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Midterm

Kin 242 Midterm Notes.docx

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Department
Kinesiology
Course
KIN 242
Professor
Mc Illroy
Semester
Fall

Description
Kin 242 Midterm Notes: Lecture 2: Cells of the Nervous System: - Neurons - Neuroglia Disease or disorder results from damage to neurons and/or glia Neurons: cells responsible for signal transmission (receive, conduct, and send signals) Parts of the Neuron Dendrites: - Receives signal from another cell Axon: - Conducts signal toward synapse Synapse: - Sends signal to another cell - Neurotransmitters serve as chemical messenger Neuroglia – glue - Provide support, insulation, nutrition, control, homeostasis, form myelin for neurons, remove pathogens - Synaptogenesis and plasticity Nervous System: CNS: - Spinal cord, brainstem, cortex - Within skeletal casing – skull, spinal column - Cortex, centers, nuclei – cell bodies – gray matter - Tracts, columns – axons – white matter PNS: - Nerves and ganglia - Outside skeletal casing o Made up of: somatic NS, ANS, enteric NS - Ganglia – cell bodies – gray matter - Nerves – axons – white matter Spinal Cord: - Fibre tracts (ascending/descending) - Entry and exit zones to/from PNS - Pools of interneurons Brain Stem: - Fibre tracts (ascending/descending) pathway passing up and down peripheral nerves//spinal cord to supraspinal regions o Nuclei involved in homeostasis (regulation) - Many important nuclei (integration region) - Cranial nerves (entry/exit) Cerebellum: - Connects to cortex via brain stem - Highly organized region with inputs and outputs through the brain stem - Important to communication to cerebral cortex - Important in control of movement, learning and non-motor activities Basal Ganglia: - Groups of nuclei connected to cortex, thalamus and brain stem o Putamen, caudate, globus pallidus, subthalamic nucleus, substanti nigra - Important in contribution to control of movement, learning, cognition and emotions Cerebral Cortex: - Important in control of voluntary behavior - Extensive connection to and from other CNS regions Motor Neurons: Lower MN: - Cell body located in the spinal cord or brainstem - Sends out axon that directly innervates skeletal muscle fibres Upper MN: - Cell body of neuron located in the cortex (M1, premotor, S1) - Axon travels via the CST and synapses on the lower MN Disruption to control of movement is dependent on the specific region that is damaged or injured Lecture 3: Healthy movement: successful, smooth, efficient, safe, adaptable Sensory inputs: - Extrinsic information about world - Intrinsic information about body Processing – sensorimotor transformation Motor output – interaction with world **Sensory input, process it and then we form the appropriate output Feedback important in making adjustments Planning (inverse) and prediction (forward): CNS can access these models in the absence of actual sensory input or motor output Feedback – adjust ongoing movement to correct for errors, not always good for rapid movements due to delays Feed forward – does not adjust movement based on feedback, good for rapid movements but no way to correct for errors Movement combination of two systems Designed to Walk: - Phylogenic adaptions of lower limbs, trunk, and neck are designed to optimize walking - Examples: o Brain stem – initiation, speed control o Cerebellum – regulates timing and intensity of descending signals o Motor cortex – incorporates vision What makes it so complex? - Progression – mobility at base of support critical for freedom to fall forward (heel, ankle and forefoot rockers) o Need mobility and ability to control rate of dorsiflexion/plantar flexion - Shock absorption – transfer of body weight features high loads and high accelerations o Impact reduced by shock absorption (eccentric contractions) - Energy conversion – efficiency, balance between other functions (pendulum gait is characterized by large vertical excursions) o Two mechanisms to minimize energy expended:  Minimize COM movement – pelvic tilt reduces vertical excursion of COM, pelvic rotation increases effective leg length, narrow step width and limited lateral COM motion  Selective muscle activation – passive posturing, generated momentum - Efficiency – forces to oppose gravitational forces applied to body (I.e. active muscle force and/or passive force) - Stability – continual adjustments of forces applied at the foot Voluntary Upper Limb Control – voluntary movement expression of additional input “goal” – damage done is VERY specific - Corticospinal pathway – PMC to lower MN – carries out motor commands - Medial and lateral pathways – many subcortical areas to lower MN – modify excitability of MN - Basal ganglia and cerebellum – coordination and feedback control Upper limb control – multi-joint behaviors – reach, grasp, object manipulation - Task specificity Reach – tight inter-joint coupling (control direction, extent, and timing) Grasp – complex multi-joint coupling (control aperture, hand orientation and timing) *Determined by sensory information about the surrounding environment Object Manipulation – complex coordination patterns of individual finger muscles (role for muscle spindle, GTO’s, joint receptors, cutaneous muscle receptors) Postural Adjustment: - CNS constantly performs adjustments to maintain desired posture in face of unexpected of expected movement o Anticipatory – expected o Automatic – unexpected - Focal movements (I.e. clear movements) require companion control of postural muscles Lecture 4: Research Tools – used to understand mechanisms or in development of new clinical tool Clinical Tools – diagnosis/injury Microneurography (needle into peripheral nerve): - Measurement of electrical potentials (arising from AP) from axons within the nerves - Can measure activity of sensory and/or motor cells – responses may represent individual or multiple cell activity - Hard to get individual cell activity Electromyography (diagnosing peripheral nerve disorders): - Study of muscle electrical signals from muscles – measures the electrical signals generated by muscles - Intramuscular EMG – measured from needle sampling few muscle fibres (MUAP) o Pathology: contraction stops but the nerve continues to fire o Measures a few fibres in the unit - Surface EMG – electrical signals measured from over skin (Summed action potentials from population of muscle fibres (CMAP)) o Placed over the muscle belly – all of the muscle fibres in the unit o Problem: cross talk o Used in research for movement disorders – noise when contraction is falling EEG: Epileptic seizures – cannot pinpoint where activity is happening - Electrical field potentials that are produced by electrical currents in the brain and measured with electrodes adhered to the scalp - Clinical/research purposes: localize function, identify specific wave forms and their modulation - Precise temporal information - Measuring EEG activity in response to specific stimuli or events (ERP’s) o Averaging of trials to see response o When increased frequency and increased amp there is a problem (amp and freq should always be opposite) MEG: - Magnetic field produced by intracellular electrical activity in the brain measured with extremely powerful amplifiers (SQUID) - Clinical and research purposes: localize pathology for research purposes, localize areas of specific function, determine function of brain areas o Electrical currents in the brain produce orthogonal magnetic field – detected by sensors - Precise temporal information and moderate spatial resolution MRI: - Noninvasive measurement of body structure/tissues – based on ability to measure energy released from protons - Static magnetic field aligns H molecules – energy from RF pulse pushes hydrogen out of alignment – when pulse stops H oscillates them back into alignment and the energy from oscillation is measured by the scanner - Detect tissue properties DTI: - MRI method mapping the diffusion process of molecules (water) in biological tissues o Reveal microscopic details about tissue architecture (normal/diseased) fMRI: - Measures brain activity by detecting associated changes in blood flow - Cerebral flood flow and neuronal activity are coupled – when an area of the brain is in use blood flow to that region also increases Lecture 5: Stimulation techniques: to evoke a controlled input to the CNS Electrical Stimulation: - application of electrical stimulus can evoke action potential in neurons or motor unit potentials in muscles o Muscle:  FES and/or TENS o Periphery (PNS/muscle):  PES - Implantable electrodes also used to stimulate CNS or PNS areas Transcranial Electrical Stimulation (TES): - Direction of current flow - Electrical field is parallel and radial to scalp - Stimulation of surface and deeply located axons - Electrical field strongest between anode & cathode Transcranial Direct Current Stimulation: - Neurostimulation that uses constant, low current delivered directly to the brain area of interest via small electrodes - Developed to help patients with brain injuries (I.e. strokes) - Can increase cognitive performance in variety of tasks (healthy people) Transcranial Magnetic Stimulation: - Direction of current flow - Electrical field is parallel to scalp - Stimulation of superficial axons – hyperpolarize/depolarize Stimulus Response Testing: Coupling specific inputs and measuring specific outputs can reveal status of CNS Nerve Conduction Testing (used for weakness, numbing): - Evaluate the function – electrical conduction of the motor and sensory nerves Reflex Testing: - Following electrical stimulation of the nerve different waveforms in the EMG can be recorded - H wave - M wave - F wave - Long latency reflex Pathology: absent, reduced or exaggerated H reflex or LLRII Motor Threshold Testing: - Stimulation: TMS to stimulate Corticospinal fibres - Measurement: EMG from specific muscles Lecture 6: Movement Disorders Conditions of neurological origin that affect the ability to produce and control movement (Abnormal movements are symptoms of underlying disorders) Hypokinesia Slow, diminished movement Akinesia Inability to initiate movements Bradykinesia Abnormal slowness of movement Hyperkinesia Exaggerated or increase in movement Dyskinesia Difficulty in controlling movement, abnormal movement Chorea Brief, irregular contractions (Huntington’s) Athetosis Writhing/wringing movements Tics Sudden, repetitive, non-rhythmic, stereotyped movement Hypotonia Decreased muscle tone (amount of resistance to movement in a muscle) – not the same as weakness Hypertonia Abnormal increase in muscle tension and a reduced ability to be stretched Dystonia (EMG gives most valuable info in clinical Sustained contractions causing twisting, repetitive diagnosis – simultaneous co-contraction) movements or abnormal postures – single muscle or group of muscles Spasticity Excessive muscle tone Clonus Series of involuntary contractions due to sudden stretching of the muscle Hyperreflexia Exaggerated reflexes Contractures Permanent shortening of muscle/tendon associated with tone Ataxia Movements characterized by lack of coordination Apraxia Inability to carry out or execute learned movements (not explained by a loss of sensation, coordination or weakness) Plegia Paralysis Hemiplegia Paralysis of one side of body Paraplegia Paralysis of lower limbs Quadriplegia Paralysis of all limbs Paresis Weakness Hemiparesis Weakness on one side of body Myopathy Neuromuscular disorders in which the primary symptom is muscle weakness due to dysfunction of muscle fibre Neuropathy Damage to the peripheral nervous system – sensory, motor and or autonomic fibres Parathesia Sensation of tingling, pricking, or numbness Transiet Pins and needles Chronic Associated with neurological disorder Lecture 7: Peripheral Neuropathy: - Result of damage to the peripheral nervous system - Damage to myelin/axon - Result of disease, trauma, illness Classification: Mononeuropathy – one nerve (small laceration – I.e. Carpal Tunnel) Polyneuropathy – multiple nerves, more symmetrical (I.e. Diabetes) Mononeuritis Multiplex – asynchronies (not symmetrical) Autonomic Neuropathy – non sensory Neuritis – inflammation of a nerve Causes: Genetic – Charcot-Marie-Tooth disease Infection/autoimmune – HIV, Lyme disease Mechanical – trauma, stress Metabolic/endocrine – diabetic neuropathy Signs and Symptoms – depends on the nerve affected Sensory Nerves (loss of sensation): - Pins and needles, burning, numbness Motor Nerves (loss of function): - Tremor, weakness, tiredness Autonomic Nerves (involuntary, cant control): - BP, HR, digestion Diabetic Neuropathy: - 60-70% of all diabetics may have some degree of neuropathy - Neuropathy implicated in 75% of amputations *High levels of glucose toxic to a system – vasoconstriction decreases O2 transport to cell – breakdown myelin and affect nerve function Symptoms: - Can affect all peripheral nerves, symptoms vary depending on nerves affected and develop gradually - Sensory: o Retain a lot of fluid o Numbness/tingling of extremeties o Abnormal sensation (dyesthesia) o Longer fibres affected to a greater degree so symptoms can occur first in the toes o Loss of proprioception - Motor: o Focal weakness o Facial, mouth and eyelid drooping o Muscle contractions - Autonomic: o Dysphasia – swallowing difficulty o Bladder problems o Regulating body temp o Sexual function Carpal Tunnel Syndrome: - 10% of adults - More common in women than men (30-60) Causes: - Idiopathic - Repetitive movements - Congenital (size of carpal tunnel) - Stress, trauma, pregnancy Symptoms: - Parathesia, numbness and pain along median nerve distribution - Unilateral/bilateral - Pain at night - Muscle weakness in thumb abduction and opposition - Hand stiffens, muscle weakness Radiculopathy (myotome – NR muscle, dermatome – skin): - Compressed nerve spine (nerve root) – as it exits the spine - Compression/irritation of nerves lead to neuropathy - Cervical and lumbar most common – not as mobile through thoracic *Often posterior/lateral off to one side Causes: - Disc herniation - Bone spur - Tumour/infection - Scoliosis - Diabetes - Trauma Symptoms: - Result in pain, weakness, numbness or difficulty controlling specific muscles - Problem at/near root however pain/symptoms may refer anywhere alone nerve distribution *Myotome dance Lecture 8: Structure of Peripheral Nerves: Endoneurium – small amount of collagen that is present between individual axons Perineurium – sheath of special, fibre like cells that ties the axons of each fascicles together Epineurium – connective tissue that surround entire nerve trunk – separate fascicles from one another Axonal Transport: - Proteins synthesized in cell body need to be moved to terminal ends – axonal transport - Fast (anterograde and retrograde) - Slow (anterograde) SEDDON: Neuropraxia: - Mild, reversible failure of propagation of AP (impaired conduction) - Cell body remains in contuity with end organ - Normal conduction on other side of focal injury - Longevity: couple of hours – temporary compression Axonotmesis: - Axonal and myelin sheath damage Wallerian Degeneration: The disintegration - Loss of continuity with cell body and end organ - All parts of nerve preserved of the axon and then myelin sheath (12-48 hrs - Wallerian degeneration occurs after injury). Myelin retracts away from the - Can observe atrophy of end organs node – disarranged and fragmented. (48-72 hrs after) axon breaks into twisted fragments - Take longer to repair (1-3mm/day) – scwaan cells and macrophages clear tubes Neurotmesis: - Greatest degree of nerve injury - Complete disruption of axon and connective tissue - Poor prognosis – surgical intervention - DOUBLE CRUSH SYNDROME o Impaired axonal transport damage may predispose distal segments to increased risk - Proximally and distally damaged Sunderland: st 1 Degree – Bruise, small stretch and good outcomes 2 Degree – disruption of myelin – scwaan cells – good prognosis if no damage to endoneureum 3 Degree – damage to axon – myelin – scwaan – not good outcome due to not as much structure to help cells grow 4 Degree – damage to all of the above and perineureum – may recover but harder for a nerve to rthenerate 5 Degree – disruption of everything – little hope of recovery – surgery Demyelination - Never does not conduct impulses well – decrease events - Few Na+ channels in contrast - Decrease chance of action potentials End Organ Denervation Changes - Peripheral end organs need innervation to survive - After
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