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Principles of Neuroplasticity:

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Andrew

on 25 September 2014

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Transcript of Principles of Neuroplasticity:

changes in the functional organization of the brain as a result of learning & experience
What is Neuroplasticity?
Principles of Neuroplasticity
:
Clinical Applications

Long-Term Potentiation (LTP)
How Does It Happen?
“When an axon of cell A … excite[s] cell B and repeatedly or persistently takes part in firing it, some growth process or metabolic change takes place in one or both cells so that A’s efficiency, as one of the cells firing B, is increased.”
-
The Organization of Behavior
Hebb's Law (1949)
Principles of Neuroplasticity
Failure to drive specific brain functions can lead to functional degradation.
Use It or Lose It
Plasticity in response to one experience can enhance acquisition of similar behaviors.
Transference
• Neuroplastic responses are altered in aged brains.
• Experience dependent synaptic potentiation (Barnes 2003) synaptogenesis (Greenough 1986) and
cortical map reorganization (Coq & Werri, 2001) are reduced in aging.
Age Matters
Andrew Tran, SPT, CSCS
UCSF/SFSU - DPT Graduate Program

Use It and Improve It
Specificity
(Skilled) Repetition Matters
Time Matters
Intensity Matters
Salience
Interference
References
Bliss, T.V., and Lomo, T. (1973). Long-lasting potentiation of synaptic transmission in the dentate area of the anaesthesized rabbit foowing stimulation of the perforant path. J. Physiol. 232, 331-356.
Cramer, et al (2011). Harnessing neuroplasticity for clinical applications. Brain. 134: 1591-1609.
Ferguson, A.R., Crown, E.D., and Grau, J. W. (2006). Nociceptive plasticity inhibits adaptive learning in the spinal cord. Neuroscience. 141, 421–431.
Ferguson, A.R., et al (2012). Maladaptive spinal plasticity opposes spinal learning and recovery in spinal cord injury. Frontiers in Physiology. 3:399, 1-17.
Hebb, D.O. (1949). The Organization of Behavior. New York: Wiley & Sons.
Johansson, B.B., and Belichenko, P.V. (2002). Neuronal plasticity and dendritic spines: effect of environmental enrichment on intact and postischemic rat brain. J. Cerebral Blood Flow & Metabolism. 22, 89-96.
Melton, A.W.; Lackum, W. J. von (1941). "Retroactive and proactive inhibition in retention: evidence for a two-factor theory of retroactive inhibition". American Journal of Psychology 54: 157–173.
Nudo, R. et al (2006). Behavioral and neurophysiological effects of delayed training following a small ischemic infarct in primary motor cortex of squirrel monkeys. Experimental Brain Research, 169:1, 106-116.
Sturm, W., et al (1997). Do Specific Attention Deficits Need Specific Training?, Neuropsychological Rehabilitation: An International Journal, 7:2, 81-103
Wohldmann, E.L., Healy, A.F., Bourne Jr., L.E. (2008). A mental practice superiority effect: Less retroactive interference and more transfer than physical practice. Journal of Experimental Psychology: Learning, Memory, and Cognition, 34, 823-833.
Spinal plasticity is known to play a role in central neurogenic pain. Recent data suggest links between the learning deficit and the sensitization of pain circuits associated with inflammation or injury (central sensitization).
Plasticity in response to one experience can interfere with the acquisition of other behaviors.
Consolidation of memories requires time. (Silva 2004)
Critical period after brain damage. Delayed training resulted in less change in cortical remapping. (Nudo 2006)
There is a major cascade of events and neuronal reactions that occurs after injury.
Early intervention
is critical!
Tough with delays in scheduling, referrals, high caseloads.
Low –intensity stimulation can induce weakening of synaptic response (LTD), whereas higher intensity stimulation will induce LTP.
Challenge patients, but make sure they are doing so safely and correctly.
Non-skilled repetitive tasks do not result in map changes or synaptogenesis.
Merzenich and Jenkins concluded. “Plastic changes in brain representations are generated only when behaviors are specifically attended. When stimuli identical to those that induce plastic changes in an attending brain are instead delivered to a nonattending brain, there is no induction of cortical plasticity.
Attention
must be paid.
Simply engaging a neuronal circuit in task performance is not sufficient to drive plasticity.
Plasticity requires not only the acquisition of a specific skill, but also the continued performances of that skill over time.
So the role of repetition in driving plasticity and learning may be critical for rehabilitation.
Induction of plasticity requires sufficient repetition
Specific forms of neuronal plasticity and behavioral changes are dependent upon specific kind of experience.
The nature of the training experience dictates the nature of the plasticity.

Connection-Dependent
: After deafferentiation (e.g. limb amputation), reorganization of cortex so muscles adjacent to amputated area have larger cortical representation.


Use-Dependent
: Motor learning alters body representation in the motor cortex. Areas used most have largest representation.
• After damage to brain, adjacent areas or contralesional areas can take over motor control.
Training that drives a specific brain function can lead to enhancement of a function.
Interference in Memory
Interference in Motor Learning
Proactive Interference
: when an old memory disrupts the learning & remembering of a new memory
ie. trying to put dishes away at a new house; baseball player difficulty learning golf swing
Retroactive Interference
: newly learned information disrupts or impedes the recall of previously learned information
ie. driving an automatic after driving a manual; switching a long-used password
Occurs during development (and throughout lifespan)
Occurs during learning
Occurs during recovery after damage/disease to sensory, motor and cognitive areas of the brain and spinal cord.
Is an active area of research at many levels: molecular, cellular, system, clinical
Ability to constantly lay down new pathways for neural communication and to rearrange existing ones
throughout life
necessary for learning, memory, and adaptation through experience.
important for
functional recovery
Neurons (among other cells) alter their structure & function in response to variety of internal & external stimuli.
Why Is It Important?
It's our job!
As little as 6 min
of uncontrollable shock to either the leg or the tail generates a learning deficit that lasts up to 48 h.
Deficits in functional locomotor recovery, sensory and autonomic recovery up to at least 6 weeks post-injury.
(comparable to ~3 human years)
Spinal cord has important role in processing nociceptive signals.
Spinal cord is vulnerable to nociceptive input after injury.
Acute nociceptive input is a common feature of polytraumatic automobile accidents (most common cause of SCI), and that pain affects
65-85%
of human SCI population.
Co-morbid peripheral injuries may also play a role in dictating both functional recovery and nociceptive sensitization.
Long-Term Depression (LTD)
Mechanisms for LTP/LTD
increase in synaptic strength
decrease in synaptic strength
Increased/decreased release of neurotransmitter
Increased/decreased number of neurotransmitter receptors
Increased/decreased sensitivity of neurotransmitter receptors
How Does It Happen?
Axon Growth & Regeneration
Synaptogenesis
Neurons that fire together, wire together.

Neurons out of sync, fail to link.
Dendritic Modifications
Standard
Enriched
Changes in dendritic:
length
branching
spine density
synapse number
size
Johansson, Belichenko (2002)
Neural plasticity may be enhanced when the movement is purposeful & related to the behavior being trained.
Motivation, reward, and attention
Training fails to produce plasticity if the subject’s attention is drawn away from the activity or stimulus.
Putting All the Pieces Together
1. Use therapy activities that are hierarchically organized (build upon success).
2. Minimize maladaptive behaviors, movement patterns, and pain.
3. Provide sufficient skilled repetition & intensity.
4. Instill patient motivation and attention to practice.
5. Ensure reinforcement of gains.
6. Make interventions functional, task-specific, and goal-oriented to each patient.
7. Actively facilitate generalization to functional activities from the start.
8. Build sense of cognitive self-efficacy.
9. Educate! Educate! Educate!
Future Directions
Animal studies not fully translatable to humans
younger relative age, more homogenous injury, less co-morbidities, 14% brain white matter volume vs. ~50% in humans
specific patient populations
optimal training/therapy parameters
"neuroprotective" effects
research on interventions in combination (ie. task-specific training + stem cell therapy)
Merzenich, 1978
Cortical somatotopic maps can be modified by sensory input, experience, and learning.
Merzenich, 1978
Induction of plasticity requires sufficient training intensity.
Training-induced plasticity occurs more readily in younger brains.
This doesn't mean you can't still create change in older patients!
The brain of a child is resilient and extremely plastic.
ie. removal of child's left hemisphere: can still learn to speak if injury happened before age of 2
We use this principle every day having patients practice several different interventions, then measuring performance against standardized outcome measures and functional tasks/activities.
In brain injuries and cognitive impairments...
Attention and/or dual task ability is often impaired.
Varying levels:
alertness
sensory/focused attention (visual, auditory, tactile)
sustained attention
selective attention (distractibility)
alternating, divided attention (dual tasking)
Impairments on a given level should be approached by training on the same or a subordinate level.
On the other hand, training for a superordinate level may lead to overload of cognitive-attentive system and result in stagnation or even deterioration to subordinate levels of attention.
Sturm et al, 1997
Only rats receiving combination of chondroitinase and specific rehabilitation showed improved manual dexterity.
Rats that received general locomotor rehabilitation were better at ladder walking, but had worse skilled-reaching abilities than rats that received no treatment.
Chondroitinase treatment opens a window during which rehabilitation can promote recovery.
However, only the trained skills are improved and other functions may be negatively affected.
Wohldmann et al, 2008
Ferguson et al, 2006
Ferguson et al, 2004
The Problem...
Main Point:
be careful
, especially with acute SCI
-uncertain of implications to other neuro injuries
Full transcript