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DEPARTMENT OF ORAL AND MAXILOFACIAL SURGERY

NEUROPHYSIOLOGY IN ORAL AND


MAXILLOFACIAL SURGERY

GUIDED BY PRESENTED BY
DR.NISHANT .R. CHOURASIA DR.MANIMALA PRIYA
PROFESSOR & HOD OF OMFS BABY
YEAR(2018-2021)
CONTENTS
 INTRODUCTION
 THE NEURON
• DEFINITION
• CLASSIFICATION
• STRUCTURE OF SENSORY NEURON
 PHYSIOLOGY OF PERIPHERAL NEVES
 ELECTROPHYSIOLOGY OF NERVE CONDUCTION
• ELECTROCHEMISTRY OF NERVE CONDUCTION
• RESTING PIOTENTIAL
• MEMBRANE EXCITATION
 IMPULSE PROPOGATION
 IMPULSE SPREAD
 PAIN
 CONCLUSION
 REFERENCES
THE NEURON

•It is the structural and functional unit of the nervous


system
•It transmits messages between the CNS and all parts
of the body
CLASSIFICATION

•Depending upon the function


•Sensory(afferent)
•Motor(efferent)
•Depending upon number of poles
•Unipolar neurons
•Bipolar neurons
•Multipolar neurons
•Depending upon the length of axon
•Golgi type 1
•Golgi type 2
SENSORY NEURONS
• They are capable of transmitting pain and consist of 3 main parts
1. Dendritic zone/peripheral process-It is composed of an
arborization of free nerve endings ,is the most distal segment of
sensory neuron.
2. Axon-Thin cable like structure that may be quite long.At it’s
mesial end is an arborization similar to that seen in the
peripheral process.
3. Cell body-It is located away from axon,the main pathway of
impulse transmission in the nerve.It’s main function is to provide
vital metabolic support
PHYSIOLOGY OF PERIPHERAL NERVES

•The function of the nerve is to carry


messages in the form of electrical action
potentials ,which are called impulses.
•Action potentials are transient
depolarization of the membrane that result
from a brief increase in the permeability of
the membrane to sodium ,& usually also
from a delayed increase in the permeability
to potassium
ELECTROPHYSIOLOGY OF NERVE CONDUCTION
•A nerve possess a resting potential. This is a negative electrical
potential of -70mV that exists across the nerve
memrane,produced by differing concentrations of ions on
either side of the membrane.The interior of the nerve is
negative relative to the exterior.
ELECTROCHEMISTRY OF NERVE CONDUCTION

•Nerve conduction depends on two factors:


1. Concentration of elecrolytes in the axoplasm
(interior of the nerve cell) and extracellular fluids
2. The permeability of the nerve membrane to sodium
and potassium ions
MODE AND SITE OF ACTION OF LOCAL ANAESTHETICS

•Local anaesthetics interefere with the excitation


process in a nerve membrane in one or more of the
following ways:
1. Altering the basic resting potential of the nerve
membrane
2. Altering threshold potential
3. Decreasing the rate of depolarisation
4. Prolonging the rate of repolarization
THEORIES OF LOCAL ANAESTHESIA

1.Acetylcholine theory
2.Calciun displacement theory
3.Surface charged theory
4.Membrane expansion theory
5.Specific receptor theory
PROPOSED MECHANISM
Displacement of calcium ions from sodium channel
receptor site

Binding of local anaesthetic agent to the receptor


site

Blockage of sodium channel

Decrease in sodium conductance


Depression in rate of electrical depolarisation

Failure to achieve threshold potential because of which


is called conduction blockade
IMPULSE PROPOGATION

•After initiation of an action potential by a stimulus,the


impulse must move along the surface of the axon.
•The stimulus disrupts the resting equilibrium of the nerve
membrane;the transmbrane potential is reversed with the
interior of the cell changing from negative to positive,and
the exterior changing from positive to negative.
•This new electrical equilibrium in this segment of nerve
produces local currents that begin to flow between the
depolarised segment and adjacent resting area.
•These local currents flow from positive to
negative,extending for several millimeters along the nerve
membrane.
IMPULSE SPREAD

•The propogated impulse travels along the nerve


membrane towards the CNS.The spread of this impulse
differs depending on whether or not a nerve is myelinated.

UNMYELINATED NERVES
•An unmyelinated nerve fiber is basically a long cylinder
with a high electrical resistance cell membrane
sorrounding a low resistance conducting core of axoplasm.
•The spread of an impulse in an unmyelinated nerve fiber
is therefore characterised as a relatively slow forward
creeping process.
MYELINATED NERVES
•Impulse spread within myelinated nerves differs
from unmyelinated nerves because of the the
layer of insulating material separating the
intracellular and extracellular charges.
•Impulse conduction in myelinated nerves
occurs by means of current leaps from node to
node ,a process termed as saltatory conduction.
•This form of impulse conduction proves to be
much faster and more energy efficient .
PAIN

•An unpleasant emotional experience usually initiated


by a noxious stimulus and transmitted over a
specialized network to the CNS where it is interpreted
as such.
THEORIES OF PAIN

SPECIFICITY THEORY
• Classical description was provided by Descartaes in
1644,when he conceived pain system as a straight through
channel from skin to the brain.

•The concept changed little untill n19th century when


Muller postulated the theory of information transmission
only by the way of sensory nerves.

•Von Frey developed the concept of specific cutaneous


receptors for the mediation of touch,heat,cold &pain.
•Free nerve endings were implicated as pain
receptors

•A pain centre was thought to exist within the brain


,which was responsible for the development of all
overt manifestations of the unpleasent experience.
PATTERN THEORY

•In 1894 Goldscheider was the 1st to propose the stimulus


intensity & central summation are the critical determinants
of pain.

•The theory suggested that particular patterns of nerve


impulses that evoke pain are produced by summation of
sensory input within the dorsal horn of spinal column
.
•Pain results when the total output of cells exceeds a
critical level.
GATE CONTROL THEORY

•The gate control theory,proposed by Melzack& Wall in 1965 &


recently reevaluated ,is presently receiving considerable attention

•Although the theory may be simply stated ,it’s ramifications are


extreme complex.
•The gate control theory postulates:
1. Information about the presence of injury is transmitted to
the CNS by small peripheral nerves.
2. Cells in the spinal cord or nuleus of 5th cranial nerve,which
are excited by these injury signals,are also facilitated or
inhibited by other large peripheral nerves that also carry
information about innocuous events.
3.Descending control systems originating in the brain
modulate the excitability of cells that transmit
information about injury.

Therefore the brain receives messages about injury by


the way of the gate control systems ,which is
influenced by:
1. Injury signals
2. Other types of afferent impulses
3. Descending control
PAIN PATHWAY

Tissue injury

Release of prostaglandins,bradykinins
and leukotreins from the injured tissue

Activation of A delta and C fibres


(first order neurons)

Second order neurons arising from the


dorsal horn cells of the spinal cord
Signal is transmitted via the brain stem to
the third order neurons in the thalamus

From thalamus it is relayed in the


somatosensory cortex where it is
perceived as pain
CLINICAL CONDITIONS
INJURY TO THE PERIPHERAL NERVES

•1.NEURAPRAXIA:
•This condition is almost equivalent to concussion,in
which there is no porganic damage to either nerve fire
or it’s sheath,but there is temporary physiological
paralysis of conduction through the intact nerve fibres.
•Neurapraxia is produced by stretching or torsion or
vibratory effect of a high velocity missile passing near a
nerve.
•There may be sensory loss or weakness of muscle
groups.
•During this time there is no degeneration of muscles.
•Recovery is complete ,which may take aperiod of
hours to even few weeks.
2.AXONOTMESIS
•In this condition there is rupture of nerve fibres or
axons within intact sheaths.
•Wallerian degeneration occurs in distal part of the
broken axons leaving nerve sheaths empty.
•Recovery takes place slowly by downgrowth of axons
into the empty distal nerve sheaths .
•There may be loss of nerve fibres owing to the blockage
of downgrowing axons by intraneural fibrosis.
3.NEUROTMESIS
•This condition is defined as an injury in which the
nerve is completely divided.
•This results in complete paralysis,the resultant
atrophy of muscl;es innervated by the nerve,and total
anaesthesia of nerve’s cutaneous disribution
•Spontaneous recovery does not occur after
neurotmesis.
•Complete recovery is not possible because of
degenerative changes that affect the target muscles
and end organs and because of disordered axonal
regrowth at the site of anastomosis.
REFERENCES

1.Guyton& Hall.Textbook of medical physiology.13thedition.2015


2.K Sembulingam.Essentials of medical physiology.5th
edition.Jaypee brothers medical publishers;2010.56-119
3.Monheim LM. Monheim’s Local anesthesia and pain control in
dental practice. 6th ed. Saint Louis: Mosby; 1978
4. Stanley.F.Malamed.Handbook of local anaesthesia.6th ed.
Saint Louis:Mosby;2013