Studied by 0 peopleCommon rodent rehab tasks
running, skills training, cognitive rehab, general enrichment
cognitive rehab for rodents usually consists of
mazes
BLANK rehab is often combined with other therapies
cognitive
common treatment parameters in rodent rehab studies
intervention delay, duration and intensity
most animal rehab studies examine
the mechanism of action
EE is
environmental enrichment
a modified montoya box is
an example of skilled teaching training
key treatment parameters in any study are
timing and intensity
what is the assumption of looking at timing and intensity of rehab in studies
we need to target the sensitive period to maximally take advantage of brain plasticity
when should rehab begin
within two days as long as the patient is stable, able, and willing
most clinicians believe that rehab is given BLANK, and begins BLANK
at one time, sooner and at higher intensity than is achievable
in an experimental study using young male rats training on reaching tasks after an MCAO, rats that got rehab sooner did
better
BLANK is a common complication to stroke recovery
pneumonia
in a mild stroke people will move from hospital to BLANK in a timeframe of BLANK
home, days
with a moderate stroke patients will move from hospital to BLANK in a timeframe of BLANK, and BLANK to home in a timeline of BLANK
rehab hospital, weeks, rehab weeks to months
with a severe stroke patients will move from hospital to BLANK in a timeline of BLANK, and then the assisted living
a transition unit, days to months
predictors of recovery
family support, injury size and location
why might cerebellar infarcts be hard to rehab
cerebellum is central to posture and balance, and full of white matter
possible assesments of funciton
bed mobility, transfers, stairs, walking, sitting and standing, balance
hypertonia
more muscle tone, harder to move
hypotonia
less muscle tone, floppy limbs
assessments of impairments after stroke are done in the following areas
strength, sensation, reflexes, tone, coordination, range of motion
what impairments contribute to the following walking deficits: strength, balance, bracing and stretching
weakness, balance deficits, spasticity
what factors make a patient a good candidate for rehab
they are making progress in acute care, they have enough cognition, language, and motivation to participate, requires one person assistance, can tolerate 2 hours sitting and 1 hour activity, has a discharge plan
external factors that effect rehab potential and outcome
age, stroke severity, aphasia and perception, motivation, family support, advocacy
major challenges of rehab
communication issues, limited resources, emotionally and physically taxing, struggle for practitioners to keep up with evidence
generally, starting rehab BLANK is a better approach
earlier
why not do an RTC when studying effects of delayed rehab
ethics
adverse effects can be seen when starting rehab within BLANK after stroke
1 month
youtube prompt: intention to treat analysis
AVERT trials mean
a very early rehabilitation trial
advantages of early mobilization
avoids harmful effect of bed rest, avoids immobility complications, takes advantage of neuroplasticity
risks of early mobilization
effects on BP and CBF, higher risk of fall, risk of bleeding
in general early mobilization is BLANK to recovery
detrimental
early rehab doesn’t really help anybody, but is especially harmful to BLANK and BLANK
hemorrhages, severe strokes
why do we do secondary analysis
the more you look for something the more likely you are to find something
youtube prompt: secondary analysis
how did the avert authors explain their findings
initial data suggested harm to those with severe stroke and ICH, rehab interactions with stroke type and severity expected, re analysis suggests more frequent and briefer mobilization was helpful but longer was not
exceeding a certain level of reaching is a BLANK
critical threshold
what is the implication of the finding that allowing rats unlimited reaching in rehab inproved outcomes
maybe a lot of rehab just isn’t often enough to make a difference
you need a certain amount of therapy to drive plasticity, without the right intensity
you don’t get enough to rewire the brain
in this type of stroke, researchers are unable o find benefit to rehab
striatal ICH
why does rehab protocal fail in striatal ICH
when you damage the striatum it damages the corticospinal tract going through it
when talking about rehab intensity, generally
more is better
problems with studying rehab intensity in animals
patients get less intense rehab than animals ( a few dozen vs 100s), human rehab focuses on ADLs where rodents may just use forced running
translational research issues in rehab studies
quality issues, insufficient consideration to species effect, clinically unrealistic treatment protocols, focus on endpoints not quality of movement, inability and diminished ability to account for stroke effects in animal models, forgetting medical stability effects, mismatch in terminology, animal studies are not strong evidence
impact of exercise varies by
personal factors, exercise type, duration
exercise, especially aerobic exercise, improves BLANK, BLANK, and BLANK
mood, cognition, memory
exercise decreases many risk factors, for example BLANK
vascular damage
exercise causes reductions in BLANK, better BLANK, less BLANK, enhanced BLANK, greater BLANK, and fewer BLANK
stress, sleep, anxiety and depression, muscle mass, flexibility, disorders
exercise results in better glucose BLANK, enhanced BLANK protection, greater BLANK defenses, better BLANK function, and alterations in BLANK pathways
control, growth factor, anxti-oxidant, mitochondrial, cell death
in general with exercise we see less BLANK, enhanced BLANK, and greater BLANK
inflammation, synaptic plasticity, stem cell response
true/false exercise promotes angiogenesis, maintains blood flow,and prevents the accumulation of protein aggregates and damaged mitochondria
true
whole brain benefits to exercise
greater cognitive reserve from enhanced synaptic plasticity, improved electrophysiological function, increases in brain volume
mechanisms of post stroke rehab vary by
patient factors, type of insult, treatment type, therapy parameters
mechanisms of normal learning and spontaneous recovery are BLANK by rehab
enhanced
dendritic and spine growth, formation of new terminals, and changed in neurotramsmitters and receptors act to
modify synaptic transmission and alter physiological function
what are some actions resulting from modifying synaptic transmission and altering physiological function
map reorganization, unmasking dormant pathways, removal of diaschisis
possible mechanisms of improvement in blood flow
opening of collateral vessels, angiogenesis
improvements in blood flow can sustain penumbral tissue and heighten activity in rewired circuits, also known as
neuroprotection
transcriptional changes leading to elevations in BDNF promote
dendritic growth and synapse formation
true/false rehab therapies are sometimes neuroprotective
true
rehab drives a lot of the same effects as
spontaneous recovery
rehab can be neuroprotective or
damaging
rehab increases dendritic BLANK after focal ischemia and ICH in rats
arborization
rehab will drive dendritic growth through BLANK
remaining structures, including distal structures
early rehab is associated with greater BLANK in the undamaged motor cortex
dendritic branching
greater dendritic branching in the undamaged motor cortex is an example of these mechanisms
unmasking and reorganization
study groups:
animals with no BNDF and rehab BLANK
animals with blocked BDNF BLANK
animals with blocked rehab BLANK
got better, did not get better, did not get better
what does it mean that if you block BDNF recovery goes down
blocking bdnf prevents rehab effects
question: is there evidence that aerobic exercise can influence recovery
yes
was forced or voluntary aerobic exercise harmful in animal rehab studies
no
will forced or voluntary aerobic exercise reduce lesion volume
forced
is early or later treatment better in animal rehab
earlier
when should rehab start in animal models for best results
a few days
exercise in animal models lessens BLANK, BLANK, and BLANK while increasing BLANK and BLANK
cell death, inflammation, oxidative injury, neurogenesis, angiogenesis
components of constraint induced movement theraopy
forced use, massed practice (5-6 hours per day), transfer package (practice on ADLS)
prompt: watch a video on constraint induced movement therapy
-
research on constraint induced movement therapy findings
mixed but positive findings
broad mechanisms of constraint induced movement therapy
neural changes like axonal sprouting, cortical re-organization and thickening, counteracting learning non-use
during learned non use…
use of the good hand is reinforced, impaired hand is punished
learned non use develops during
initial period with the greatest neurological impairment
forced use therapy timeline
2 weeks, 80% of waking hours, massed practice 506 hours a day, transfer package for ADLs
why does constraint induced movement therapy work
counteracts learned non use
true/false many studies demonstrate the benefit of CIMT models of sensory deafferentation, cerebral ischemia, hemorrage, and TBI
true
one problem with CIMT
very early CIMT in animals not demonstrated in patients
one study found that casting the good limb in animals
greatly increased brain damage
mechanisms of use dependent injury
use dependent effects are model and timing dependent with effects mediated by stress and/or excitotoxicity
in CIMT early forced use was BLANK and delayed was BLANK
harmful, not
how does use dependent injury drive exitotoxicity
using impaired circuits releases glutamate
alternative hypothesis to use dependent injury model
using a limb drives up brain temperature and hyperthermia is harmful in early stages of stroke, stress induced fever causes damage
a rat study found that restraining an impaired limb, bit not a ipsilateral limb, while forcing brain temp higher had this effect
worsened brain injury
why might fever be a mechanism of injury after rehab
infection because if gut is degrading more likely to get bacteria into your bloodstream, or temperature regulating areas like hypothalamus are damaged
when is fever damaging after stroke
the first few days
the combination of CIMT and BLANK drives progress in rehab
exercise
possible reasons that clinical data on CIMT do not match with animal studies
timing issue, poor quality studies
illustrate a group breakdown for a study in which you test timing, intensity or rehabilitation in a rat model of ICH. Provide specific hypothesis regarding the individual impact of timing and intensity on recovery
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what is constraint induced movement therapy often used for (type and location) state the underlying mechanisms that CIMT is counteracting. State 3 components of CIMT. Does clinical data support the use of CIMT after stroke
why does the type of stroke matter in rehab
risk factors and risk for death are different, response to treatment is different
should we assume that plasticity responses are the same in ishcemia and hemorrhage
likely not because of differences in pathophisiology and outcome
Note
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