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  • Hysiology OF Nerve Conduction

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    Muhammad Huzaifah Jusoh
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    The document discusses the physiology of nerve conduction and the molecular basis of pain. It describes how [1] local anesthesia interrupts the pathway that carries sensory information from the periphery to the central nervous system, achieving pain control. It then covers [2] the anatomy of nerves including the myelin sheath and nodes of Ranvier that allow saltatory conduction. Finally, it discusses [3] how various molecules and ions released during inflammation, such as cytokines, histamine, and prostaglandins, lead to pain sensation at the cellular level by stimulating nerve activity and lowering pain thresholds.

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    The document discusses the physiology of nerve conduction and the molecular basis of pain. It describes how [1] local anesthesia interrupts the pathway that carries sensory information from the periphery to the central nervous system, achieving pain control. It then covers [2] the anatomy of nerves including the myelin sheath and nodes of Ranvier that allow saltatory conduction. Finally, it discusses [3] how various molecules and ions released during inflammation, such as cytokines, histamine, and prostaglandins, lead to pain sensation at the cellular level by stimulating nerve activity and lowering pain thresholds.

    Copyright:

    Attribution Non-Commercial (BY-NC)
    Download as PPTX, PDF, TXT or read online from Scribd
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    15 views16 pages

    Hysiology OF Nerve Conduction

    Uploaded by

    Muhammad Huzaifah Jusoh
    The document discusses the physiology of nerve conduction and the molecular basis of pain. It describes how [1] local anesthesia interrupts the pathway that carries sensory information from the periphery to the central nervous system, achieving pain control. It then covers [2] the anatomy of nerves including the myelin sheath and nodes of Ranvier that allow saltatory conduction. Finally, it discusses [3] how various molecules and ions released during inflammation, such as cytokines, histamine, and prostaglandins, lead to pain sensation at the cellular level by stimulating nerve activity and lowering pain thresholds.

    Copyright:

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    Download as PPTX, PDF, TXT or read online from Scribd
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    of 16

    PHYSIOLOGY OF NERVE CONDUCTION

    LOCAL ANASTHESIA
    Has been introduced to the clinical world for more than 100 years. Simple & predictable (GA vs LA) Corner stone in dentistry Normal people (not dentists) usually tend to judge dentists according to the local anesthesia.

    PAIN CONTROL
    1. Removing the stimulus
    2. Interrupt pathway that carry information of the stimulus from periphery CNS

    Stimulus = instrumentation during dental tt By definition, cant be stopped

    Achived by application of LA to the sensory nv supplying the area of stimulation

    A.

    LOCAL NERVE CONDUCTION

    Physiology & pathophysiology of pain

    CNS

    1. Motor (CNS periphery/skeletal muscle)

    2. Sensory (Stimulus at periphery CNS) 3. Proprioception (the reception of stimuli produced within the organism)

    NERVE ANATOMY

    Myelin sheath

    Insulates nerve Prevents current flow

    Nerve (axon) Nodes of Ranvier (myelin sheath gap/esposed nerve)

    Occurs at regular intervals between segments of myelin sheath along a nv axon Unmyelinated Allow rapid passage of excitatory impulse along the nerve, effectively jumping from one node to another (saltatory conduction)

    CONT.

    Propagation of an A-P

    Passage of information as an impulse

    Synapse
    Junction between one nerve & another Coordinate nervous activity Ensure unidirectional flow of A-P

    Saltatory conduction: the propagation of action potentials along myelinated axons from one node of Ranvier to the next node, increasing the conduction velocity of action potentials.

    Basis of A-P: Balance of ions Resting membrane potential (-70 mV)

    ELECTROGENIC PUMP

    Results in a distribution of ions that produces a membrane potentioal = 70mV

    1. DIAMETERS OF NERVE FIBERS

    2. ION CHANNEL

    Voltage gated

    Chemical gated

    3. PASSAGE OF AN ACTION-POTENTIAL
    b.

    Rest (-70mV): Na/K ATPase

    Change reaches -55 mV (threshold) Na-gated channel permits Na influx

    Reaches +30mV K-gated channel open permits K outflow

    a.

    Stimulus
    Eg: trauma inflammation

    Minimal change Na-K ATPase restore to resting value

    Cant reach +60mV (eq potential of Na): 1. short-lived 2. reversed electrcal gradient 3. K-gated is open

    Ionic imbalances/change
    Inflammation K & H release acidic

    Membrane potential alteration

    B. MOLECULAR BASIS OF PAIN

    PAIN SENSATION AT CELLULAR LEVEL


    Trauma 1. Physical 2. Thermal 3. Chemical Infection

    Histamine & serotonin (5-hydroxyIonic imbalances (K & H) Tissue Cytokines (IL & GF) Cytokines (IL, GF) damage tryptamine) [] pain P Substance PG & related metabolites - lymphocyte, MO, osteoblast Mast cell Histamine & seratonin K: - NTM - PGE: pain & inflammation - lysis Direct / cells indirect Potent vasoactive of - Vasodilatation & amine - LKB4 ~ PG (WHY??) Ionic imbalances (H & K) Stimulate PG production pruritus (itch; mild irritating - lysosomal Nerve hyperexcitability activation - [] AA metabolites Localized pain @ pain) Immobility - Lowering threshold inflammation Substance P
    PG & metabolites

    MOLECULES & IONS IN INFLAMMATORY PROCESS


    Cytokines (IL, GF) - lymphocyte, MO, osteoblast - Direct / indirect - Stimulate PG production
    Ionic imbalances (K & H) - [] pain - K: - lysis of cells (WHY??) - Nerve hyperexcitability - Lowering threshold

    Histamine & serotonin (5-hydroxy-tryptamine) - Mast cell - Potent vasoactive amine - [] pruritus (itch; mild irritating pain @ pain)

    Substance P - NTM - Vasodilatation & lysosomal activation

    PG & related metabolites - PGE: pain & inflammation - LKB4 ~ PG - AA metabolites

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