Psych 403 quiz 4

BLANK is the stimulus for repair. The implication of this is

injury, by blocking injury you may also block repair

true/false most animals have considerable recovery in the days and weeks after injury and often recover faster than humans

true

recovery depends on

injury and task conditions

when you test recovery more carefully this tends to emerge

residual deficits

on an easy scale in recovery you are more likely to see BLANK, and on more difficult scales you will see BLANK

recovery, residual deficits and compensation

true/false ipsilateral deficits are also seen

true

are contralateral or ipsilateral deficits generally worse

contralateral

NDS

neurological deficit scale

after an ICH into the striatum, recovery in rats in generally seen at BLANK when measured on the neurological deficit scale

1 week

deficits are ICH in rats are seen in BLANK tests

more demanding skilled reaching

after an ICH blood infusion into the striatum, these deficits are observed

modest deficits in the contralateral stroke forelimb, no deficits ipsilaterally

generally, a more BLANK stroke will also affect the ipsilateral side

severe

examples of compensation on the staircase task

dragging pellets up, licking

why is the single pellet test better to assess recovery compared to the staircase test

it is harder to compensate on the single pellet test

true/false the single pellet test still shows compensatory movements

true

skilled reaching tasks are often used because they are BLANK relevant

biologically

why do animal studies focus on skilled reaching tasks

important to humans, lots of tests available, mechanisms of control in the brain are similar to humans

BLANK function is an important predictor of recovery

hand

true/false even good recovery has residual compensatory movements

true

why might compensation be more pronounced on some tests

crude tests and endpoints do not reflect the residual impact of stroke

BLANK impairments occur when the motor cortex is damaged

ispilateral

potential mechanisms of bilateral deficits following injury

bilateral control, ipsilateral projections, inter-hemispheric interaction in the corpus callosum

ipsilateral deficits are more pronounced BLANK

earlier after injury

what happens in broad terms when you damage one side of the brain

the brain can swell, causing distal damage and metabolic changes occur

why might ipsilateral damage dissapear with time

it make be due to inflammation and swelling, or it may be engaged in compensation

important factors of plasticity

location and time

possible ipsilateral outcomes following stroke

boost in plasticity or damage

is proportional recovery seen in rats

yes

a non fitter is a subject that

does not fit with proportional recovery

characteristics of “fitter” animals

milder initial impairment, smaller infarct, less striata injury, intense rehab

why does striata damage decrease potential for recovery

involves a lot of white matter tract damage

early recovery stems partly from

resolving harmful processes that lead to abnormal neural activity

examples of harmful processes leading to abnormal neural activity just after stroke

stress reaction, impairments in CBF in affected but surviving structures, toxic cellular debris, inflammation, abnormal ionic gradients, distal matabolic derangements like diaschisis, sub lethal structural perturbations

true/false even though plasticity contributes to early improvements many animals will show spontaneous recovery

true

edema is a big contributor to BLANK, and as edema resolves patients generally BLANK

initial impairment, have a better outcome

diaschisis

remote functional depression in areas distal but connected to the site of injury

cerebral edema may compromise BLANK

CBF

how does edema compromise CBF

edema osmotically drives increase in water inside tissues

how to you weigh edema in animals

a wet dry measurement: take a piece of brain, weight it, bake it, weight it again

edema is BLANK and BLANK

cytotoxic, ionic, vasogenic

cytotoxic mechanisms of edema

early rise in intracellular water driven by entry of sodium and chloride entry into cells causes spines and dendrites to swell and disappear. Cell body may swell to the point of rupture

ionic mechanisms of edema

rise in extracellular fluid and elements from ion imbalance causes effort to normalize, which pulls components from the vasculature, pulling water into the brain

in ischemia edema can arise before BLANK

BBB damamge

vasogenic component of edema

delayed increase in extracellular water through a damaged BBB which permits osmotically important molecules to enter the brain

BBB damage arises from BLANK or directly from BLANK

ischemic damage to vasculature, cerebral bleeds

BLANK directly alters brain osmolarity

cerebral bleeds

brain swelling can cause BLANK and swelling can impair BLANK

herniation, CBF

brain swelling impairs CBF notably through the BLANK

lower pressure vasculature

high ICP can substantially impair BLANK

CBF

pathway of brain swelling to death

swelling causes herniation and impairs CBF, high ICP impairs CBF, further ischemia and edema augment cell death

high ICP makes it harder to

get blood into the brain

true/false high ICP can increase ischemia

true

ICP and edema generally resolve over BLANK

days and weeks

BLANK are temporally linked to behavioural recovery

ICP and edema resolution

true/false ICP can increase blood pressure very quicklu

true

possible treatments for edema

drugs to remove water from the brain, hemicraniectomy

why is swelling so detrimental to the brain

the brain has a fixed space to exist in

elevated BLANK is linked to poor outcomes

ICP

elevated ICP results from edema and in hemorrhages from the BLANK

hematoma

mass effect

edema and hemotoma cause elevated ICP, perpetuating the cycle

If patients have elevated ICP but not above 20mg mecury, as pressure goes up chances of BLANK go down

staying alert

Mass effect is

adding something extra to the skull to create more strain

an extra mass in the brain can be one of the above

hematoma, tumour, edema, blockage in CSF drainage

reductions in venous blood and BLANK occur to counteract mass effect, this is known as BLANK

CSF, intracranial compliance

as the system of intracranial compliance becomes overwhelmed

downstream blood flow is impaired

CPP=

MAP - ICP

as CPP decreases and ICP increases mean arterial pressure changes, which is what

impedes brain function and promotes cell death

survivors with swelling in the brain are at increased risk of

neurological function and mortality

ways to treat brain swelling

producing less or draining CSF, reducing venous blood in the brain

midline shift

one hemisphere is pushing the other one over due to swelling

ICP above BLANK puts you at risk of dying

20

prompt: watch youtube videos on mechanisms of edema and treating edema

\-

BLANK is used to measure BBB injury

gadolinium extravasation

you will see low BLANK levels in the peri-hematoma

potassium

Edema changes the BLANK concentrations around stroke sight, which results in BLANK

element, messed up function

As BLANK resolves in edema tissue function around injury begins to normalize

element concentrations

true/false edema both directly and indirectly impairs neural function and worsens outcome

true

development of edema is linked to worsened BLANK

worse brain function, risk of death

spontaneous resolution of edema is linked to BLNAK

improved behaviour outcomes

why treat edema

improve mortality, improve outcome, improve behaviour

some of the effects of edema are explained by the BLANK response

ICP and CBF response

broad mechanisms of impact in edema

ICP and CBF response, element concentrations

in ICH element level perturbations result from BLANK , BLANK and BLANK

BBB injury, edema, serum extrusion from blood clot into surrounding tissue

the best recovery is possible when

you have some damaged area left to work with

in big strokes, the brain outside of the damaged area gets BLANK

smaller

volume of BLANK areas decrease in cell volume following ICH

CA1. CA3, S2, striatum

in ICH do cells unaffected by stroke or edema reduce in volume

yes

we know cells in distant region decrease in volume, but what about density?

they increase in density

tissue compliance

because of the mass effect the brain compensates by shrinking other parts of the brain

Data shows that distal brain cells BLANK in a process called tissue compliance

transiently shrink

tissue compliance would act to counteract BLANK

high ICP after severe strokes

side effect of cell volume reductions

abnormal behaviours

does tissue compliance cause functional impairments, and does the phenomenon exist in humans?

we dont know yet

what is the most sensitive region to look for in ischemia

CA1

true/false inflammation always occurs after brain injury

true

dual role of inflammation

inflammation removes debris and damaged tissue to promote remodelling

broad mechanism of inflammation removing debris

neutrophils and macrophages act via signalling molecules like cytokines

inflammation occurs rapidly and peaks in BLANK

a week, but may persist for months

BLANK are rapidly organized in the inflammation response following stroke

microglia

broad mechanisms of inflammation removing damaged tissue

phagocytizing dead cells from infarcts and blood clots and wall off damaged areas. astrocytes in the scar secrete growth promoting and inhibting factors