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In rat studies “skilled reach training” was found to cause what?
Reorganization of cortical movement representation.
Results: Significant inc in wrist and digit representation, but not the elbow and shoulder representation.
In rat studies motor skill was found to develop before what?
Structural reorganization and persists w/out continued performance.
Result: Reorganization not evident until 10days of training but once it has occurred, persists w/out training up to 220 days
Animal studies have shown cortical reorganization is associated with?
Inc in synapse number (due to Skilled reach training).
What is the key to structural plasticity?
Skill acquisition, as it has been shown to inc synapse number and size of the cortical map
Does the development of motor skill and plasticity w/in the motor cortex occur at the same time?
No. significant inc in Skill level occur before changes in synapse number, which also occurs before reorganization
Based on animal studies does strength and endurance training induce cortical reorganization?
No, but skill learning does
What should you do to drive neuroplasticity for your patients?
Give them a task to learn
What are the 10 principles of Neuroplasticity?
Use it or lose it
Use it and improve it
Specificity
Intensity matters
Repetition matters
Time matters
Salience matters
Age matters
Transference or generalization
Interference
What do Animal studies inform us about representation in the infarcted zone?
Movements formerly represented in the infarcted zone do not reappear in adjacent cortical regions w/out post-infarct training.
What allows for substantial retention of the spared hand area?
Rehabilitative training regimen (based off monkey study)
What does the squirrel monkey study regarding forced training inform us about?
That the group who was given the jacket (forced training) performed slightly better than the control group but they still lost over 50% spared hand area.
What can we conclude based off of studies regarding forced training?
It’s not sufficient to drive structural neuroplasticity after stroke.
Does repetitive motor activity alone produce structural reorganization? What instead is required to drive plasticity?
No, motor skill/learning is a prerequisite in driving plasticity
In rats it has been shown that acrobatic training improved functional performance and enhanced homotopic synaptogenesis. What can we do as therapist to create a similar effect with our patients?
The use of obstacle has been shown to challenge neuromuscular control of LE and structural neuroplasticity
What role does social environment play in rehab (based of rat study)?
Can improve sooner and slightly when placed in enriched environment
What efffect would a unilateral lesion to the sensorimotor cortex cause on contralateral homotopic cortex?
Inc in dendritic arborization. Meaning the other side of the brain will be used since affected side isn’t working.
What is “forced use” or “constraint-induced movement therapy”? (Traditional vs. modified)
Traditional:
1. Unaffected UE restrained during 90% of waking hours x 2 weeks
2. Intensive, graded practice of the paretic upper limb to enhance task-specific use of the affected limb for up to 6 h a day for 2 weeks
3. Adherence-enhancing behavioral methods designed to transfer the gains obtained in the clinic/lab to patients’ real-world environment
Modified CIMT:
30 min x 3x/week x 10 weeks shaping therapy
5 hours x 5x/week of CIMT
Is there evidence for structural plasticity occuring after training?
3% change w/ 0.2% error rates for brain volume changes
What treatment dose is necessary to obtain MRI-detectable structural changes?
90min of balance training drove gray matter volume inc
(0min of balance training over 2 weeks in PD inc gray matter volume
What are possible mechanisms for map changes (neuroplasticity)?
Resolution of edema and removal of necrotic tissue
Restitution of damaged pathways
Modulation of GABAergic intracortical inhibition
Changes in synaptic efficacy
Alteration in transcallosal inhibition
Substitution from ipsilesional parallel pathways
Activation of ipsilateral (contralesional) pathways
Long term potentiation
Does cortical representation of a muscle expand with CIMT?
Yes, it does expand and its COG changes
What are synonymous terms for Skill acquisition?
Task novelty
Challenging task
Does intensity matter for neuroplasticity?
No, but training at higher intensities does show a that “challenge” is a key ingredient in driving improvements in fxn
When should rehabilitative strategies begin for post-stroke pts? What do you want to avoid w/ these pts? When is rehab considered safe?
Within first 2 weeks (optimal time still unknown). Avoid rehab within the first 24hrs (especially intensive rehab). Rehab considered safe beyond 24hrs
What does motor priming help facilitate?
Motor learning and improve neuroplasticity
Whats the theory of motor priming?
A prior method of activation is generally more responsive to the accompanying training. Which can enhance LTP-like mechanisms.
Types of motor priming?
Stimulation-based motor priming
Movement-based priming
Pharmacology-based priming
Mental practice/motor imagery priming
Sensory priming
What are the 4 categories of stimulation-based motor priming?
Repetitive transcranial magnetic stimulation (rTMS)
Transcranial direct current stimulation (tDCS)
Paired associative stimulation
Peripheral nerve stimulation (PNS)
What is repetitive transcranial magnetic stimulation (rTMS)?
Goes through cranium via magnet to stimulate cortical regions
What causes an inc and Dec in excitability in rTMS?
Increase corticospinal excitability = high-frequency (5–20 Hz) rTMS trains over M1
Decrease corticospinal excitability = long trains of low frequency rTMS (1 Hz) applied over M1
What is Transcranial direct current stimulation (tDCS)?
Low-intensity direct current (0.5-2 mA) through active electrode on the scalp modulates neuron potentials by altering the conductance of sodium and calcium channels. Mechanism may be due to LTP and LTD
How does Transcranial direct current stimulation (tDCS)
Anodal current (+) = upregulation of cortical excitability
Cathodal current (-) = downregulation of cortical excitability
Diff montages (placement) should be used to stimulate affected area.
What is transcranial direct current stimulation (tDCS)?
Theory of asymmetric hemisphere excitability post stroke. Often ipsi hemi has Dec excitability, while contra hemi has inc excitability. Thus, this method tries to correct for the imbalance between hemispheres but suppressing activity on one side and exciting affected side.
What is paired associative stimulation (PAS)?
What is transcranial direct current stimulation (tDCS)
PAS emphasizes the potent interaction of somatosensory input and cortical
motor circuits
How does PAS work?
Increased excitability = afferent peripheral volley is timed to arrive prior to the TMS stimulation
Decreased excitability = afferent peripheral volley arrives just after TMS stimulation
What is movement based priming?
Repetitve or continuous movement that is done to enhance the effect of an accompanying therapy
Why is it best to do bilateral or mirror symmetric movement for movement based priming?
There’s strong evidence that improvement in motor fxn coincides w/ normalization of transcallosal inhibition, resulting in greater balance between the hemispheres
Aerobic exercise promotes neuroplasticity via what?
BDNF
What does BDNF help with? (5)
Involved in motor learning and post-stroke motor rehabilitation
Facilitates LTP
Secreted in the CNS through both a constitutive and an activity-dependent pathway
Aerobic exercise increases BDNF
Exercise-induced increases in BDNF benefit cognitive function
What are the 4 main neurotrophic?
BDNF, GDNF, IGF, VEGF
Although aerobic exercise has shown to be beneficial for brain health, we shouldn’t forget about resistance training for which reason?
The positive effect it has by utilizing muscle as an endocrine gland
Does aerobic exercise improve cognitive fxn?
Yes
What can you do for a post stroke pt to “prime” their system?
Can use aerobic exercise for BDNF release. Which will prime motor learning task later in the session.
To induce large positive effects on cognition and BDNF levels, exercise should include? (4)
Aerobic sessions of >30 minutes
Training intensities of approximately 70% EHRM
Frequency of 4 days per week
Combination of aerobic and resistance exercises
What are mirror movements? Whats the purposed theory for this?
Concomitant activation of a limb that may reproduce voluntary movements on the contralateral homotopic area. Small uncrossed corticospinal pathways in adult humans are thought to underlie this phenomenon
In what instances do mirror neurons fire when observing a task?
When performing a task and observing someone else perform a task (monkey study)
What advantages do mirror neurons provide from an evolutionary standpoint?
Revs up system or help activate downstream motor areas
Does imagining an action, intending to perform an action and execution of an action share the same functional networks in the brain?
Yes
What are the 5 pharmacological agents proposed to enhance motor recovery?
Amphetamines
Dopaminergic agents
Cholinergic agents
SSRIs
Whats sensory priming?
Modulation of sensory input through sensory stimulation and sensory deprivation
Changes in somatosensory cortex influences what? and why?
Motor cortex due to strong connections btwn these two cortical areas
What are the sensory priming mechanisms? (3)
Peripheral nerve electrical stimulation
Vibration of agonist and antagonist muscles
Sensory deprivation (tourniquet, nerve blocks, anesthetic cream)
What is temporary functional deaffernation?
Dec in intercortical inhibition from the deafferented cortex of the unaffected limb regions will cause the adjacent injured limb region to work harder
What should you consider about the timing of priming? (5)
Priming should be done in close proximity to the training
Priming during motor training appears to enhance learning more than priming applied prior to training
Priming after training does not appear to be effective
Pre-workout supplements
Nootropics (drugs, suppose and other substances)