Neuroplasticity and aging

Age

associated changes that involve structural and functional changes that affect a person’s ability to function or survive

Disuse

decline in physical function associated with decline in activity

Pathology

decline in function occurs due to a disease or pathology

Reasons older adults may have impaired sensation

Decline in sensation with touch, hearing, vision, taste, smell, proprioception, and vestibular function are typically observed after 60 y.o. due to changes in the cellular system as a whole

What is the impact of impaired sensation on movement and motor control with aging

Necessary to learn new movements, Keeps movement on track with error detection, Critical for balance responses

Effects of aging on muscle function

Gradual decline in motor behaviors due to atrophy, sarcopenia, motor unit application, etc.

Effects of aging on anatomic changes

Brain undergoes atrophy, losing around 5% of volume per decade after 40, Frontal lobe decreases by about 12%, Certain subcortical areas are more impacted than others (Thalamus, BG, hippocampus)

Effects of agin on biochemistry of NS

Changes in nerve cell morphology, Decrease in size, density, myelin coverage, Purkinje cells, Senile plaques form

What does the decrease in size, density, myelin coverage and purkinje cells result in

slowing of movement and worse adaptability

Abnormal neurofibers distort the cell bodies causing

dementia

Effects of aging on metabolic changes of NS

Decrease in cerebral blood flow with increased resistance which leads to decreased oxygen consumption

Effects of aging on autonomic NS

Impaired ability to maintain internal homeostasis due to endocrine and neural control issues, Parasympathetic activity decreases

Neuroplasticity

the ability of neurons to change their function, chemical profile (NT types), and/or structure

Neuroplasticity occurs as

the brain encodes and learns new behaviors, or relearn lost behaviors in response to rehab of brain damage

Habituation

a decrease in response to a repeated, benign stimulus, allows us to pay attention to more important information

Short term habituation

presynaptic changes in decrease of excitatory neurotransmitters

Long term habituation

post synaptic changes with prolonged repeated stimuli

Habituation and therapy

certain techniques are used to decrease neural response to a stimulus

Experience dependent plasticity positives

persistent and long lasting effects, as tasks become more plastic, the multiple brain regions activity required becomes less

Experience dependent plasticity negatives

during initial phases, large amount of brain regions is required to learn a task

Declarative memory

explicit, facts and events

Non declarative memory

implicit

Nonassociative learning

reflex pathways

Associative learning

classical and operant conditioning with emotions and skeletal structure

Procedural skills

skills and habits

Learning

persistent change

Performance

one time event involving a person’s ability to complet a skill

Long term potentiation

conversion of silent synapses to active ones

Long term depression

conversion of active synapses to silent ones

Long term potentiation and depression can affect therapy by

changing the presynaptic membrane to up to downregulate the nervous system when performing activities

Astrocytes influence the

synaptic plasticity by modulating NT release, expression, or uptake in the synaptic cleft (helps remodeling in re

Cerebral Cortex cerebellum loop

particularly important in early stage learning, cerebellum very active post stroke

Cerebral Cortex BG loop

later stage learning, BG motor loops stay active even after a task is well learned, some gains require time to become effective

Degenerative following severance of an axon

axon degenerates and myeline is broken down, leaving debris behind, cells undergo metabolic changes and presynaptic terminals are retracted, post synaptic cells degenerate

Wallerian Degeneration

severed segments retract away from each other,

The distal segment undergoes WD

myelin sheath pulls away and the axon swells while breaking down, terminal rapidly degenerates, which causes death of the distal segments, glial cells scavenge the area, cleaning debris

What are the two types of sprouting

collateral and regenerative

Collateral sprouting

denervated target is reinnervated by intact axons from neighboring branches

Regenerative

injured axons send out side sprouts to a new target

CNS recovery following injury

Has similar processes like the PNS (Wallerian degeneration and severance), Damage evolves over time (Hours to days later due to a cascade of cellular events)

What does not occur during CNS recovery following injury

Functional axon regeneration

Edema occurs

2 to 3 days post injury and leaves about a week post onset

Cytotoxic edema

accumulation of fluid

Vasogenic edema

fluid leakage and BV damage

Excitotoxicity

is cell death caused by overexcitation of neurons (causes can be oxygen deprivation, increased extracellular water, or increased glycolysis)

PNS recovery following injury

More immediate effects like sprouting can occur, Nerve growth is stimulated by Schwann cells

Synaptic changes following an injury

Reduction of local edema can return synaptic effectiveness, denervation hypersensitivity, synaptic hypereffectiveness, unmasking of a silent synaps

Denervation hypersensitivity occurs after

destruction of presynaptic neurons deprive NTs from system so the postsynaptic neurons develop new receptors at the remaining terminals

Synaptic hypereffectivenss

Presynaptic terminals are lost, and NTs accumulate in undamaged terminals so the active terminals are hyperactive

Unmasking of a silent synapse

NDMA receptors are present at postsynaptic membranes, they cannot propagate APs

Functional reorganization/remapping

Researchers map the functional areas of cortex according to stimulation patterns, The cortical areas constantly adjust and are modified

How long does reorganization take

years

BDNF (brain derived neurotropic factor)

is a gene that plays a role in reorgainization/remapping

Neurogenesis

Stem cells are involved in remodeling, This is an exciting avenue for the discovery of novel therapies used to treat brain injuries or disease

Potential effects of rehav on neuroplasticity

may have direct effects on integrity and reorganization of the motor complex mapping

Recovery of neuronal function is influence by

intensity and timing of rehab

What are the neuroplastic principles used to devise appropriate therapy for improved outcomes

use it or lose it, use it or improve it, repetition matters, salience, intensity, specificity, age, time, transference, interference