Factor Influencing recovery

psychology 301

anosognosia

lack of awareness of impairment. related to a network that modulates knowledge of impairment rather than one specific area of brain

dysexecutive syndrome

disinhibition, aggression, impulsiveness, disruptions in planning and working memory, (frontal lobe syndrome)

anosognoa and recovery

poorer functional outcomes, worse recovery

recovery and age

if lesions happen early in life recovery is better due to high neuroplasticity

prefrontal lesions before 16 months old

associated with an inability to learn social and moral rules later in life

size of lesion

bilateral lesions show less recovery than unilateral, larger lesions have larger impairments

chronic vs acute dysfunction in recovery

brain constantly accommodates for damage through neuroplasticity so fast onset can be more devastating than a slow and large lesion

secondary recovery

neurons are temporarily dysfunctional but after a while become functioning again

edema

swelling in the brain (protective in nature, but still a force that may render neurons dysfunctional)

edema after stroke

may mask or distort functions in essentially intact regions

restitution of function

true recovery after the swelling where neurons become functional again

constant swelling

can permanently kill neurons

diaschisis

when a lesion causes dysfunction in an area remote to it because of its strong connections with that area. Other regions can become temporarily hypofunctional when they’re missing input.

diaschisis recovery in PET

reduction in metabolic depression in cerebral areas remote to the regions (areas stop looking ‘cooler’)

environment in recovery

may affect the amount of functional recovery after TBI. (First and biggest predictor of stroke recovery is social network.)

constraint induced movement therapy

forcing patients to use the part that is recovering rather than the healthy part. e.g. children with lazy eye covering their good eye, stroke patients using the side of their body that was affected

compensatory strategies

ways to adapt to new sensory, motor, or cognitive impairments. substituting neurons instead of true recovery because the original neurons are gone forever

rich club of neurons

variety of neurons that are responsible for more things and fire fast

poor club of neurons

tend to fire slowly and have less connections but more neuroplasticity (reorganization of synaptic connections)

cortical representation

maps inside of the brain that represent parts of our body and environment. not static, grows and shrinks based on lack of use or overuse

neuroplasticity due to damage

When unused neurons (after damage) reorganize and respond to nearby areas, strengthening them

neuroplasticity due to use

when repeated practice strengthens and expands neural representation of used area (e.g. violin players having a bigger cortical representation of their left hand)

neuroplastcity and phantom limbs

After limb loss, cortical areas (e.g., hand) lose input and are taken over by nearby regions (e.g., face), causing sensations in the missing limb when those areas are stimulated