Psych 403 quiz 6

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1
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Common rodent rehab tasks
running, skills training, cognitive rehab, general enrichment
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cognitive rehab for rodents usually consists of
mazes
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BLANK rehab is often combined with other therapies
cognitive
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common treatment parameters in rodent rehab studies
intervention delay, duration and intensity
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most animal rehab studies examine
the mechanism of action
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EE is
environmental enrichment
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a modified montoya box is
an example of skilled teaching training
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key treatment parameters in any study are
timing and intensity
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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
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when should rehab begin
within two days as long as the patient is stable, able, and willing
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most clinicians believe that rehab is given BLANK, and begins BLANK
at one time, sooner and at higher intensity than is achievable
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in an experimental study using young male rats training on reaching tasks after an MCAO, rats that got rehab sooner did
better
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BLANK is a common complication to stroke recovery
pneumonia
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in a mild stroke people will move from hospital to BLANK in a timeframe of BLANK
home, days
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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
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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
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predictors of recovery
family support, injury size and location
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why might cerebellar infarcts be hard to rehab
cerebellum is central to posture and balance, and full of white matter
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possible assesments of funciton
bed mobility, transfers, stairs, walking, sitting and standing, balance
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hypertonia
more muscle tone, harder to move
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hypotonia
less muscle tone, floppy limbs
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assessments of impairments after stroke are done in the following areas
strength, sensation, reflexes, tone, coordination, range of motion
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what impairments contribute to the following walking deficits: strength, balance, bracing and stretching
weakness, balance deficits, spasticity
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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
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external factors that effect rehab potential and outcome
age, stroke severity, aphasia and perception, motivation, family support, advocacy
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major challenges of rehab
communication issues, limited resources, emotionally and physically taxing, struggle for practitioners to keep up with evidence
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generally, starting rehab BLANK is a better approach
earlier
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why not do an RTC when studying effects of delayed rehab
ethics
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adverse effects can be seen when starting rehab within BLANK after stroke
1 month
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youtube prompt: intention to treat analysis
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AVERT trials mean
a very early rehabilitation trial
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advantages of early mobilization
avoids harmful effect of bed rest, avoids immobility complications, takes advantage of neuroplasticity
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risks of early mobilization
effects on BP and CBF, higher risk of fall, risk of bleeding
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in general early mobilization is BLANK to recovery
detrimental
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early rehab doesn’t really help anybody, but is especially harmful to BLANK and BLANK
hemorrhages, severe strokes
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why do we do secondary analysis
the more you look for something the more likely you are to find something
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youtube prompt: secondary analysis
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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
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exceeding a certain level of reaching is a BLANK
critical threshold
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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
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you need a certain amount of therapy to drive plasticity, without the right intensity
you don’t get enough to rewire the brain
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in this type of stroke, researchers are unable o find benefit to rehab
striatal ICH
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why does rehab protocal fail in striatal ICH
when you damage the striatum it damages the corticospinal tract going through it
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when talking about rehab intensity, generally
more is better
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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
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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
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impact of exercise varies by
personal factors, exercise type, duration
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exercise, especially aerobic exercise, improves BLANK, BLANK, and BLANK
mood, cognition, memory
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exercise decreases many risk factors, for example BLANK
vascular damage
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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
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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
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in general with exercise we see less BLANK, enhanced BLANK, and greater BLANK
inflammation, synaptic plasticity, stem cell response
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true/false exercise promotes angiogenesis, maintains blood flow,and prevents the accumulation of protein aggregates and damaged mitochondria
true
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whole brain benefits to exercise
greater cognitive reserve from enhanced synaptic plasticity, improved electrophysiological function, increases in brain volume
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mechanisms of post stroke rehab vary by
patient factors, type of insult, treatment type, therapy parameters
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mechanisms of normal learning and spontaneous recovery are BLANK by rehab
enhanced
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dendritic and spine growth, formation of new terminals, and changed in neurotramsmitters and receptors act to
modify synaptic transmission and alter physiological function
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what are some actions resulting from modifying synaptic transmission and altering physiological function
map reorganization, unmasking dormant pathways, removal of diaschisis
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possible mechanisms of improvement in blood flow
opening of collateral vessels, angiogenesis
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improvements in blood flow can sustain penumbral tissue and heighten activity in rewired circuits, also known as
neuroprotection
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transcriptional changes leading to elevations in BDNF promote
dendritic growth and synapse formation
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true/false rehab therapies are sometimes neuroprotective
true
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rehab drives a lot of the same effects as
spontaneous recovery
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rehab can be neuroprotective or
damaging
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rehab increases dendritic BLANK after focal ischemia and ICH in rats
arborization
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rehab will drive dendritic growth through BLANK
remaining structures, including distal structures
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early rehab is associated with greater BLANK in the undamaged motor cortex
dendritic branching
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greater dendritic branching in the undamaged motor cortex is an example of these mechanisms
unmasking and reorganization
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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
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what does it mean that if you block BDNF recovery goes down
blocking bdnf prevents rehab effects
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question: is there evidence that aerobic exercise can influence recovery
yes
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was forced or voluntary aerobic exercise harmful in animal rehab studies
no
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will forced or voluntary aerobic exercise reduce lesion volume
forced
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is early or later treatment better in animal rehab
earlier
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when should rehab start in animal models for best results
a few days
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exercise in animal models lessens BLANK, BLANK, and BLANK while increasing BLANK and BLANK
cell death, inflammation, oxidative injury, neurogenesis, angiogenesis
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components of constraint induced movement theraopy
forced use, massed practice (5-6 hours per day), transfer package (practice on ADLS)
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prompt: watch a video on constraint induced movement therapy
\-
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research on constraint induced movement therapy findings
mixed but positive findings
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broad mechanisms of constraint induced movement therapy
neural changes like axonal sprouting, cortical re-organization and thickening, counteracting learning non-use
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during learned non use…
use of the good hand is reinforced, impaired hand is punished
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learned non use develops during
initial period with the greatest neurological impairment
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forced use therapy timeline
2 weeks, 80% of waking hours, massed practice 506 hours a day, transfer package for ADLs
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why does constraint induced movement therapy work
counteracts learned non use
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true/false many studies demonstrate the benefit of CIMT models of sensory deafferentation, cerebral ischemia, hemorrage, and TBI
true
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one problem with CIMT
very early CIMT in animals not demonstrated in patients
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one study found that casting the good limb in animals
greatly increased brain damage
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mechanisms of use dependent injury
use dependent effects are model and timing dependent with effects mediated by stress and/or excitotoxicity
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in CIMT early forced use was BLANK and delayed was BLANK
harmful, not
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how does use dependent injury drive exitotoxicity
using impaired circuits releases glutamate
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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
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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
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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
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when is fever damaging after stroke
the first few days
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the combination of CIMT and BLANK drives progress in rehab
exercise
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possible reasons that clinical data on CIMT do not match with animal studies
timing issue, poor quality studies
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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
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why does the type of stroke matter in rehab
risk factors and risk for death are different, response to treatment is different
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should we assume that plasticity responses are the same in ishcemia and hemorrhage
likely not because of differences in pathophisiology and outcome