Recovery and Outcome Expectations Post Stroke

primary or direct damage to neurons resulting in neuronal death
disrupts afferent and efferent connectivity

an indirect effect
-damage to one area impacts connections to other healthy brain areas
-causes the other healthy brain areas to have decreased neuronal activity and metabolic dysfunction
-so initial deficits are a combination of the actual damage and then the healthy areas being like wtf
-presents as loss of function, impedes neural reorganization

indirect effect
each side supposed to activate itself, and inhibit other hemisphere
acute (1 week): decreased same side activation/inhibition
subacute (6 mos): spontaneous recovery, risk of healthy side becoming overactive
chronic (>6mos): restore balance, but risk of continued overactivity from healthy side impacting recovery

neural reorganization

involved repair or redundancy
adaptive plasticity

involves perilesional and distant areas
leads to incomplete recovery or maladaptive plasticity

the peripheral tissue of the lesion
restore/create new connections

the capacity of the brain to reorganize - remodeling and functional recovery!
-happens in reponse to activity and task specific training
-aka learning and skill acquisition
-at the level of synapses, dendrites, axons, and cortex

resolution of neural shock/diaschisis
denervation super-sensitivity
recruitment/ unmasking of silent synapses
regenerative and reactive sprouting

edema reduction around injury
synapse recovery
restore impulses and neural blood flow
resolution of diaschisis
occurs over days to weeks
-low capacity functional intervention

post synaptic response to the loss of synaptic inputs
changes in post synaptic membrane that makes the neuron more sensitive to neurotransmitters (good bc theres not much left, #upregulation, #desperate)

-recruitment of previously silent synapses
-suggests structural synapses are present in many areas of the brain that may not be functional because of competition within neuronal pathways
-appears to be a "use-dependent" competition among neurons for synaptic connections

-surviving neurons generate new axons (axonal sprouting and dendritic remodeling) to replace connections lost due to infarc
-target denervated areas, supporting the restoration of disrupted circuits and contributing to regained motor and sensory functions
-takes weeks to months, usually less effective, leads to dysfunction
how? specific motor stimulation

resolution of diaschisis
restoration of interhemispheric balance
many neural networks and cortical reorganization
shifting of functional representations of motor and sensory systems to other areas
can be adaptive or maladaptive

immediately after - irreversible injury
-> then reversible dysfunction, lower levels of function initially
-> with remapping comes up to a new functional level which is better than immediately post stroke but still below baseline
improved through targeted therapy

the motor experience

salient, intensive, goal directed task practice

increase density of blood vessels in motor cortex-> angiogenesis
facilitates growth factors (BDNF)

increase the number of synapses at the level of the spinal cord
(not cortical mapping)

it interferes with recovery and results in persistent behavioral deficits after a brain injury

restoring fxn in neural tissue initially lost due to injury vs
residual neural tissue takes over a function due to injury

restoring ability to isolate movement patterns in SAME manner as prior to injury vs performing movements in a manner different from how it was performed prior to injury

restoring the ability to perform a task the same way vs not

secondary response over time
affected limb is used less often
compensatory strategies develop which negatively impacts recovery

multifactorial and biopsychosocial determinants
objective: potential recovery, ambulation ability, discharge destination

higher dose = more recovery
not time dependent

rapid assessment and diagnosis
hyperacute access to interventions
physiologic and nuerologic monitoring to reduce complications
Early and intensive rehab and secondary prevention

improved outcomes at 1 year
reduced rates of death or institutionalization
outcomes improved with >2 hours/day of rehab care

quantitative assessment tool to measure acute stroke related neurologic deficits at the body structure and function level

Very severe: >25
Severe: 15-24
Mild to mod severity: 5-14
Mild: 1-5

<5: d/c home
6-13: acute rehab
>14: long term care

4.7 days

18-54
male
white ppl
private insurance
ambulate with assist
larger hospitals or stroke unit

>55
more co-morbidities
Black, hispanic
medicare, medicaid
unable to ambulate

accessibility at home and workplace

family care capacity
marital/partner status
cognition and depression
low level of illness acceptance
limited self efficacy

manage patient expectations
tailor rehabilitation goals
use time and resources most effectively for the best outcomes

health condition
patient goals

activity and participation

available evidence based predictive factors
modifiers: previous activity and endurance levels, previous engagement and success with PT, access to rehab, support

hand function and ADL domains

gait function and health related QOL indicators

discharge location
older -> care facility more likely

lower functional recovery and HRQOL

T1 weighted anatomical imaging
Diffuse tensor imaging
functional MRI

useful for locating lesion
extent of lesion overlap with posterior limb of internal capsule -> motor impairment
overlap between lesion and CST -> upper limb recovery potential
Severe white matter disease or hemorrhagic transformation -> poor outcomes

useful for assessing structural integrity of white matter pathways
greater damage -> greater impairment
strong predictor of upper limb recovery
measures at 3 weeks post stroke -> UE function at 6 mos

cortical activity during voluntary movement of paretic limb -> reduction of impairment
functional connectivity between cortical and subcortical areas -> capacity for reorganization

most people have upper limb dysfunction, and about half stays 5 years post stroke

lower subjective well being and HRQOL

prediction made based off evidence that sparing of descending white matter pathways is related to bettwe upper limb recovery

identifies 4 subsets of recovery potential
efficient for half of stroke individuals

1. Safe score: sum MRC and MMT grades at 72 hours post stroke
2. Transcranial Magnetic Stimulation
-test functional integrity of corticospinal pathways originating from lesioned primary motor cortex
+ response = good recovery potential

TUG score at 4 months post stroke

Sitting Balance Scale (28.5)
Trunk Impairment Scale (16.5)
Trunk Control Test (82)
Postural Assessment for Stroke Scale (10.5)

4 items: rolling weak vs strong side, supine to sit, sitting balance
0 - unable
12 - able but not typical
25 - able "normally"
>=50: recovery of walking
<40: higher potential to be non-ambulatory

LOS and 10MWT

+ correlation between TCT and

5 items - postural control
supine to sit and sitting items
items are scored 0-3
strong correlation with ADL function at 6 months
12.5/36: independent ambulation >10m at discharge from inpatient rehab
>17.5: acute stage is predictive of a high functional potential of recovery

6 months

less likely to regain independence

discharge destination and level of participation and disability post stroke

independent walking

lower limb motor impairment
stroke severity
trunk control and balance
lower limb sensory impairment

predicts at week 1 post stroke time to independent walking
includes:
TCT: static and dyn trunk control
MRC strength grade hip extension
determines probability for independent ambulation at 6 months