Chapter 3 - Neuroanatomy of Pain Control.pdf
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THE NEUROANATOMY AND NEUROPHYSIOLOGY OF PAIN CONTROL CHAPTER 3 LEARNING OBJECTIVES Explain normal mechanisms of nerve impulse generation and conduction Define resting state, slow depolarization, firing threshold, rapid depolarization, and recovery Explain the significance of the Schwann cell...
THE NEUROANATOMY AND NEUROPHYSIOLOGY OF PAIN CONTROL CHAPTER 3 LEARNING OBJECTIVES Explain normal mechanisms of nerve impulse generation and conduction Define resting state, slow depolarization, firing threshold, rapid depolarization, and recovery Explain the significance of the Schwann cell sheath and nodes of Ranvier on the ability of the LA agents to block nerve impulses Describe the significance between sensory and motor neurons Discuss the different types of nerve fibers related to pain perception Identify the nerve fibers that normally transmit pain sensations from dental and periodontal structures Differentiate between myelinated and unmyelinated nerves Discuss anatomic barriers to the diffusion of LA solutions Describe the location of the dental neural plexus Discuss the action and effects of LA on the neural membranes WHAT ARE WE GOING TO TALK ABOUT? ▪ The anatomy and physiology of nerves prior to administering local anesthetics The mechanisms of the normal generation and conduction of pain signals to the (CNS) The effects of local anesthetic drugs on conduction of pain signals NERVOUS SYSTEM BASED ON FUNCTION Somatic nervous system (SNS) External sensory organs (including skin) Skeletal muscles Gland cells Autonomic nervous system (ANS) Involuntary smooth muscles, cardiac muscle, glandular tissue 2 divisions Sympathetic division Parasympathetic division 6 NEURONS There are two types of neurons in the Somatic Division: Sensory neurons Afferent(sensory) – carry incoming impulses from the body to the CNS for processing Motor neurons Efferent(motor) – carry impulses away from the CNS to effector cells, tissues, and organs The basic structure of these two neuronal types differ significantly Anatomy of Sensory and Motor Neurons sensory motor STRUCTURES OF NEURONS Nerve cell anatomy Nerve axons, cell bodies, and membranes Nerve myelination Saltatory conduction Nerve fiber types Peripheral nerve anatomy Dental neural plexus NEUROANATOMY One of the most important aspect of delivering profound and reliable local anesthesia comes from a solid understanding of neuroanatomy THE NEURON The neuron or nerve cell is the structural unit of the nervous system. It is able to transmit messages between the CNS and the body. ANATOMY OF A NEURON Peripheral nerves - made up of many axons that are bundled, protected, and provided with metabolic support. Axon (nerve fiber) single nerve cell Endoneurium covers each nerve fiber Fasciculi Bundles of 500-1000 nerve fibers Mantle and Core bundles ANATOMY OF A NEURON Perineurium covers fasciculi Perilemma* inner layer of perineurium *the perilemma is the greatest anatomical barrier to diffusion of local anesthetics CORE AND MANTLE BUNDLES Mantle (outer) bundle fibers innervate structures in close proximity to them Core (inner) bundles innervate structures at some distance away Bundles have an impact on the order in which anesthesia develops when exposed to local anesthetic drugs. CORE AND MANTLE BUNDLES & LOCAL ANESTHESIA Mantle Bundles Outermost - receives greatest concentration of local anesthetic drug Innervate most proximal areas - soft tissues, Ex: IA - Mandibular molar area Core Bundles Innermost - receives lesser concentration of drug Innervate distal areas - pulp, Mandibular incisor/canine area Drug Uptake Concentration of uptake decreases from mantle to core bundles THE NEURON – AN EXCITABLE CELL For neurons to carry out the tasks of receiving, processing and sending information they must have specialized structures. Conduct electrical impulses and communicate with other neurons through cellular extensions axons and synapses. They maintain concentration of ions across their membranes. MANTLE AND CORE BUNDLES DISTRIBUTION OF CORE AND MANTLE BUNDLES CORE AND MANTLE BUNDLES Example: inferior alveolar (IA) nerve block ▪ Deposition site near mandibular foramen ▪ Mantle bundle fibers innervate the molar region ▪ Core bundle fibers innervate the anterior mandible including the chin and lips DENTAL HYGIENE CONSIDERATIONS Large nerve trunks are myelinated A fibers Large nerve trunks require more local anesthetic volume to successfully block the core fibers 23 CORE AND MANTLE BUNDLES Significance Molar regions anesthetize earlier and more easily. Lips, chin, and anterior dentition and supporting structures anesthetize later and with more difficulty. Incomplete anesthesia of labial and mental soft tissue after an (IA)injection indicate core bundles are not yet adequately anesthetized. Insufficient volume has diffused. NERVE CONDUCTION The Key Players of Nerve Conduction: Neurons Dendritic zones Axons Cell bodies Terminal arborizations SENSORY NEURONS SENSORY NEURONS ▪ Dendritic zone (Peripheral process) Most distal portion of cell Composed of an arborizations of free nerve endings Nerve endings responds to stimuli in the tissues Contain numerous organelles When stimulated by impulse, release neurotransmitters that convey information along the axon Impulses or signals are initiated by chemical, thermal, mechanical, or electrical stimuli and are processed in the ganglia in the CNS SENSORY NEURONS CONT. Axon – The single nerve fiber, the axon is a long cylinder of axoplasm, encased in a thin connective tissue sheath, the nerve membrane or axolemma (sometimes referred to as the neurolemma.) Contains axoplasm. Distributes incoming (sensory impulses to their appropriate sites with in the CNS for interpretation) Conduct impulse from periphery to the CNS Synapse with nuclei in CNS Smaller than motor SENSORY NEURONS CONT. Cell Body (Soma) Located above the axon (the axon is the main pathway of impulse transmission in this nerve). Not involved in impulse transmission Primary function is to provide metabolic support for the entire neuron MOTOR NEURONS MOTOR NEURONS Dendritic zone Mesial portion of cell Axon branch into endings as a bulbous terminals or synaptic knobs (buttons). Synapse with muscle cells Responds to stimuli MOTOR NEURONS CONT. Axon Contains axoplasm – encased in a thin connective tissue sheath = nerve membrane. Separated from extracellular fluids by the nerve sheath. 70 to 80 angstroms thick (1/10,000 of a micrometer) Some nerves covered by an insulating lipid rich layer of myelin. Conduct impulses from the CNS toward the periphery Larger than sensory nerves Long (100-200 cm) MOTOR NEURONS CONT. Cell body Interposed between the axon and dendrites. INTEGRAL part of impulse transmission Provides metabolic support for the cell NERVE MEMBRANE NERVE MEMBRANES (SHEATH) Biological nerve membranes are structured to block the diffusion of water-soluble molecules Selectively permeable to specific molecules via specialized pores or channels Convert information through protein receptors in responsive to chemical, physical stimulation by neurotransmitters or hormones (chemical) or light, vibration, or pressure (physical) Membrane is flexible, non- stretchable consisting of lipid molecules (bilipid layer of phospholipids), proteins, and carbohydrates. NERVE MEMBRANES ▪ Nerve membranes = Neurolemmas (aka axolemma, nerve membrane) ▪ Comprised of phospholipids ▪ Lipids are oriented with their hydrophilic (polar) ends facing the outer surface and their lipophilic (non-polar) ends projecting to the middle of the membrane. ▪ Lipophilic (“fat loving”) ▪ Hydrophilic (“water loving”) NERVE MEMBRANES CONT. Creates a fatty core. Fatty core allows small lipophilic molecules of local anesthetic molecules (neutral bases) to pass through freely Water soluble substances, such as sodium ions, can only pass through the membrane at designated channels. HYDROPHILIC AND LIPOPHILIC COMPONENTS “water loving” How does each “end” behave? “fat loving” NERVE MEMBRANE CHANNELS NEUROLEMMAS Encase each axon Separate axoplasm from extracellular fluids Function: to block diffusion of water- soluble molecules 70-80 angstroms thick (1/10,000 micrometer) NERVE MYELINATION Let’s look at nerve myelination …. ▪ Nerves are classified as myelinated or non-myelinated. Schwann cells – produce myelin and are specialized connective tissue cells that surround and protect peripheral nerves. Insulate and protect nerve membranes from their surrounding environments. The axon and associated Schwann cells are collectively referred to as a nerve fiber. Isolate neurons from changes in their environment, minimizing nerve fiber to injury. Facilitates healing and regeneration Nonmyelinated cells do not regenerate. Demyelination of the axon is the cause of the neurologic symptoms seen in multiple sclerosis. NERVE MYELINATION CONT. These protective features are important and significant obstacles to the diffusion of local anesthetic solutions. Anesthetic solutions cannot diffuse through myelinated nerves except in the areas where there is direct contact with the nerve membrane at the nodes of Ranvier. NERVE MYELINATION CONT. ▪ Nodes of Ranvier – minute gaps in myelinated nerves of unprotected nerve membranes. Located at regular intervals, approx. every.5 to 3mm between Schwann cells and their myelin spirals. Nerve membrane is exposed directly to the extracellular medium. NERVE MYELINATION CONT. Non-myelinated nerves or unmyelinated nerves ▪ Have a Schwann cell, but groups of unmyelinated nerves shared the same sheath. ▪ Free nerve endings ▪ Smallest nerve fibers, ▪ C fibers ▪ Most numerous fiber in the PNS Myelinated nerves are enclosed by multiple spiral layer of Schwann cells. ▪ the layers wrap around myelinated neurons. As many as 300 times. The insulating properties of the myelin sheath enable a myelinated nerve to conduct impulses at a much faster rate than an unmyelinated nerve of equal size. NERVE MYELINATION Myelinated vs. non-myelinated neurons Provides: A Lipid layer of “insulation” More efficient (faster) impulse transmission SCHWANN CELLS NERVE MYELINATION Now, let’s look at Schwann cells …. Schwann cell sheath NERVE FIBERS Are all nerve fibers the same? NERVE FIBER TYPES Nerve fibers are typed as A, B, and C, with numerous subcategories. C fibers Most numerous of peripheral nervous system Non-myelinated, conduct more slowly Provide sensations of dull and aching pain Larger-diameter A fibers require more anesthetic volume than smaller C nerve fibers to provide complete nerve block. NERVE FIBER TYPES A fibers (A delta or Aδ) Lightly myelinated, conduct more rapidly Provide sensations of sharp, stabbing pain Both A and C fibers have been found in dental pulps Greater distribution of C fibers than A fibers DENTAL NEURAL PLEXUS An interwoven, interconnecting network of nerves supplying the teeth and their supporting structures ▪ The maxillary dental plexus derives from the terminal branches of the 2nd division of the trigeminal nerve. ▪ The mandibular dental plexus derives from the terminal branches of the 3rd division of the trigeminal nerve. These networks of nerves innervate the maxillary and mandibular teeth and their supporting structures. DENTAL NEURAL PLEXUS Maxillary Plexus Mandibular Plexus NEUROPHYSIOLOGY NEUROPHYSIOLOGY Nerves carry messages from one part of the body to another. Messages are electrical action potentials, impulses. Impulses are initiated by chemical, thermal, mechanical, or electrical stimuli. Neurons are electrically excitable, and maintain voltage gradients across their resting membranes by sodium ion pumps. ▪ Specific thresholds must be achieved before transmission of impulses to CNS occurs. ELECTROCHEMICAL SIGNALS ACROSS THE GAP - SYNAPSE NEUROPHYSIOLOGY In Sensory nerves Energy from an impulse is duplicated and transferred to succeeding impulses along the axon toward the CNS ▪ Impulses are identical in size and nature to the original – known as action potentials. The process of sequential impulse generation to the processing area in the CNS is referred to as impulse propagation. GENERATION AND CONDUCTION OF NERVE IMPULSES The generation and conduction of nerve impulses occur over a series of phases, or “states.” Resting state Depolarization Slow depolarization and firing thresholds Rapid depolarization Repolarization ACTION POTENTIALS There are four stages of potentials in the process of impulse conduction. To achieve anesthesia we must disrupt this process. RESTING POTENTIAL A nerve possesses a resting potential. Negative electrical potential of -70mV produced by differing concentrations of ions on either side of the membrane. The interior of the nerve is negative compared to the exterior. In a resting state the nerve membrane is: Slightly permeable to sodium ions (Na+) Freely permeable to potassium ions (K+) Freely permeable to chloride ions (Cl-) RESTING POTENTIAL CONT. However: K+ remains within the axoplasm, despite its ability to diffuse freely due to the electrostatic charge. Cl- remains outside the nerve membrane instead of moving into the nerve cell, because the opposing and nearly equal electrostatic charge. Na+ is prevented from moving inward due to concentration gradient and electrostatic charge. STAGE 1 - RESTING POTENTIAL Characteristics of Resting Potential: Electrical potential of axoplasm - 70mV (range -40 to -95 mV) Potential is maintained by Na+ and K + ions Cl - ions participate with the Na+ ions to maintain the resting membrane potential Ion channels are “gated” by Ca+2 ions at specific receptor sites INTRACELLULAR AND EXTRACELLULAR ENVIRONMENT … a nerve is in the resting state when it receives little to no stimulation RESTING POTENTIAL (RESTING STATE) Potential maintained by Na+ and K + , Cl - participates Channels are “gated” by Ca+2 SUMMARY RESTING POTENTIAL Nerve membrane slightly permeable to sodium ions (Na+) freely permeable to potassium ions (K+) freely permeable to chloride ions (Cl-) Intra: Extra-cellular fluid ratio potassium (27:1) sodium ions (1:14) chloride ions (1:11) STAGE 2 - DEPOLARIZATION Once a nerve is stimulated: Ion channels respond by opening their gates Release Ca+2 from receptor sites (gate keepers of resting state) Gates open, Na+ enters axoplasm Membrane depolarizes by 15 to 20 mV to -55 to -50 mV (firing threshold) DEPOLARIZATION (SLOW PHASE) nerve is stimulated Ion channels open gates in response to Ca+2 Slow depolarization occurs ~ 15 to 20 mV Until axoplasm is -50 to -55 mV = firing threshold IMPULSE GENERATION FIRING THRESHOLD The firing threshold is reached once the axoplasm has depolarized to -50 to -55 mV. IMPULSE GENERATION FAILURE If Na+ ion influx is insufficient to depolarize the membrane ~15 to 20 mV, no impulse is generated. STAGE 3 - RAPID DEPOLARIZATION Once the firing threshold has been achieved, the nerve quickly depolarizes due to the flood of positively charged Na+ ions. The impulse propagates Potential is +40 mV Further Na+ ion influx is prevented Sodium pump moves Na+ ions out of axoplasm DEPOLARIZATION (RAPID PHASE) Once enough Na+ floods the axoplasm Firing threshold is achieved Rapid depolarization generates an impulse DEPOLARIZATION SUMMARY DEPOLARIZATION Depolarization - membrane excitation ▪ Slow depolarization phase widening of ion channels influx of sodium begins firing threshold -50 to -55 mV ▪ Rapid depolarization phase rapid influx of sodium peak action potential +40mV NERVE IMPULSE Once an impulse is initiated by a stimulus, the amplitude and shape of that impulse remains constant. Does not lose strength as it passes along the nerve Imagine a fuse of gunpowder. Once lit, the fuse burns steadily along its length, with one burning segment providing the energy to ignite it’s the next. This is impulse propagation. IMPULSE PROPAGATION Unmyelinated Myelinated slow impulse spread rapid impulse spread step progression salutatory conduction 1.2 m/sec energy efficient 14.8 to 120 m/sec NERVE IMPULSE In sensory nerves, energy from an impulse is duplicated and transferred to succeeding impulses along the axon in the direction of the CNS. SALTATORY CONDUCTION Nerve impulses in non-myelinated nerves, “creep” along their membranes. ▪ move in increments ▪ Saltatory conduction – impulses are more rapidly conducted along myelinated nerves. ▪ Move from one node to the next node ▪ Much faster and has more energy ▪ Progresses from one node to the next, ▪ The current flow can skip over a blocked node. ▪ Anesthetic solution must block a minimum of 8 to10mm to be effective and ensure a thorough blockade. STAGE 4 - REPOLARIZATION Once a nerve has attained a potential of approximately +40 mV, the process begins to reverse. Recovery phase Sodium pump moves Na+ ions out of axoplasm Potential returns to -70 mV REPOLARIZATION (RETURN TO RESTING STATE) Reversal of ion concentrations in recovery phase = repolarization Nerve potential = ~ +40 mV Na+ ions exit the nerve (passive diffusion through channels and active transport of Na+ ion pumps). SUMMARY REPOLARIZATION Repolarization decreased permeability to sodium active transfer of sodium begins (sodium pump) axoplasm returns to -60 to -90 mV REFRACTORY STATE The inability to successfully re-stimulate the membrane after impulse generation and conduction. REFRACTORY PERIOD IMPULSE GENERATION FAILURE Absolute refractory Relative refractory is a cannot be re- partial resting state a stimulated no matter larger stimulus is required how great the stimulus to achieve a firing threshold RETURN TO RESTING STATE Re-attainment of a -70 mV potential Membrane has fully recovered Entire process requires only one millisecond for nerve membrane to react and recover after a successful impulse-generating stimulation INTRODUCTION TO LOCAL ANESTHESIA Local anesthesia may be defined as a temporary loss of sensation in a specific, usually small, area of the body. A primary distinction between local and general anesthesia is that when local anesthesia alone is in affect, patients remain conscious. INTRODUCTION TO LOCAL ANESTHESIA What is local anesthesia? ▪ Loss of sensation in circumscribed area without loss of consciousness ▪ Induced by a chemical drug ▪ Effects are reversible, transient Effects of local anesthesia: ▪ Depression of sensory nerve endings ▪ Inhibited impulse conduction in peripheral nerves LOCAL ANESTHETICS LOCAL ANESTHETICS are the only drugs that actually PREVENT PAIN LOCAL ANESTHETIC DRUGS AND HOW THEY WORK Local anesthetic molecules have a greater affinity for protein receptor sites within the nerve membrane compared with Ca+2 ions and subsequently displace them. This prevents depolarization of nerve membranes and impulse conduction. IMPULSE EXTINCTION The event where impulse propagation may be interrupted by local anesthesia is known as non-transmission, or impulse extinction. ▪ Local anesthetic drugs block Na+ ion influx Sodium-dependent depolarization is prevented ✓ Impulse conduction is prevented IMPULSE EXTINCTION LOCAL ANESTHETIC DRUGS AND HOW THEY WORK Prevents both the generation and conduction of a nerve impulse. Impulse is aborted and is prevented from reaching the brain and cannot be interpreted. Creates chemical roadblock Impulse does not reach brain No pain sensation
