Lecture Five: Neural Plasticity and Recover of Function Flashcards
(40 cards)
MOTOR CONTROL:
ANATOMICAL PROCESS/STRUCTURES
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
Neural Plasticity
- 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
CNS and Learning
- 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
Plasticity: Changes in neural structure and function during learning
Short term learning vs Long term learning
Initial skill phase vs Autonomic skill phase
Short term learning
Intercellular level changes occur in the efficiency of synaptic connection
Long term learning
Structural changes occur in the organization and number of neural connection
Initial Skill Phase
- Increased attentional demands
- Associated with activity in widely distributed areas of the brain, predominantly cortical areas
Autonomic Skill Phase
- 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
Intercellular level plasticity
Changes between neurons at the synaptic level
Network level plasticiy
Changes in patterns of neural activation and cortical remapping/reorganization
Synaptogenesis
The formation of synapses between neuron in the nervous
Synaptic Pruning
Process of elimination through apoptosis of synapses that are not strengthened through use
Synaptic Plasticity
Changes in the strength of connections between synapses, in response to increases or decrease in their activity
Recovery of Function after CNS injury
- Spontaneous recovery: Initial or early , not related to external interventions
- Activity-induced recovery: Improvements related to specific activities and training
Recovery of Function- Mechanisms
Restorative( Direct), Compensatory( Indirect)
Restorative( Direct)
Resolution of temporary changes in neural tissue, and recovery of injured neural tissue after injury
Compensatory (Indirect)
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
Neural systems initial injury: Intercellular level
- 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
CNS Response to Injury: Mechanisms of Recovery
Unmasking silent synapses
Regenerative synaptogenesis/Neural regeneration
Reactive synaptogenesis/Collateral Sprouting
Unmasking silent synapses
Structural synapses that are present but have not contributes to function pre-injury (silent) may be unmasked
Regenerative Synaptogenesis/Neural Regeneration
Injured axons begin sprouting to reestablish synaptic connections
Reactive Synaptogenesis/Collateral Sprouting
Adjacent ( uninjured) axons sprout to innervate synaptic sites that were previously activated by axons that are injured
NEURAL SYSTEM RESPONSE TO INJURY: NEURONAL REGENERATION
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
RECOVERY OF FUNCTION:
STRUCTURAL LEVEL – CORTICAL REORGANIZATION
- 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