Pathophysiological Basis of Motor Control (plasticity) (unit 1)

what is neural plasticity

- is the ability to show modification

- is neural modification

> occurs on a continuum

> short term changes: efficiency or strength of synaptic connections

> long term changes: structural changes in the organization and numbers of connections among neurons

learning

- acquisition of knowledge or ability

- recall: motor learning is measured via changes in behavior

- is the process by which we acquire knowledge

memory

- the retention and storage of knowledge or ability

- is the product of that process

non - associated learning

- form of implicit learning

- subject learning about properties of a stimulus that is repeated

- can be short term or long term

habituation

- related to a decrease in synaptic activity between sensory neurons and their connections to interneurons or motor neurons

- reduction in the amplitude of synaptic potentials

- can be a reduction in: amount of NT release, number of synapses, reduced receptors on the target neuron

sensitization

- strengthening that response between two neurons

- typically preceded by an intense or noxious stimulus

- may be short or long term

- more complex than habituation

> the action potential is prolonged

short term sensitization

changes in pre-existing proteins

long term sensitization

o: synthesis of new proteins (ie structural changes)

what is classical conditioning

- Learning to predict relationship between stimuli

- timing is the important factor

- An initial weak stimulus (conditioned stimulus) becomes highly effective in producing a response when it becomes associated with another stronger stimuli (unconditioned stimulus)

- Specific stimuli = specific response

- When they converge, facilitation takes place (Timing is critical)

what is operant conditioning

- learning to associate ones behavior with a consequence

- behavioral relationships

- Same mechanisms that involve predictive relationships

- Predict the outcome of specific behaviors

- Same mechanisms

what are physiological basis of associative learning

- Changes are through synaptic efficiency

- Activation of 2 neurons together = protein modification (short-term)

- Long-term association = new synaptic connections

- Mechanisms of classical and operant conditioning are similar

procedural learning

- More complex form of implicit learning with an element of automaticity (Acquisition of skills and habits, Sequence learning)

- Involves both cerebral cortex, cerebellar structures, and the caudate nucleus (basal ganglia)

- Habit, navigating the world, avoiding objects = habitual movement patterns that are learned throughout life

declarative / explicit learning

- Requires a conscious process (i.e., awareness or attention) and results in knowledge that can be expressed consciously.

- Temporal lobe & hippocampus: critical for acquiring long-term declarative memories BUT not part of the memory-storage area

long term potentiation (LTP)

- Basic neuronal electrical properties

- Similar mechanisms as Sensitization as LTP increases presynaptic NT release

- Increases spatial memories, cognition, and improves learning of different locations and space between objects

- has 3 phases:

> short term: 1-3 hours, no protein synthesis but function changes

> long term: at least 24 hours, involves CAMP and structural changes

The Shift to Automaticity

- Fitts and Posner state that the development of motor skills can be characterized as a shift towards automaticity

- Automation: Increased neural resources to become available for additional tasks (Increases the ability to perform a second attention-demanding task simultaneously)

- Pathology: Neurological diseases may alter automaticity, thus increasing the amount of attentional resources required for a task

two time dependent phase

- initial phase: attention demanding

> actively is widely distributed with predominate activity in cortical regions (prefrontal, sensorimotor, parietal)

- later stages of learning

> decrease in primary motor cortex and increase in subcortical motor regions (cerebellar dentate nucleus, thalamus, putamen)

what happens at the individual level when Neural activity associated with the shift to automaticity

- Perception -> summation of sensory information -> meaningful interpretation

- Motor/action -> change in motor cortex activity

Shift to automaticity in older adults

- Older adults can achieve automaticity in both simple and complex learning tasks

- requires:

> More learning (practice) compared to younger adults

> Greater brain activity compared to young adults (for the amount of automaticity)

- Age-dependency and neural plasticity: This is also seen in other fields that elicit neural plasticity

Shift in automaticity in Parkinson's Disease

- Many can perform simple tasks, but are unable to perform complex tasks automatically

- Complex dual-task performance is impaired, even with extended practice

- Greater brain activity during "automatic" movements compared to healthy adults

> The increased activity is thought to compensate for the BG dysfunction

Neural Plasticity and Recovery of Function

- Plasticity occurs at many levels:

> Brain (glial and vascular support)

> Network levels (changes in patterns of neural activation and cortical remapping)

> Intercellular level (changes between neurons at the synaptic level, including synaptic sprouting)

> Intracellular (mitochondrial and ribosomal)

> Biochemical (protein conformation, enzyme mobilization)

> Genetic level (transcription, translation)

direct or restorative

- Resolution of temporary changes and recovery of injured neural tissue itself

> Restitution = achieving functional/goal the SAME WAY as before

- Nearby neural tissue takes over identical function

> Some say restitution, we've identified this as adaptation (see early slides)

indirect / compensatory

Completely different neural circuits enable the recovery of lost or impaired function

short term memory

- working, momentary memory

long term memory

- process of learning

- continumum

- change of synaptic efficiency -> which leads to structural changes