Neural Plasticity Flashcards
(34 cards)
neuroplasticity
The ability of the nervous system to respond to intrinsic or extrinsic stimuli by reorganizing its structure, function, and connections
mechanisms involved in establishing a short term memory and converting it to a long term memory
Presynaptic facilitation and inhibition can be used to create short and long term memories
Facilitation inputs can presynaptically affect neurotransmitter release and later signal need for protein synthesis via CREBs
Similarly, long term potentiation can enhance synaptic transmission via long term high frequency stimulation – this forms short term memories that can later be converted to long term memories if a CREBs cycle is initiated
relationship btwn learning/memory and neuroplasticity
When therapists use treatment techniques with a patient, the patient is using the same biochemical mechanisms to learn as they use to form new memories. Because neuroplasticity is an ongoing change in our brain structure and function in response to new experience (i.e. learning), therapists can utilize it to create new pathways by which patients can deal with pain and/or accomplish a task.
3 mechanisms for cell death
Ischemia
Excitotoxicity – too much glutamate (hyperexcitation of cells lead to premature cellular destruction)
Target deprivation
recovery/remediation
the ability to accomplish a goal using the same strategies as prior to the injury
compensation
switching to a different means of accomplishing the task
factors that affect recovery
Age at the time of damage – the younger, the better the chances of full recovery
Size/proportional area of damage – typically, the smaller the lesion the better
Speed of onset – slower progressing lesions cause less severe deficits than sudden onset lesions which also increase the risk of deficit permanence
Past experience – if someone had a great deal of experience with a task/activity/movement prior to the injury, they may recover that same task faster than someone who had no prior experience
Training/rehab post injury – the quicker a patient receives rehab therapy post injury, the more effective rehab will be
5 mechanisms that account for CNS recovery
- neural shock resolution
- denervation hypersensitivity
- hyperinnervation
- recruitment of silent synapses
- collateral sprouting
neural shock resolution and tx
recovery of temporary dysfunction or diaschisis*
Tx implication: If compensation is attempted early, the damaged part of the system will not be challenged to recover. However, if therapy challenges these dysfunctional synapses, the potential for recovery may be greater
denervation hypersensitivity and tx
remaining receptors become more sensitive to neurotransmitters following a lesion, thus yielding a greater reaction with less input
Tx implication: Stimulation of appropriate remaining descending neural pathways may enhance the ability to produce movement by stimulating denervation hypersensitivity. It must be noted that this phenomenon may also cause an unwanted response, spasticity. Caution is warranted.
hyperinnervation and tx
some neurons are not yet active or specialized (i.e. stem cells) – more relevant in younger pt’s
Tx implication: These neurons can be activated and trained to take over functions lost by damaged neurons.
recruitment of silent synapses and tx
connections from neurons to certain pathways which exist but which are not utilized or not as strong as other inputs – possibly too far away from the trigger zone to cause sufficient depolarization
Tx implication: With a thorough knowledge of anatomy, therapists can stimulate these synapses to make them more sensitive/increase their potential in order to yield motor movement from a different circuit than the one damaged by a lesion.
collateral sprouting and tx
new branches sprout from an axons’ terminal ends to take over vacant receptor sites on a cell body following a lesion
Tx implication: Therapists can stimulate the collateral sprouting to regain motor function lost by a lesion. However, this can also cause spasticity and so again caution is warranted.
which mechanisms/theories account for cortical recovery and reorganization?
- expansion of ipsilateral areas
- recruitment of contralesional primary motor area
- bilateral retained activation of primary motor and supp motor areas
expansion of ipsilateral areas
Unmasking of pre-existing inactive representations
Recruitment of new connections (i.e. axonal sprouting)
Changes in synaptic efficiency (i.e. denervation hypersensitivity)
recruitment of contralesional primary motor area
Recruitment of uncrossed corticospinal tracts (referred to as CST in notes)
Reduced transcollosal inhibition
Tasks are processed as complex tasks which normally recruit the bilateral motor cortices
bilateral retained activation of primary motor and supp motor areas
Both areas contribute to corticospinal tracts and may constitute a substitution for the loss of the ipsilesional cortex
how does neural recovery of one function in a child affect later functions
The recovery of a lost function may occur at the expense of another learned function later in life
As was previously stated, this is because inactive or unspecialized neurons take over for the ones that were damaged or lost—which in turn means they will not be available later in life
what drug is used for embolic clots to reduce stroke impact
tPA
what type of stroke is tPA used for/how soon does it need to be given
Used for ischemic strokes (i.e. strokes caused by a blood clot that block the flow of blood to brain tissue thus depriving it of oxygen) to help dissolve the clot quickly and restore blood flow to brain tissue
Should be administered within 6 hours
Should NEVER be administered to patients with hemorrhagic strokes because it is essentially a specialized blood thinner and so it would make these patients bleed even more
what drugs improve or block recovery of CNS damage
d-amphetamine – stimulates some aspects of recovery if used with exercise or activity
CNS depressants (ex: haloperidal or diazepam) – these appear to slow or block recovery but are commonly used to treat agitation or spasticity in patients with TBI and stroke
Acetylcholine – improves motor function and cognitive function in patients with stroke and Alzheimer’s
recovery timeline for stroke
Most recovery occurs during the first 6 months post-stroke
recovery timeline for TBI
Most recovery occurs within 12-18 months post-injury
key issues to consider for successful neurorehabilitation
Rehabilitation should begin as soon as possible.
Rehabilitation should not focus on compensation early in the disease process, as it will not challenge neurological recovery or neural plasticity.
Motor learning literature 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 and do not promote neural plasticity.
Therapy in conjunction with drugs or transplantations/medical interventions will be more effective than these medical treatments alone.
Many times the patient’s insurance will run out before they have reached their maximum potential. It is the obligation of the rehabilitation professions to continue to engage in and support research to document our effectiveness and to provide support for expanding the amount of therapy allocated to patients with neurological injuries or diseases.
