Psycho_Motor_Learning_Notes.docx

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Department
Kinesiology
Course Code
Kinesiology 1080A/B
Professor
Matthew Heath

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Psycho-Motor Learning Topic #1 Plasticity  it is the ability to acquire & learn new skills within the Central Nervous System (CNS)  New neural connections are being formed; motor neurons are running down the axons (repetition)  This plasticity slowly deteriorates as the person gets older and it affects the person’s ability to acquire & learn new skills How does an individual reacquire skills if injured (head injury)? Optogenetics  A technique used in behavourial neuroscience, combination of techniques (optics & genetics), to control the activity of individual neurons in the living tissue (light to activate nerves) Skeletal Muscle  Extrafusal Muscle Fibers  Power producing muscle fibers  They run in parallel dimensions  Intrafusal Muscle Fibers  Kinesthetic sense  They are design to detect stretch  These fibers are important because they tell the Central Nervous System the location of the limb in perspective to the rest of the body  Peripheral Neuropathy  It is a disease to not feel the stretch Motor Learning and Control Defined 1) Motor Learning  A set of internal processes associated with practice or experience leading to relatively permanent gain in performance capability  This is a learning effect that coaches a primary tactic, while the performance effect is temporary (Learning benefit vs. Performance Effect)  Learning benefit (permanent change) 2) Motor Control  An area of study dealing with the understanding of the neural, physical, and behavioural aspect of movement  It is how the brain develops a motor program and how that information is transferred from the brain to the extrafusal muscle fibers Psychology  Our ability to learn movements and learn cognitive is totally different  Perception, Cognition & Action 1) The brain is a computer: serial nature of information 2) Memory for different tasks: motor tasks vs. cognitive tasks  In our brain, the information needs to be first processed and only then the new information can be taken in afterwards  Shiffrin  He was interested in how we learn and store information  Particularly interested in how our short term memory system affects our learning system (The processing of short term information)  He was also interested in symantic information (factual, cognitive), which led to the acquiring of new movements Human Engineering 1) Arthur Melton - Pilots can be selected based on specific individual abilities - Disproven 2) Paul Fitts - Too many air plane accidents the result of faulty human/machine interface - There was incompatible spatial mapping in the cockpit of the airplanes  They had to redesign the cockpit (make it direct spatial mapping) - He is the forefather of the field of ergonomics - He layed the ground work for machine and person interaction - How we process information influences our interactions with machines and computers  Developing our motor control Neuroscience: Reciprocal Innervation (reciprocal inhibition)  First understood by C.S. Sherrington  Suppresses activity of an antagonist muscle when agonist muscle is active  These inactive and active muscles work together (reciprocal inhibition)  This explains the phenomenon such as walking and reaching  Final common path at the spinal cord produces the muscular contraction  However, if you have co-contraction, contraction of both antagonist and agonist, the muscle will not be able to move because both of those muscles are contracting at the same time Physical Education - Franklin M. Henry  He examined the whole body movements and developed experimental approaches to understanding how we ‘learn’ to produce complex movements  He examined gross body movements  whole body movements (techniques)  complex movements - MRI of the brain  used for theoretical research  Left is right, right is left  Relating movement impair with damaged cortical structures The Nervous System Topic #2 Division of Nervous System - Two division: Central Nervous System (CNS) and Peripheral Nervous System (PNS) - CNS consists of the brain and the spinal cord and it is the branch of the nervous system - The PNS consists of the Autonomic division and Somatic division - Autonomic division  regulates the internal environment and it carries information from the CNS to organs, blood, vessels and glands - The autonomic division also has sympathetic and parasympathetic branches - Sympathetic - arouses the body - Parasympathetic - calms the body after arousal - Somatic division  It carries the information to the CNS from the senses and from the CNS to the skeletal muscles - This division uses the intrafusal muscle fibers (muscle stretch and sense); this will allow for connectivity with the central nervous system (The intrafusal muscle fibers make the connections with the CNS – this allows us to connect with neurons, interneurons and the spinal cord) Hierarchy Organization of the CNS  Think of the Cerebral Cortext as the ‘big boss’ as it tells everyone else what to do and when to do it  Cerebral cortex  most advanced component of the central nervous system (billion neurons)  Lesions to the this cortext (from a stroke) can affect fine digit control and allow the person to only have a power grip  it affects the person’s ability to live independently  Think of the thalamus, basal ganglia, pons, and cerebellum as being second in command  Anything below this cerebral cortex is known as sub-cortical structures  These sub-cortical structures are mainly known for modifying the information sent from the cerebral cortext (change in signals)  The brainstem is third in command  This is simply a relay station, where all information goes through here (original and modified info goes through here in order to reach the spinal cord)  It plays no role in modifying the information signals  The spinal cord is a ‘slave’ system to all of the above  Common pathway  No role in modification Locked in Syndrome - Very limited ways to talk with others  this is due to the damage to their brain and cannot access the spinal cord (problem in the brainstem) - The signals are unable to go to the spinal cord (unable to respond to the stimuli) - Example: a patient was able to blink, so letters are presented and the patients would blink to respond to stimuli Luigi Galvani - Interested in how muscles contract - The contemporary thought was fluid movement – WRONG - He was also interested in static electricity and the electric rod caused the frog body to twitch - Hence he concluded that for our muscles to have the ability to move is related to bio-electrical energy -> transmit signals Neuron – Building Block of the CNS - Learning a new skill  Developing new neurons (young children) - But in older individuals, we are laying down new neural pathways - The more we use the neural pathways (repeated exposure to the task), the better they are going to be able to communicate with each other (increase dendritic arborization)  The efficiency increases, more connections - Developing more dentritic (axomal) branches – spread out and touch more neurons; by doing this, we are able to acquire new motor skills  There is myelin sheath on the neuron  allows for efficient axomal transmission  Heavy sheath:  Faster convey of information  Rapid conduction of impulses  90m/s Neurons and the Neuromuscular System - Motor Unit: A single alpha motor neuron connected to extrafusal muscle fibers (power producing) - It innervates 3 muscle fibers - Alpha motor neuron = extrafusal muscle fibers - There can be a direct communication between this neuron and the neuron in the primary motor cortex (neuron on the cerebral cortex) - Damage to the alpha motor neuron is known as an alpha motor neuron disease, also referred to as a lower motor neuron disease - Upper motor neuron disease  damage to neurons in the cerebral cortex Speed of Nerve Conduction  Helmhotz (1850s)  He was interested in the speed of nerve conduction  Used isolated muscle and motor nerve of a frog (CNS – alpha motor neurons)  He stimulated these neurons and see how long it would take for the muscles to twitch  Measured time between the electrical stimulation and the muscle contraction  He would stimulate the cell body of the alpha motor neuron and see how long it would take for the muscle to twitch  He would also put the stimulus at different locations and then measured how long it took for the muscles to contract from different locations  Close to the cell body, away from the cell body (electrical stimulus to two points)  Nerve conduction velocity very fast (35-60m/s)  Diseases of the nerve 1) Disease of the nerve influences the amplitude of the nerve conduction (fidality of the signal) e.g. quality of the radio signal diminishing as you move farther away from the city  Amyotrophic Lateral Sclerosis (ALS) or more commonly referred to as Lou Gehrig’s disease  alpha motor neurons become less and less effective in depolarization 2) Disease of the myelin influences conduction speed  Scarring on the axon  Difficulty transferring information from axon to muscle fibers  Mutiple Sclerosis (MS)  It destroys the myelin in patches along the central nervous system  The white areas (right scan) indicate multiple cortical lesions  areas without myelin (demyelination)  MS has a systematic impact on CNS around the cerebral cortex Different Types of Neurons 1) Motor Neurons (Efferent)  Transmit motor commands down the spinal cord 2) Sensory Neurons (Afferent)  Transmit signals to and up the spinal cord Phrenology and Modern Neuroscience - It was suggested that there were different parts of your brain for things like courage, hope, love, etc… - Modern Neuroscience – FMRI and MRI - Thinking of initiating a motor task, and a part of the brain activates (lights up on the FMRI scan) - MRI – structure, FMRI – structure & function - MRI  used clinically - FMRI  Used clinically and experimentally Cortical Structures  Occipital Lobe: visual cortex  Contains primary and secondary visual areas  Primary Visual Cortex – V1 (spatial frequency & orientation, maybe even colour of the object)  V1 – most visual inputs from our eyes end up in this area  It processes the elementary information coming into the cortex  Demonstrates cortical magnification  Cortical magnification is where there are more neurons in V1 (central vision), which explains why we cannot read with our peripheral vision (there aren’t enough neurons in our peripheral vision)  There is uneven distribution of neurons on our eyes which leads to high spatial resolution in the central vision  Lesions to the primary visual cortex lead to cortical blindness  Individuals are unable to see the visual stimuli (images)  They have no conscious awareness that they are looking at an object  They cannot see objects but can use vision to navigate  Nothing wrong with their eyes, but high level processing of visual information takes in their damaged V1, hence they cannot see the object  These individuals cannot use vision to see or identify objects but they can use vision to move (navigate through environment)  Dissociation in how we use vision for perception activities (identifying objects) and using vision for action  navigate through environment  Blindsight: the individual isn’t aware that his brain could process visual information on both sides even though he wasn’t aware of it  V1, V2, V3 & V4 are damaged and they are unable to see consciously see things, but can grasp things in front of them even though they have no idea what that object is or how it looks like  V2 – Responsible for binocular vision  Its class of cells (binocular disparity neurons)  Specialized neurons which allows us to generate a 3-D image in our mind  It allows us to perceive depth  David Hubel  He investigated the origins of binocular disparity cells  Single cell recording of V1 in the awake cat  Binocular cells in V1  He patched one eye on cats and when taking it off after 6 weeks, he compared the vision from one eye to vision from 2 eyes  He noticed that by patching the eye, binocular disparity neurons never develop (cannot see depth  stereo vision)  Hence at early stages of development, it is very critical for these neurons to develop  During the experiment, 2 different classes of neurons were discovered in the primary visual cortex  Blobs and Interblobs  Blobs  Specialized cells in V1 for colour and determining whether or not something is in cylindrical shape  Interblobs  Orientation sensitive (Determines orientation of an object)  Infants born is lazy eye, ophthalmologists used to patch the good eye and force the infants to see with the lazy, but if this is done too early on, this would prevent the development of binocular disparity neurons  V3 – has two areas  V3 &dV3 v  Visual information that passes through V3 ordginates from V1, which then goes to the parietal cortex (V1  V3 d Parietal Cortex) This pathway is important because it supports the vision for action (Ex. Taking notes in class)  Visual information that passes through V3 alvo originates from V1, but this pathway goes to the temporal lobe (V1  V3  vemporal Lobe) This visual pathway is for perception  the ability to make judgment on different colours  V4 – works in junction with V1  Involved with more sophisticated processes; orientation or the size properties of an object  Identification of simple geometric shapes  Lesions of this V4 would make that individual confuse their shapes; mistake a triangle for a square, etc  V5 – Movement  It uses visual information to detect movement (self-motion or motion within the environment)  Critical motion detecting motion (area MT)  Parietal Lobe: Contains Primary Somatosensory Cortex (S1) - It is responsible for the planning and control of movement - Visuo-spatial processing skills  It can serve as an interface between sensory and motor command  Inferior Parietal Lobe (IPL)  Critical for planning a movement  Lesions here would lead to difficulty in initiating movement  Superior Parietal Lobe (IPL)  Control of action (Online or feedback of the action)  This is during the action (feedback) to make corrections while making the movement; feedback from the environment to make corrections for a successful movement  Lesions here would lead to difficulty with feedback (mistakes)  Visual Spatial Neglect  Happens to individuals with lesions right hemisphere of the parietal lobe  It is a high level disorder because these individuals have difficulty with making a single image from the entire scene; they don’t have any issues processes, but they have difficulty attending  People with lesions to the right side of the parietal lobe neglect the left side (left visual field  They do not attend their impaired visual field) And this would be vice versa if lesions to the left side of the parietal lobe due to crossed visual pathways  These people can see the visuals on that side, but they are simply not attending to it  Prism Goggles  they shift visions to the unattended visual field; these only last a couple of hours (transient)  Anterior Inter-Parietal (AIP)  Provides our movement system with critical information to support grasping  Lesions here would make individuals have difficulty with grasping  Parietal Occipital (PO)  It controls the transport of the limb to the object; transport phase of movement  Lesions here would make individual have difficulty with transportation of limb during a movement  Temporal Lobe: Functions in visual object recognition - Controlling movement and speech production - Contains primary auditory cortex - It is the location of hippocampus (memory & learning) - Haptic information which is essentially touch information is retained in the temporal lobe - Visual information is mediated within the temporal lobe  Lateralize function  comprehend speech on the left side of the brain (left cerebral hemisphere primary auditory cortex)  Hippocampus (subcortical structure)  Temporal Lobe is not the location of the hippocampus but the temporal lobe has lots of connections with the hippocampus  It plays a very important role in formation of new explicit memories  Explicit memory is cognitive/factual information (test, exam information)  Lesions to or removal of the hippocampus would result in loss of ability to formulate new long term memories  However, these patients would still be able to acquire new motor skills (movements) because that is controlled by the cerebellum  Frontal Lobe: Functions in working memory - Contains primary & secondary motor areas - Labatomy  It is who we are  it maintains our personality; self-awareness  Finius Cage  railway worker; rod went through his brain  He survived, but he had a striking change in his personality  M1 – Primary Motor Cortex  it known to the final common pathway to action  It will send signals to the spinal cord allowing us to move  SMA – Supplementary Motor Area (Secondary Motor Area)  PM – Pre-motor Area (Secondary Motor Area) Sub-cortical Structures  Brain Stem: Plays a role in basic attention arousal and consciousness - All the information to and from our body passes through the brainstem on the way to or from the brain - Regulates autonomic processes  Heart rate/Respiration  Debunks one critical component of the classic view of the organization of the central nervous system (Hierarchy)  There are actually structures on the brain stem that in and of themselves can control functional movements  Superior Colleculus  It is responsible for making saccades  They are goal-directed eye movements (voluntarily)  This is an exception to the hierarchical system of the brain function (CNS)  Cerebellum: Important in learning and producing movement - Involved in the coordination of voluntary motor movement, balance, equilibrium and muscle tone - Involved in formulating implicit memories (motor memories)  These motor skills are retained in the cerebellum - Minor hemisphere  Head injury causing the damage of the cerebellum will cause the person to lose his ability to acquire new motor skills (long term implicit memories)  If damaged, you lose previously acquired motor skills (riding a bike)  Lesions to the Cerebellum  Cerebellar Attaxia: Leads to the deficit cerebellar gate; it is a movement defecit  Cerebellum is involved with the timing of movement  The timing of firing different neurons to different muscles (CNS)  Cerebellum can be the clock that measures the timing of a movement  Soft Deficit  stuttering individuals have a soft deficit in their cerebellum causing a difficulty with the timing due to cerebellum lesions  Basal Ganglia: They are a bundle of neurons connected to numerous subcortical structures; it is a subcortical structure - Group of varied origin nuclei connected to the thalamus and cerebral cortex - Plays an important role in the excitation of the primary motor cortex; Basal Ganglia causes the PMC to be active  leading to movement - The basal ganglia receives and sends many connections to the cerebral cortex (frontal lobe of the cerebral cortex)  Parkinson’s Disease: it is a neuro-disorder (effecting the basal ganglia) which makes it difficult to initiate movement; In these individuals, the basal ganglia does not allow for the activation of the primary motor cortex  With parkinson’s disease, you can have damage to any one of the below structures  Parkinson’s disease causes tremors but with medicine, the movement is slowed considerably - The nuclei that comprises the basal ganglia are:  Striatum: it receives information from cortex and then sends it to only the other nuclei of basal ganglia  Globus Pallidus (GPe): It receives input from thalamus and then sends out inhibitory output to movement related centers  Substantia Nigra: Responsible for producing dopamine and it is critical neurotransmitter that is lost as a result of Parkinson’s disease; it is a source of dopamine  Subthalamic Nuclei: It is critical for producing primary excitatory neurotransmitters in the brain (Glutamate) Direct Pathway: Has both inhibitory and excitatory input (blue & red)  Cortex sends excitatory input to the striatum  After the striatum becomes active, it sends inhibitory input to the Substantia Nigra and GPe  Then the Substantia Nigra and GPe send inhibitory input to the thalamus (inhibiting the thalamus)  The inhibition of the thalamus leads to the excitation (excitatory input) of the motor areas on the cortex  Hence the direct pathway is the combination of both inhibitory and excitatory control that activate the excitatory neurons in the cortex - People with Parkinson’s disease have an inhibitory cortex
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