Neuroplasticity (quiz 2)—7

A damaged adult brain need what to rebuild

"Neuroplasticity jump start" -practicing particular movements over and over; constrain- induced movement based therapy

Brain plasticity and learning

- an enormous amount of research has revealed that the brain never stops changing and adjusting

Adaptive plasticity

- brains ability to compensate for lost functionality due to brain damage as well as in response to interactions with the environment by reorganizing structures -compensation from brain injury and in adjustment to new experiences -neuronal changes occur through sprouting and rerouting -occurs over the lifespan but is more efficient and effective during infancy and early childhood

Developmental plasticity

- changed in neural connections as a result of interaction with the environments (our experiences during childhood) as a consequence of developmental processes -It predetermined and occurs in response to initial processing of sensory information by the immature brain - neuronal changes (synaptogenesis, synaptic pruning, neural migration, myelination) - occurs over lifespan but diminishes with age

1 study small area of monkeys brains damaged which resulted in loss of hand movements

- due to lack of hand activity even the neurons surrounding the damaged brain area withered, resulting in further impairment of hand movement (These observations confirm the notion that it is important to provide stimulation to neurons in order for them to remain active and form new connections, promoting rehabilitation)

Adaptive brain plasticity; injury and hemispheric compensation

- just as brain changes in response to environmental conditions it can also change and rearrange in response to injury or disease

Synaptic pruning

- reduction in the number of synaptic connections - determined by experience - unused connections are mostly pruned

Neuroplasticity allows neurons in the brain

-adjust neuronal activities in response to new situation or to changes in their environment (developmental plasticity) - to compensate the loss from injury and neural disease (adaptive plasticity)

Neuroplasticity

-can be described as brains ability to reorganizeitself by forming new neural connectios throughout the life - neuronal connections are continuously being created and broken and all modeled by our exeriences and states of health and disease

Plasticity occurs on a variety of levels

-cellular changes involved in learning - large scale changes involved in cortical remapping in response to injury

NESS H-200

-device with electrical stimulation -electrically stimulate patients hand and arm muscles to perform task like grasping -if patient practices functional activities with this device, brain gets stimulated gets mediagenic that the arm wants to be utilized in a functional way -if done repeatedly in patient following stokes (8-10wks) brain can reorganize itself

Developmental plasticity and synaptic pruning

-following birth, the brain of a newborn is flooded with information from the baby's sense organs - this sensory information must somehow reach to the brain where it can be processed - to do so, nerve cells must make connections with one another, transmitting the impulses to the brain

Similar network of cerebral structures is activated when

-normal control subjects execute physically or imagine a sequence of up-down foot movements

Synaptogenesis

-rapid expansion in synaptic formation in order to deal with bombardment of sensory input - inenables more efficient synaptic configurations (thus more efficient brain functioning hence ongoing learning)

Effects of rehabilitation on plasticity

-recovery of neuronal function after brain injury is influences by the intensity of rehab and the timing of rehab relative to the injury EARLY rehabilitation is necessary for IMPROVED outcome

Problems with regeneration

-sprouting by peripheral axons can innervate the wrong target (peripheral nerve injury, motor axons may innervate different muscles than previously, causing unintended movement SYKINESIS)

Retrograde degeneration

-the degeneration of axon stump proximal to the lesion -proceeds from distal to proximal REVERSIBLE if regeneration occurs

Axonal injury, axon is severed

-the proximal end is Separate from the distal segment -once isolated from cell body the distal segment undergoes wallerian degeneration -the axon terminally readily degenerate and their loss Is followed by death of the entire distal segments -glial cells scavenge the area, cleaning up the debris from degenerating axons - associated cell body undergoes degenerative changed called chromatolysis (leads to cell death) -sometimes post0synaptic cells undergo degenerative changes and die

Axonal sprouting

-undamaged axons grow new nerve endings to reconnect surrounding neurons whose links where injured or severed -undamaged axons can also sprout nerve endings and connect with other undamaged nerve cells, forming NEW neural pathways to accomplish needed functions -neurological research indicated that experiences can actually change both the PHysical and FUnctional organization of the brain

According to durbach (2000) there are 2 major types of modifications taking place in the brain with learning

1. A change in the internal structure of the neurons (most notably the synapses) 2. An increase in the number of synapse between neurons

Long term potentiation appears to change the following synapses

1. Conversion of silent synapses to active synapses 2. Changes the shape of postsynaptic membrane

3 principles of neuroplasticity

1. Habituation 2. Learning 3. Cellular recovery after injury

By the time an infant is. 2-3 years old the number on synapses per neuron is

15,000 synapses

At birth each neuron in the cerebral cortex has approximatley

2500 synapses

How many average synapses are in an average adult brain

7500-800 About 1/2 of infant because of pruning

In order for the brain to have a chance to repair

A certain (yet unknown) number of neurons must remain intact

Mental practice with motor imagery can be used as

A therapeutic approach to keep active the neural circuits involved in locomotion, and hence facilitating the rehabilitation of patients who sustained damage to the brain

Neuroplasticity

Animals when raised in presence of challenging environments develop more synapses and dendritic branches than animals without stimulation

Habituation clinically

Applied to physical therapeutic interventions -patients with specific types of vestibular disorders exhibit dizziness and nausea can be stopped with repeated induction of dizziness and nausea movement of head - reversible, if the stimulus is withdrawn, the reflexive behavior may elicit again

Excessive vigorous rehabilitation of motor function too soon after injury

Are counterproductive

Learning as an example of neuoplasticity

As we learn, we acquire new knowledge and skills through instruction or experience -in order to learn or memorize a fact of skill, there must. Be persistent functional changes in the brain that represents the new knowledge -this ability of the brain to change with learning is due to neuroplasticity

Building on the principle that neuronal activity promotes new connections rehabilitation therapy...

Attempts to stimulate particular neurons (that have not been active in some time) through specific motor activities

If an area of the brain is extremely damaged, then its natural ability to reorganize will

Be insufficient to regain the loss of function (Huntington's disease)

As we age brain reorganization

Becomes more difficult

Simple brain exercises such as presenting oneself with challenging environments, interacting in social situations, and getting involved in physical activity will

Boost the general growth of connections

Forming new neural connections is a delicate process that must be done

Carefully by making balance between the intensity and frequency of exercise (although repetition is the key for making neuronal connection )

Huntington's disease and other neurodegenerative diseases

Cause neuronal death The death of many cells may render the brain unable to reorganize corrective connection s

Some evidence supports the concept the STM depends upon

Chemical and electrical events Not structural changes

In retrograde degeneration the following changes take place

Chromatolysis of cell Body Swelling of cell body and fragmentation of ER

Types of neuronal sprouting

Collateral Regenerative

Neuroplasticity enables the brain to compensate for

Damage

Research on non-human animals indicated that if an injured limb is used immediately after brain area had been damaed

Damage to the brain will increase further

A person who has suffered from brain damage and does not practice the lost movement shows

Damaged neurons as well as surrounding neurons are starved of stimulation and will be unable to reconnect

Habituation

Decreased response to a repeated stimulation - Charles Sherrington observed that certain reflexive behaviors (withdrawal reflex in response to painful stimulus) can be stopped after repeated stimulation with same stimulus -due to decreased synaptic effectiveness of the stimulated pathways or decreased release of excitatory transmitters

Injuries that damage the axons of neurons cause

Degenerative changes but may not result in death of the cell

Generally synkinesis

Disappears when individuals relearn muscle control

Constraint induced movement of an impaired limb immediately after an experimental lesion of the sensorimotor cortex in adult rats showed

Dramatically increase neuronal injury and result in long-lasting increase in neuronal injury and result in long-lasting deficits in limb placement decreased response to sensory stimulation and defective use of the limb for postural support

Long term potentiation

Excitation through multiple inputs with cooperatively, associativity, and specificity to the enhancement of EPSP and formation of memory

Recent research had shown that the brain can sometimes

Generate new neurons not just new connections -these neurons can sometimes "migrate" within the brain This raises the possibility that, under certain condition s, new neurons could migrate to damaged areas, form new connections, and restore some or all lost function

Over the first few years of life the brain

Grows rapidly -each neuron matures, it sends out multiple branches (axons, which send info out, & dendrites which bring info in) increasing the number of synaptic contacts

Key principle of neuroplasticity is

In activity promotes brain reorganization

Repetition of specific stimulus causes

Increase in synthesis and activation of new proteins that alter the neurons excitability and promote new synaptic connections

How do non-neuronal cells play a role in plasticity

Increased connections between astrocytes and neurons are observed in rats raised in challenging environments

Neuropraxia

Injury that causes transient loss of function (conduction block ischemia) No degeneration occurs here Nerve functions reverse

Neurotmesis

Injury that damages the nerve tissue with total severing the nerve fibers -damage is irreversible due to lack of regeneration

Axonotmesis

Injury that damages the nerve tissue without severing the nerve -wallerian degeneration takes place distal to the injury (crush injury)

Learning and memory

Involve persistent, long lasting changes in strength of synaptic connection - has been observed that during initial phase of motor learning, large and diffuse areas of the brain show synaptic activity - when the task has been learned, only small, distinct regions of brain show increased activity during performance of the task

With repetition of specific stimulus we can

Learn THR specific experience and can have long term memory

Widely recognizes forms of plasticity are

Learning, memory and recovering from brain damage

After a period of time Informaion has to be moved to a more permanent type of memory

Long term memory It's the result of anatomical and biochemical changes that occur in the brain (structural and functional)

Transcranial magnetic stimulation and functional magnetic imaging show that task specific rehab training produce

Long-lasting cortical reorganization in the brain areas activated

The cellular mechanism for formation of memory is called

Long-term potentiation (Function of hiooocampus in temporal lobe)

Task specific training induces

More regular patterns of brain activation compares with the general use training of upper extremity in individuals with stroke

Regenerative sprouting

Occurs when an axon and its target have been damaged and the injured axon sends out side sprouts to a new target -now joins another/ two feed into one

Collateral sprouting

Occurs when enervated neurons attract side sprouts from nearby undamaged axons -one splits to two

When a nerve fiber is injured the part distal to the site undergoes degeneration called

Orthography degeneration (wallerians degeneration) -the degeneration moves from proximal to distal on distal stump

Functional regeneration of axons occurs most frequently in

PNS because of the production on nerve growth factor (NGF) by Schwann cells and their recovery process is low (1mm/day)

The growing number of selectively responding neurons discharge with

Positively stronger temporal coordination (distributed synchronicity)

Wallerian degeneration

Process where myelin sheath pulls away from the segment The axon swells and breaks into short segments

If behaviorally important stimuli repeatedly excite cortical neuron populations the neurons will

Progressively grown in number

Some neurons have the ability to do what to their axons

Regenerate

The brain compensated for damage in effect by

Reorganizing and forming new connections between intact neurons

Initially newly leaned data are stored as

Short term memory STM

Repetitive, behaviorally important stimuli processed in

Skilled learning lead to progressively greater specificity in the spatial and temporal dimensions

If one brain hemisphere is damaged the intact hemisphere can

Sometimes take over some of the functions or the damaged one (Anna)

Regeneration of damaged axons take place through

Sprouting

STM

Temporary for which an individual will have the ability to recall a few pieces of information

Adaptive plasticity

The brain compensate for damage by reorganizing and forming new connections between intact neurons -reorganization takes place by (axonal sprouting and rerouting)

Physical therapy must take advantage of

The brains natural flexibility for forming new neural connections s

If the cell body Is injured...

The cell will die

New connections can form at an amazing speed but in order to reconnect

The neurons need to be stimulated through activity

There should be some limits on practice, If one activity is practiced millions of times per month over years...

The pattern of connection scan grow so much that it inhibits or "squeezes out" other patterns or connection , resulting in inability to perform other movements

If the axon of the CNS is damaged....

There will be no regeneration -b/c of lack of NGF and inhibition of growth by oligodendrocytes

An important aspect of the rehabilitation therapy is

Timing

To be successful rehab must

Wait a week or two Use active exercise using injured limb stimulates damages connection s that would otherwise atrophy without input

Synaptic pruning eliminates

Weaker synaptic contacts while stronger connections are kept and strengthened (Experiences determine which will be strengthened and which will be pruned) Connections that have been activated most frequently are preserved

Wallerian degeneration definition

When nerve fibers are injured, the distal to the injured fibers undergo degenerative changes -distal stump separated from cell body, showed rapid loss of neural transmission - degeneration of myelin sheath on nerve fiber distal to injury leading to loss of myelin (neurolemma membrane remains intact)