Unit 4_Neuroplasticity Flashcards
What is defined as the ability of the nervous system to respond to intrinsic or extrinsic stimuli by reorganizing its structure, function and connections?
Neuroplasticity
Neuroplasticity reorganization happens _______ as we learn and establish new memories. Unfortunately, in forms of dementia and as we approach senescence, we lose memories or capability of forming long term memories.
everyday
The nervous is capable of neuroplasticity ________ life.
throughout
Thousands and thousands of people with neurologic lesions were not given the fullest neurorehabilitation until the ______ _____ ______ even though scientists had clearly demonstrated this capability in the mid 20th century and possibly even earlier.
late 20th century
Today understanding and utilizing neuroplasticity forms the basis of much of what we do in what?
Neurorehabilitation
What can be used to create short and long-term memories?
Presynaptic facilitation and inhibition
What can “presynaptically” affect neurotransmitter release and later signal need for protein synthesis involving second messengers?
Facilitating inputs
With presynaptic inhibition there could be loss of what?
synaptic contacts
What are accompanied by increased synaptic contacts?
Long-term habituation and sensitization
What occurs when a person is said to recover from a CNS deficit if they are able to accomplish a goal using the same strategies as prior to the injury?
Recovery
What means that the person has switched to a different means of accomplishing the task?
Compensation
What happens when there is a lesion in the nervous system?
A sequence of changes follows all lesions, and that perhaps one never achieves an equilibrium. There are immediate changes, and changes occurring over seconds, hours, days, weeks, months and indeed years.
What can mechanical damage - crush, shear, cut cause cell death to?
PNS
What can Ischemia (80% of strokes are ischemic) cause cell death to?
CNS
What can (Glutamate) Excitotoxicity cause cell death to?
CNS
(It may be the final common pathway for most CNS cell death)
What can target (or input) deprivation cause cell death to?
It may cause a cascade of changes with the CNS
What have to talk to each other for proper function and in addition when communication is cut off neurons can become unhealthy because of target deprivation? This can be short or long-term depending on the type of lesion.
Neurons
What is continually modified in healthy adults in response to activity, behavior, and skill acquisition?
The cortical representation of the body
What opens a window of increased neural plasticity in the CNS?
A lesion
As therapists we are interested in activity dependent changes in the structure and function of the CNS following what?
injury
Removal of target in periphery, such as with amputation can cause what?
major changes in CNS
Post stroke, the following occurs to what changes in the cortical maps?
Unmasking of pre-existing inactive representations.
Recruitment of new connections-axonal sprouting.
Changes in synaptic efficiency-denervation hypersensitivity.
Expansion of ipsilesional areas of the cortex
Post stroke, the following occurs to what changes in the cortical maps?
Recruitment of uncrossed CST
Reduced transcallosal inhibition
Tasks are processed as complex tasks which normally recruits the bilateral motor cortices.
Recruitment or Inhibition of contralesional primary motor cortex
Post stroke, the following occurs to what changes in the cortical maps?
Both contribute to CST tracts and may constitute substitution for loss of ipsilesional primary motor cortex
Bilateral Retained Activation of Pre-Motor Area and SMA
What two primary processes are signs and symptoms of CNS damage?
Actual cell death caused by the event
Diaschisis
Damage to neurons in CNS can cause death and they don’t regenerate as commonly as PNS cells.
Actual cell death caused by the event
Physiological shut down of other neurons near the area or that are associated with the damaged area.
- There is a functional stand still or abolition of all electrical impulses in neuronal areas that are connected to the damaged area.
- This is often due to shock, edema or partial denervation of post-synaptic neurons.
Diaschisis
What is the final common pathway resulting in neuronal injury for many seemingly unrelated disorders, including ischemia, trauma, seizures, hypoglycemia, hypoxia and even some neurodegenerative disorders?
Excitotoxicity
What is reduced function of a region of the brain (and spinal cord) due to a lesion at a remote site which normally supplies background excitation to the neurons in that region?
Diaschisis
Progression of functional depression of the spinal cord following an injury to the motor cortex.
Diaschisis Corticospinalis
Functional depression of the contralateral cerebral cortex after injury to one hemisphere.
Diaschisis Commissuralis
What do the following factors influence?
1. Age at time of damage
2. Nature of the lesion
3. Size or proportion
4. Speed of onset
5. Past Experience
6. Training after injury
7. Post-lesion environment
Influence recovery
Young children and adolescents’ recovery to a larger extent than older adults do but this is not to say there is not capacity for recovery in adults which apparently exists throughout life.
Part of the functional recovery of a child may occur at the expense of another function that was supposed to develop later in life.
The ability for younger children to recovery faster and more completely may be due to hyperinnervation.
Age influences recovery
Generally, the smaller the lesion, the smaller the deficits. However, the proportion of area damaged is also important.
Although all of this can break down when you have lesions outside of the cerebral cortex (Internal capsule, brainstem and spinal cord because so many structures and/or pathways are close to each other)
Lesion size and location influences recovery
A slow progressive lesion produces less severe deficits than the same lesion presenting suddenly.
It is likely that the CNS accommodates to the slow growing lesion as it grows and provides collateral sprouting etc. to minimize functional deficits.
In a sudden lesion, the CNS first is in shock and then must provide a massive re-organization all at once.
Speed of onset influences recovery
Once the deficits associated with a slow growing lesion do present to the patient, they are often more permanent because the CNS has already maximized the ability to re-organize and accommodate for the lesion.
In contrast, the deficits associated with a sudden lesion may be more severe initially, but they may have a greater potential to resolve.
Speed and recovery
There is evidence to suggest that “overtraining” a certain brain function prior to injury leads to sparing of function or a reduction of deficits post-injury.
(I practice using both limbs when I draw in case, I have a stroke)
For example, individuals who have a great awareness of movement through exercise prior to a stroke may recover better motor function than someone who did not (particularly if we can limit secondary damage).
Past experience influences recovery
Evidence for the importance of post-lesion exercise or training in animals has existed since the early 1900’s.
Research has suggested that early rehabilitation is more effective than later and that more intensive therapy will produce better outcomes. That said there are now many examples of successful training many years after a lesion.
In addition, functional goal specific therapy is better than non-functional activities.
Training and post injury environment influences recovery
What are the following mechanisms:
Neural shock resolution
Denervation Hypersensitivity
Hyperinnervation
Recruitment of silent synapses
Collateral Sprouting
Recovery Mechanisms and Treatment Implications
The recovery of temporary dysfunction or diaschisis caused by shock or edema etc.
Treatment Implications
Some symptoms will recover regardless of rehabilitation due to natural recovery. Edema decreases, blood flow returns, and this produces a recovery of synaptic effectiveness which in turn leads to a recovery of function.
Neural Shock Resolution
Cells that lose some of their pre-synaptic terminals become more sensitive to transmitter effects from the remaining excitatory sensory pathways. Therefore, the remaining pathways produce a stronger effect.
Denervation Hypersensitivity
This is a more potent factor in young patients:
- We have neurons not currently in use. When a lesion occurs, these neurons can become active and take over function for damaged cells.
- In this scenario, these cells have no functional connections yet. They are just cells in waiting. They are probably stem cells that are not fully formed.
Treatment Implications
Stimulation is required in order to activate these inactive cells and guide their connections. There are now protocols being developed to train new or inactive neural circuits.
Hyperinnervation
There are connections from cells to certain pathways which exist, but which are not utilized. Most often during development they were not activated as much.
When other primary axon pathways are ablated or shut down, these silent synapses become more effective and can produce a response.
Recruitment of “Silent” Synapses
When inputs to a neuron are ablated, other axons can sprout branches from their terminal ends and take over synaptic spots on the cell body and/or dendrites.
This occurs within 4-5 days (or sooner) and occurs only from tracts/cells closely associated with the injured area.
Contralateral Sprouting
Most of the neurological and functional recovery post stroke and SCI occurs within the first ____ months.
six
Recovery from traumatic brain injury is generally slower and most recovery occurs within the first year to ____ months.
18
Recent evidence suggests that certain functions may recover even many years ______.
post-injury
Constraint of the less-affected limb in a glove, sling or puppet that prevents use of that limb combined with intense functional task practice.
- Combats learned non-use
- 2-week training
- Typically performed 3-6 months post stroke
Constraint Induced Movement Therapy (CIMT)
Goals
- Increased excitability in the affected hemisphere.
- Decreased or increased excitability in the unaffected hemisphere.
Neuromodulation
What seems to stimulate some aspects of recovery if presented with exercise or activity? Stroke patients who received this drug and then immediately engaged in physical therapy performed better than those who received a placebo did. Acetylcholine also improves motor function and cognitive function in patients with stroke and Alzheimer’s.
d-amphetamine
What CNS depressants are commonly used to treat agitation or spasticity in patients with TBI and stroke appear to slow or block recovery?
haloperidol or diazepam
What may improve spinal cord function after SCI which affects motoneuron excitability?
Acute Intermittent Hypoxia (AIH)
Rehabilitation should begin ___ _____ ____ ______.
as soon as possible
Rehabilitation should not focus on _________ early in the disease process, as it will not challenge neurological recovery.
compensation
What suggests that rehabilitation should focus as much as possible on functional real life activities? Activities that are practiced out of context do not transfer as well to real life situations.
Motor learning literature
