Psych 403 quiz 5

new neurons and glia are produced BLANK, but BLANK

throughout life, mainly at a younger age

cells produced in the subgranular zone migrate to the

dentate gyrus

cells produced in the subventricular zone migrate to the

olfactory bulb via the RMS

subventricular cells may also migrate to the

striatum and cortex

true/false new cells can functionally integrate into circuitry and contribute to behaviour

true

growth factors are

proteins and steroids that stimulate cell growth, proliferation, differentiation, and survival

after injury some cells migrate to other areas, but most migratory cells do this

die off

true/false cavities in the brain can be filled in with an endogenous stem cell response

false

prompt- watch a video on BNDF

\-

BNDF promotes BLANK

neurogenesis and survival

TNF-alpha BLANKs neurogenesis

blocks

BNDF is BLANK after a stroke

beneficial

BNDF production is stimulated by BLANK activity

NMDA and AMPA

short term effects of BNDF

neuronal depolarization, affects ion channels, potentiating transmitter release

long term effects of BNDF

alters neurotransmitter production, changes excitability and metabolism, enhances synaptic transmission and increasing long term potentiation, modulating neuronal structures, affects neuronal survival and differentiation, promotes angiogenesis

BNDF improves BLANK and aids in recovery by promoting BLANK

memory, plasticity

why does BNDF lessen injury when given soon after insult

it reduces oxidative stress

Does the CA1 zone spontaneously regenerate after global ischemia

unsure, most say no

bendel et al 2005 major finding

the reapperance of 40% of CA1 after global ischemia, with time

what model did bendel 2005 use

11 min 2-VO ischemia

major contrary finding to bendel 2005

eventually, a lot of the regenerated cells die off

plasticity responses peak in the BLANK and BLANKS that follow injury

days, weeks

plasticity has a BLANK period

sensitive

why is the sensitive period of plasticity important

that is when rehab therapy can manipulate processes

plasticity can restore BLANK areas, retrain BLANK, and recruit BLANK

damaged and diaschisis regions, locally, other brain regions within the injured hemisphere and contralaterally

role of restoration, retraining, and recruitment varies depending on

insult severity, age, system affected, extent of connection, redundancy

what factors enter at the acute phase of stroke to contribute to BBB repair

BNFP< VEGF, TGF-A, HIF, ERO

downstream effect of BBB repair

angiogenesis

the release of MPPs after stroke leads to BLANK

ECM digestion

describe the process of intracorticial projections changing functions after stroke

right after injury the the uninjured area is somewhat taken over by projections from the injured side, then there is a period of disinhibition 3-4 weeks after stroke, then 4-8 weeks after stroke the injured side takes over some of the space of the injured side

hours to weeks after stroke there is a period of BLANK-excitability

hypo

3-4 weeks after stroke there is a period of BLANK- exictability

hyper

4-8 weeks after stroke the intracortical projections do this

have greater specifity

Homeostatic plasticity

occurring to restoring a not normal level of activation in these networks

training drives BLANK plasticity to increase activity in co-active nodes

hebbian

structural changes after stroke are evident in shape and number of BLANK, there are also changes in receptors and BLANK

dendrites, neurotransmitters

prompt- watch a video on postsynaptic potential and inputs

\-

true/false cells changing their response means they are growing new axons from hindlimb to forelimb

false

what does it mean when cells change their response after stroke

projections that already exist have been unmasked via plasticity

the cortex changes based on how BLANK maps it

input

homeostatic plasticity is

trying to get things to go back to normal levels

hebbian plasticity

neurons that fire together wire together

true/false cortical maps will change overtime due to plasticity

true

how does the cortical map change after a giant stroke

there is little to no local retraining, you have to recruit from farther

true/false the contralateral to stroke hemisphere can facilitate OR impair recovery of the more impaired limb

true

factors determining the role of the contralateral hemisphere

age, stroke severity, time since stroke, type of deficit

anatomical data supporting the role of the contralateral hemisphere in recovery

existing pathways support a role for the contralateral hemisphere in recovery, and structural and metabolic changes have been demonstrated in non damaged contralateral pathways

other data supporting the role of the contrallateral hemisphere in recovery comes from there studies

animal studies using serial lesions, activation and inactiviation studies with drugs and non invasive brain stimulation, imaging data from patients

NIBS

non invasive brain stimulation

plasticity can occur BLANK along a circuit

anywhere

the vast majority of corticospinal tracts BLANK, but some projections do not cross

decussate

“while the vast majority of corticospinal tracts decussate some projections do not cross” is a statement that provides evidence in support of BLANK

ipsilateral control

ipsilateral projections can sprout with BLANK

time and therapy

major evidence for the role of ipsilateral projections

extreme loss after stroke where function can be regained

what is a major factor in ipsilateral recovery

age

true/false after a stroke a much broader network tends to be activated

true

many structural changes that occur in the perinfarct zone also occur in the BLANK to a lesser extent

contralateral

patients that don’t have as good of a recovery tend to rely on the BLANK hemisphere

contralateral

structural changes shared by the peri-infarct zone and contralateral hemisphere

growth factors, angiogenesis, synaptogenesis, dendritic branching

these zones show increased activation after stroke

perinfarct, contralateral zone

initial contralateral activation declines in favour of BLANK in patients with good recovery

ipsi-lesional activity

could the contralateral hemisphere impair recovery

yes

ispilateral control is generally evident in those with BLANK and BLANK lesions but not bLANK lesions

intermediate, large, small

possible explanation for ipsilateral control

normal ispilateral pathways filling the deficit, or fibres crossing over in the spinal cord

whatever function is happening after a large lesion is generally mediated by the BLANK pathway

ipsilateral

true/false bilateral deficits can occur after unilateral brain injury

true

improved learning in the ipsilateral to stroke limb is due to

enhanced plasticity in the undamaged hemisphere

the BLANK hemisphere plays a role in reaching in the contralateral to stroke forelimb

contralateral

why might learning and compensation in the non affected side be advanced after stroke

the contralateral to lesion side undergoes considerable plasticity and increased activation

why is it an issue to encourage reverse handedness and other forms of compensation

you don’t switch back as the other hemisphere recovers, losing the potential to redefine connections

compensatory movement

switching to the use of non preferred limbs

compensatory movements arrise due to

plasticity

what is the best long term strategy for movement recovery

focus on real recovery in the damaged hemisphere

why is it important to focus on real recovery in the damaged hemisphere instead of compensation

the other limb will be there forever, but if real recovery is not practiced with therapy during the critical period of plasticity following stroke the patient might lose the ability to have true recovery forever

of the motor cortex (MC), rostral MC (RMC) or caudal MC (CMC) what is more important to recovery and why

the CMC, has a larger circuit

of the motor cortex (MC), rostral MC (RMC) or caudal MC (CMC) , list size of deficit from largest to smallest

MC, CMC, RMC

what task are the MC, CMC, and RMC important for

skilled reaching

true/false LC lesions on the side of an initial MC lesion is worse than injuring the opposite MC

true

LC lesions on the side of an initial MC lesion is worse than injuring the opposite MC- why?

if you have damage to your motor cortex the residual fibres on the same side are most important to recovery

discuss potential harmful roles of the contralateral to stroke hemisphere in recovery and how this varies with lesion size

may be some compensation that you do not want, hemisphere can inhibit recovery in residual tissue

discuss potential beneficial roles of the contralateral to stroke hemisphere in recovery and how this varies with lesion size

with large strokes where an entire area is knocked out and there is little hope for recovery, engaging the contralateral side and developing compensation can contribute to functional recovery

discuss the type and nature of injury occuring after damage to the internal capsule (ischemic or hemorrhagic stroke) what role would this have in behavioural recovery

if you have a lot of damage to the circuit, the more you take out in the motor system the less likely there will be any recovery there

diaschisis theory is associated with

Von Manaco

high vulnerability to ischemia is found in region

CA1

Iron toxicity results from this type of stroke

ICH

What components will make up an infarction

dead neurons, glia, vasculature

SVZ is a BLANK zone

neurogenic

aspects of evidence based practice

clinical expertise, best research evidence, patient concerns

why use evidence based practice

effectiveness and safety, meaningfulness, appropriateness, feasibility

types of primary evidence

case studies or case series, case contral study, cohort studies, RCT

case studies and case series are BLANK quality evidecen

low

what is the best possible form of primary evidence and why

RCTs, minimizes bias and gets a good sample size

types of secondary evidence

expert reviews, systematic reviews, meta analyses

examples of clinical summary resources

evidence based reviews, stroke best practices, cochrane reviews, stroke engine

ture/false animal data drives factors heavily into a decision on whether or not a therapy is clinically effective

false

stroke rehabilitation is aimed at BLANK

enabling a person with stroke related impairment to reach their optimal cognitive, physical, emotional, communicative, and social functional level

true/false rehab is not a setting

true

what is rehab

a process that includes a set of activities begining soon after event once a patient is medically stable and can identify goals for rehab, recovery, and participation

broad goals in rehab

maximize recovery, teach compensation, increase participation, help return to work, prevent complications, minimize pain and distress

do we start aggresive rehab at time of stabalization

no, moderate