NPNR

Question 1

neurplastic changes post stroke

Answer 1

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.

Task specific training leads to an increase in the area of motor cortex that controls the muscles used during the task.

Therapeutic modulation of neuronal 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))

Question 2

neuroplastic changes associated with motor impairment and recovery post stroke can include

Answer 2

changes to existing neuronal pathways

formation of new neuronal connections

overactivation of primary and association motor areas

Question 3

post stroke - changes to existing neuronal pathways

Answer 3

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 contribute to behavioral deficits

Question 4

formation of new neuronal pathways - cortical remapping

Answer 4

Reorganization of movement representations within the motor cortex.

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

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

Question 5

post stroke - Overactivation of primary and association motor areas (perilesional and contralesional)

Answer 5

**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 neuropalstic changes after stroke, but its role in motor recovery is unlear (it may play a greater role in the presence of large ischemic infarct). Persistent recruitment of contralesional motor areas often appears in patients with poorer functional outcomes

Question 6

Neuroplastic changes and motor impairment/recovery - post SCI

Answer 6

Various events depress motor function after SCI.

Direct damage to the spinal cord (severed, bruising), spinal shock, and inflammation

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 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

Question 7

Cortical reorganization occurs due to

Answer 7

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

Question 8

Neuronal dysfunction below the lesion primarily occurs due to

Answer 8

Neuronal dysfunction below the lesion primarily occurs due to immobility and decreases in appropriate afferent input, resulting in a loss of activity and a change in spinal reflex behavior

Question 9

spinal shock

Answer 9

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

Question 10

More specific neuroplastic changes
post SCI

Answer 10

• 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.

Question 11

In general, movement disorders after SCI are due to

Answer 11

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

Question 12

Spontaneous plasticity involves

Answer 12

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).

Question 13

Training-induced plasticity and recovery:

Answer 13

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.

Question 14

neurorehab definition and role of PTs

Answer 14

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.

PTs

contribute expertise as movement system specialists by assessing and designing treatment interventions aimed at improving motor function, patient independence, and quality of life.

Question 15

Organized multidisciplinary rehabilitation has been shown to be associated with reduced

Answer 15

reduced odds for death, institutionalization, and dependency compared to other non-specific, general rehabilitation approaches.

Question 16

10 principles of neuro rehab

Answer 16

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

Question 17

what is interference

Answer 17

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

Question 18

what is transference

Answer 18

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

Question 19

age matters

Answer 19

training induced plasticity occurs more readily in younger brains

Question 20

salience matters

Answer 20

the training experience must be sufficiently salient to induce plasticity

Question 21

time matters

Answer 21

different forms of plasticity occur at different times during training

Question 22

intensity matters

Answer 22

induction of plasticity requires sufficient training intensity

Question 23

repetition matters

Answer 23

induction of plasticity requires sufficient repetition

Question 24

specificity

Answer 24

the nature of the training experience dictate the nature of palsticity

Question 25

use it and improve it

Answer 25

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

Question 26

use or lose it

Answer 26

failure to drive specific brain functions can lead to functional degradation

Question 27

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

Answer 27

When taking part in motor practice and training, patients need to be an active participant. The task has to be challenging enough, and at a high enough training intensity, to induce adaptive neuroplastic changes. It is important to allow for error feedback/adjustment, so the patient learns how to monitor and adjust motor output.

Question 28

how are cortical maps very dynamic

Answer 28

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

Question 29

strategies to enhance neural plasticity include

Answer 29

• 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 – 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.

Question 30

read?

Answer 30

Rehabilitation training and pharmacological interventions can enhance spontaneous internal neuroplastic processes following CNS injury.

Stroke induces various cortical changes and reorganization on the anatomical and molecular level, yet the optimal timing, intensity, and type of rehabilitation training to further enhance plasticity remains unclear.

Optimal therapeutic approaches can only be designed with a greater understanding of the neurobiology of spontaneous and training-induced recovery.

The presence of critical time windows post-stroke (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.

Thus, potential future rehabilitation schedules may include the following to optimize plasticity and motor recovery post-stroke

Question 31

3 step model for rehab schedules

Answer 31

1. determination of the metabolic and plastic status of the brain
   - state of aart imaging and biomarkers
2. enhancement of the plastic status of the brain and spinal cord
   - application of growth and plasticity promoting factors
3. selection and stabilization of newly formed functional connections
   - rehab training

Question 31

motor recovery as health condition (neuronal)

Answer 31

restoring function in neuronal tissue that was initiallly lost after injury

may be seen as reactivation 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 and in the diaschisis

Question 32

motor recovery as body function/structure (performance)

Answer 32

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

this may occur through the reapperance of premorbid movement patterns during task accomplishment (voluntary joint ROM, temporal and spatial innerjoint coordination, etc)

Question 33

motor recovery as activity (functional)

Answer 33

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

Question 34

motor compensation as health condition (neuronal)

Answer 34

neural tissue acquires a function that is did not have prior to injury

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

Question 35

motor compensation as body function/structure (performance)

Answer 35

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 b/w movements of adjacent joints, etc)

Question 36

motor compensation as activity (functional)

Answer 36

successful task accomplishment using alternative limb or end effectors

opening a pack of chips usin gmouth not hands

Question 37

*Compensation can be adaptive, which is 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.

Question 38

use of biomarkers to guide neurorehab

Answer 38

Clinical predictors and biomarkers (e.g., neural markers via TMS or MRI, blood markers) may be used to predict motor recovery and response to therapy after stroke. Such insight can be used to:

• improve accuract of functional motor recovery prognosis
• target therapeutic interventions (personalized medicine)
• optimize patient resources/inform discharge planning

Question 39

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 prediction tools have been developed for these outcomes.

The use of prediction tools in healthcare can assist rehabilitation and goal setting and increase equity of access to therapeutic services.

For these tools to be useful, they must

Answer 39

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.

Question 40

examples of current predcition models for stroke outcomes

Answer 40

independence and disability
UE recovery potential
walking prediction models

Question 41

what is the primary predicted outcome

Answer 41

upper limb functional recovery [as assessed via the Action Reach Arm Test (ARAT)] at 3 months post-stroke. Based on the patient’s predicted category, a suggested rehabilitation focus is outlined.

Question 42

Future work is needed to investigate the potential role of neural (e.g., TMS/MRI measures) and blood (e.g., serum levels of BDNF, other markers associated with immune response) biomarkers in walking recovery post-stroke, and to differentiate between different levels of walking ability.

Question 43

Despite improvements in the medical management of acute stroke, many patients still suffer from long-lasting deficits. Prediction of motor recovery and response to therapy is an evolving field, and further research will help pave the way for eventual use of this information clinically. Selecting optimal treatment strategies for individual patients based not only on their clinical evaluation, but also on 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.