7. salience matters
8. age matters
9. transference
10. interfernece

27
Q

what is interference

A

plasticity in response to one experience can interfer with the ocquistion of other behaviors

28
Q

what is transference

A

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