Neural Plasticity Flashcards
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)
