Neurophysiology 2019
NEUROPHYSIOLOGY OF LOCAL ANESTHESIA
THE NERVOUS SYSTEM
Components:
CNS (Central Nervous System): Brain, spinal cord
PNS (Peripheral Nervous System):
Autonomic: Involuntary control
Somatic: Voluntary control
Sensory Pathways:
Cranial Nerves: Transmit sensory information
Afferent Nerves: Carry sensory information to CNS
Efferent Nerves: Carry motor information from CNS
SENSORY NERVE ANATOMY
Neuron:
Transmits messages between CNS and body parts
Dendrite:
The distal segment with free nerve endings that respond to stimulation
Axon:
Transmits impulses; encased in neural cytoplasm (axoplasm)
Cell Body:
Provides metabolic support, not involved in impulse transmission
MYELIN SHEATH AND NERVE CONDUCTION
Myelin Sheath:
Lipoprotein layer covering myelinated nerve fibers
Specialized Schwann cell form
Nodes of Ranvier:
Constrictions between Schwann cells; 0.5 to 3 mm apart
Exposed nerves; enables rapid impulse conduction
IMPULSE SPREAD
Unmyelinated Nerves:
Slow conduction method
Myelinated Nerves:
Utilize saltatory conduction (leaps from node to node) for faster impulses
If conduction blocked at one node, can skip to the next
Local anesthesia must cover 8 to 10 mm for effective blockage
NERVE CONDUCTION MECHANISM
Voltage Changes:
Resting potential: -70 mV
Initial depolarization phase: Need 15 mV decrease
Firing threshold: Rapid depolarization to +40 mV
Process timeline:
Depolarization: 0.3 msec
Repolarization: 0.7 msec
DEPOLARIZATION AND REPOLARIZATION
Depolarization Process:
Increased Na+ permeability
Rapid influx causing potential increase from resting (-70 mV) to +40 mV
Repolarization Process:
Na+ channels close; active transfer of Na+ out
K+ channels open; K+ influx
Returns nerve to resting state
ACTIONS OF LOCAL ANESTHETICS
Definition:
Chemicals that prevent generation and conduction of nerve impulses
Mechanism:
Must diffuse through nerve cell membrane, binding to Na+ channel
Decreases Na+ permeability, leading to little or no depolarization
PROPERTIES OF LOCAL ANESTHETICS
Typical Structure:
Composed of aromatic lipophilic part, intermediate chain (ester/amide), and amine hydrophilic part
Main Types:
Most are tertiary amides; some are secondary amides like Prilocaine
LOCAL ANESTHETIC STATES
When Added to Solution:
Exists in both uncharged (weak base) and charged (salt) forms
pH Influence:
Tissues' pH affects predominant form of LA
Action Factors:
Include diffusion through nerve sheath and binding at receptor sites
FACTORS AFFECTING LOCAL ANESTHESIA DURATION
pH Levels:
Acidification decreases effectiveness
pKa:
Higher pKa means slower onset due to fewer RN molecules available to diffuse through nerves
Examples:
Mepivicaine (7.7, 2-4 min), Lidocaine (7.7, 2-4 min), Bupivacaine (8.1, 5-8 min)
INFLUENCING FACTORS OF LA ACTION
Absorption: Into non-neural tissues
Lipid Solubility: Affects membrane penetration
Vascularity: Affects dilution and distribution
Protein Binding: Determines duration of action based on type and size of nerve
INDUCTION OF LOCAL ANESTHESIA
Diffusion Process:
From extra neural site to nerve
Higher initial concentration leads to faster onset
Mantle vs. Core Bundles:
Mantle fibers innervate proximal regions first, while core fibers innervate distal points
RECOVERY FROM LOCAL ANESTHESIA
Reverse Diffusion:
Mantle bundles lose anesthesia faster than core bundles
Disparity in recovery time between proximal and distal innervations
REINJECTING LOCAL ANESTHETICS
Profound Anesthesia:
Reinjection can increase concentration, leading to rapid onset
Tachyphylaxis: Tolerance increases with repeated doses; more likely if pain sensation returns