Lecture Five: Neural Plasticity and Recover of Function Flashcards

1
Q

MOTOR CONTROL:

ANATOMICAL PROCESS/STRUCTURES

A

Task example: Reaching to pick up glass of milk
First
• Sensory inputs come in from periphery for: • Body in space information
• Information related to task: how big is glass, how heavy
• Send info to cortex as sensory map, for motor planning to perform action

Second
From sensory map, make a movement plan (parietal lobes, premotor cortex)
• Plan sent to motor cortex: Muscle groups for action are specified
• Plan also sent to cerebellum and basal ganglia: Modify plan to refine the movement
• Cerebellum sends update of movement output plan to motor cortex and to brainstem
Third
Descending pathways from motor cortex and brainstem activate spinal cord networks→spinal motor neurons activate muscles→ reach for glass of milk
• If glass has more milk than you anticipated: spinal reflex pathways compensate for the difference in weight and activate more motor neurons
• Sensory input is evaluated→cerebellum will update movement pattern

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2
Q

Neural Plasticity

A
  • Ability of neurons to change function, chemical profile, or structure
  • Both changes in synaptic connections, and structural changes in cortical organizations and number of neural connections
  • Neural plasticity occurs
    • During development
    • During learning process
    • In response to CNS injury
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3
Q

CNS and Learning

A
  • The brain is continuously remodeling its neural circuitry to encode new experiences( learning) and enable behavior change
  • For each learning event, there is a change in the nervous system that supports the learning to occur
  • Learning modifies( changes) the structure and function of neurons in the brain
  • This change is evidence of Neural Plasticity- adaptation of brain and neural system to experiences
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4
Q

Plasticity: Changes in neural structure and function during learning

A

Short term learning vs Long term learning

Initial skill phase vs Autonomic skill phase

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5
Q

Short term learning

A

Intercellular level changes occur in the efficiency of synaptic connection

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6
Q

Long term learning

A

Structural changes occur in the organization and number of neural connection

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7
Q

Initial Skill Phase

A
  • Increased attentional demands

- Associated with activity in widely distributed areas of the brain, predominantly cortical areas

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8
Q

Autonomic Skill Phase

A
  • Task becomes more automatic or habitual- decreased attentional demands
  • Associated with decrease in activity on the primary motor cortex and an increase in subcortical motor regions
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9
Q

Intercellular level plasticity

A

Changes between neurons at the synaptic level

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10
Q

Network level plasticiy

A

Changes in patterns of neural activation and cortical remapping/reorganization

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11
Q

Synaptogenesis

A

The formation of synapses between neuron in the nervous

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12
Q

Synaptic Pruning

A

Process of elimination through apoptosis of synapses that are not strengthened through use

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13
Q

Synaptic Plasticity

A

Changes in the strength of connections between synapses, in response to increases or decrease in their activity

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14
Q

Recovery of Function after CNS injury

A
  • Spontaneous recovery: Initial or early , not related to external interventions
  • Activity-induced recovery: Improvements related to specific activities and training
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15
Q

Recovery of Function- Mechanisms

A

Restorative( Direct), Compensatory( Indirect)

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16
Q

Restorative( Direct)

A

Resolution of temporary changes in neural tissue, and recovery of injured neural tissue after injury

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17
Q

Compensatory (Indirect)

A

Different neural circuits/structures take over the last or impaired function- Plasticity

  • Function enabling plasticity: Changes in neural structure that improve motor function
  • Function disabling plasticity : changes in neural structure that reduce motor capabilities or sensation
18
Q

Neural systems initial injury: Intercellular level

A
  • Injuries in central and peripheral nervous systems involve damage to axons
    • Axotomy - Injury that divides axon in two
    • Results in loss of synaptic connection
    • Also causes damage to adjacent neurons: presynaptic and postsynaptic
  • Initial transient impact after injury
    - Diaschisis: Reduction in blood flow and/or metabolism to structurally intact brain areas that are adjacent to site injury, causing further loss of function- may be reversible
    • Cerebral edema: Compresses axon and physiological blocks nerve conduction- reduction of edema typically results in restored function to non damages areas
19
Q

CNS Response to Injury: Mechanisms of Recovery

A

Unmasking silent synapses
Regenerative synaptogenesis/Neural regeneration
Reactive synaptogenesis/Collateral Sprouting

20
Q

Unmasking silent synapses

A

Structural synapses that are present but have not contributes to function pre-injury (silent) may be unmasked

21
Q

Regenerative Synaptogenesis/Neural Regeneration

A

Injured axons begin sprouting to reestablish synaptic connections

22
Q

Reactive Synaptogenesis/Collateral Sprouting

A

Adjacent ( uninjured) axons sprout to innervate synaptic sites that were previously activated by axons that are injured

23
Q

NEURAL SYSTEM RESPONSE TO INJURY: NEURONAL REGENERATION

A

Severe damage to axon often leads to death of neuron
• Neurogenesis can occur in humans in hippocampus and olfactory bulb
• New neurons extend axons and dendrites, form synapses, integrated into circuits
• Stem cells are the source of neurons in embryo and in adults

24
Q

RECOVERY OF FUNCTION:

STRUCTURAL LEVEL – CORTICAL REORGANIZATION

A
  • Cortex mapping: Corresponding area of brain in somatosensory and motor cortices related to region of body - Cortex maps are dynamic
  • Capable of reorganizing after peripheral or central injury
  • Adjacent areas of brain extend to cover damaged areas
  • Non-dominant pathways (pre-injury) take over functional connections
25
Q

CORTICAL REMAPPING

A

Typically: Sensory and motor maps in the brain are constantly changing with the type & amount of activation by peripheral inputs
• Rehabilitation/training can strengthen peripheral input for brain plasticity • Each person’s brain mapping is unique

26
Q

RECOVERY OF FUNCTION:

ACTIVATION OF BRAINSTEM LEVEL PATHWAYS

A
  • In stroke patients – corticospinal lesion was found to result in an increased activation of reticulospinal pathways from the brainstem
  • Reticulospinal activation both supports and constrains functional recovery
  • Increases recruitment of flexor motor neurons to strengthen arm/hand (supports recovery)
  • Also constrains recovery, as the increased flexor activation is not balanced with increased extensor muscle activation
  • UE flexor synergy is common pattern seen in individuals after CVA
27
Q

NEURAL PLASTICITY

A

Synaptic connections and cortical remapping are dependent on use/experience

28
Q

PRINCIPLES OF EXPERIENCE-DEPENDENT NEURAL PLASTICITY

A

1)Use it or Lose it
2) Use it and Improve it
3) Specificity:
Repetition matters
5) Intensity matters
6) Time matters
7) Salience matters
8) Age Matters
9)Transference
10) Interference

29
Q

Use it or lose it

A

CNS needs to be actively engaged in tasks or will further degrade after injury

30
Q

Use it or Improve It

A

Skill training is associated with neural plasticity and improvement in function

31
Q

Specificity

A

Training needs to be specific to skill being learned

32
Q

Repetition Matters

A

High reps in practice needed to change neural networks

33
Q

Intensity Matters

A

Sufficient practice volume is need for neural plasticit

34
Q

Time Matters

A

There are time windows when training is most effective for making use of neural plasticity. Time of onset of rehab matters- don’t wait. Some interventions maybe more effective at particular times in recovery

35
Q

Salience matters

A

Training need to be meaningful to the individual for plasticity to occur

36
Q

Age Matters

A

Experience- dependent plasticity potential reduces with age. However, plasticity can still occur, but may be slower to occur and have decreased effects

37
Q

Transference

A

Plasticity that occurs from training on skill may enhance acquisition of similar skills

38
Q

Interference

A

Plasticity from learning one behavior may interfere with learning other behavior/skills

39
Q

Neural plasticity and neurodegenerative disease

A

Experience- dependent principles apply

  • Preventive factors: Activity can delay onset, progression of symptoms by strengthening neural connections
  • Prolong function
  • Neuroprotective: Activity continues to strengthen pathways with use
40
Q

Other considerations for rehab

A

Enriched Environment enhances synaptic plasticity and functional recovery ( salience, intensity, opportunities for repetition)
-Importance of aerobic exercise for increase blood flow