NCP Seminar

NERVE CONDUCTION

PHYSIOLOGY

CONTENTS:

INTRODUCTION TO NERVOUS SYSTEM

NERVE FIBRE :

CLASSIFICATION

ORGANIZATION

SYNAPSE :

CLASSIFICATION

FUNCTION

PROPERTIES

NEUROTRANSMITTERS

PROPERTIES OF NERVE FIBRE

TRANSMISSION AND PROCESSING

OF SIGNALS IN NEURONAL POOL

RECEPTOR

CLASSIFICATION

PROPERTIES

FACTORS AFFECTING NEURONAL GROWTH

APPLIED SCIENCE

CONCLUSION

REFERENCES

INTRODUCTION:

The human nervous system consists of billions

of nerve cells plus supporting cells. Among these

neurons are those which are able to respond to stimuli ,

conduct impulses, and to communicate with each other

and with other types of cells like muscle cells.

COMPONENTS OF NERVOUS SYSTEM

Nervous system

Central nervous system

BrainSpinal cord

Peripheral nervous system

Autonomic nervo

us syste

m

Sympathetic division

Parasympathetic division

Somatic

nervous

system

CELLS OF NERVOUS SYSTEM:

1. NEURON

Structural and functional unit of nervous system

2. NEUROGLIA

Supporting cell of the nervous system

NEURON

Structural and functional unit of nervous system

100 billion neurons are present in Human nervous

system

Both electrically active and excitable

CLASSIFICATION OF NEURONS:

Number of poles

Unipolar

Bipolar

Multipolar

STRUCTURE OF NEURON:

Each neuron is made up of three parts:

a) Nerve cell body

b) Dendrite

c) Axon

NERVE CELL BODY:

Soma or parykaryon

Irregular shape

Single large centrally placed nucleus.

Nissl bodies and neurofibrils

NISSL BODIES: Named after the discoverer F.Nissl

Tigroid substance

Small basophilic Membranous granule

Protein synthesis.

Absent in axon hillock

Flow into the dendrite but not into axon

NEUROFIBRILS:

Thread like structures

Microfilaments and microtubules

DENDRITE

Branched shorter process of neuron

May be absent, one or more in number.

Conductive in nature ( DECREMENTAL CONDUCTION)

AXON

Longer process of nerve cell

One per neuron

Arise from axon hillock

First portion of axon : Initial segment

Internal structure of axon-

Long central core called axis cylinder covered by neurolemma

Axis cylinder = Axoplasm+ Axolemma

Can be myelinated or non-myelinated

Nodes of ranvier

• Periodic constrictions ( Myelin is absent)

• Internode

• Faster conduction

NEUROGLIA

Supporting cell of the nervos system

10-50 times than neuroms

Present in both CNS and PNS

NEUROGLIA IN CNS:

1. ASTROCYTES Star shaped Present throughout the brain

Two types Fibrous (white matter) & Protoplasmic (Gray matter)

Function- Forms blood brain barrier Supporting network Maintain appropriate concentration of

ions and neurotransmitters.

2. MICROGLIA (MACROPHAGES OF CNS) Smallest Scavanger cell Derived from monocytes

3. OLIGODENDROCYTES Short with few process. Myelin sheath formation (multiple fibre)

2.Satellite cells:

Provide support to neuron. Regulate chemical environment

of ECF around neuron

1. SCHWANN CELLS:

Major glial cell in PNS Function: Myelination: Single neuron Nerve regeneration

NEUROGLIA IN PNS:

ORGANIZATION OF NERVE:

ENDONEURIUM SUROUND EACH AXON

PERINEURIUM SURROUN FASICULUS

EPINEURIUM SURROUND COMPLETE NERVE

CLASSIFICATION OF NERVE FIBRES:There are various classification:

1. On the basis of structure:Myelinated & Non myelinated

2. On the basis of distribution: Somatic & Visceral/autonomic

3. On the basis of origin:Cranial & Spinal

4. On the basis of function:Sensory & Motor

5. On the basis of neurotransmitter secreted:Adrenergic & Cholinergic

CLASS OF NERVE FIBER

DIAMETER OF FIBER /THIN OR THICK(MU)

VELOCITY OF CONDUCTION (M/SEC)

IDENTITY OF NERVES

Aα 12-22 120-70 Motor & proprioceptive

Aβ 12-6 70-30 Afferents for touch

Aγ 6-3 30-15 Motor for intrafusal muscle fibers of the spindle

Aδ 5-2 30-12 Afferents for thermal senses

B Less than 2 10-3 Preganglion fibers of the autonomic system

C 1.5-0.3 2-.05 Afferents for pain, post ganglionic sympathetic

6. On the basis of diameter and conduction speed: (Erlanger & Grasser classification)

7. Sensory nerve classification (Classification used by sensory physiologist):

NUMBER ORIGIN FIBRE TYPE

Ia

Ib

Muscle spindle, annulo-spiral endingGolgi tendon organ

Aα

Aα

II Muscle spindle, flower-spray ending, touch, pressure

Aβ

III Pain and cold receptors,Some touch receptors

Aδ

IV Pain, temperature, and other receptors

Dorsal root C

8. On the basis of sensitivity to hypoxia and anaesthesia

SUSCEPTIBILITY

MOST SUSCEPTIBLE

INTERMEDIATE

LEAST SUSCEPTIBLE

HYPOXIA B A C

PRESSURE A B C

LOCAL ANAESTHESIA

C B A

SYNAPSE :

Junction where presynaptic cell (axon or some portion of

one cell) terminate on postsynaptic cell (dendrite,

soma or

axon of another neuron)

Growth cones :

Present at the growing tip

Right synaptic connections.

Guided by attractant and repellant secreted by glial cell.

Semaphorin protein & Neurolignin protein :

Moderate actual synapse formation

CLASSIFICATION:

Anatomical classification

Axo-axonic synapse

Axo-dendritic synapse

Axo-somatic synapse

FUNCTIONAL CLASSIFICATION-

1. Electrical synapse 2. Chemical synapse

ELECTRICAL SYNAPSE:

Physiologic continuity between Pre & Postsynaptic neuron because of GAP JUNCTIONS

ELECTRICAL SYNAPSE:

Gap junction form low resistance bridges

through which ions pass with relative ease.

Synaptic delay is less.

Transmission in either direction.

CHEMICAL SYNAPSE:

More commonly seen

Presyaptic terminal is separated from Postsynaptic terminal

by a space called Synaptic cleft (20-40 nm)

ANATOMY OF CHEMICAL SYNAPSE:

PRESYNAPTIC AXON TERMINAL:

Branches of axon of presynaptic neuron.

Various types:

Round or oval knobs

• Terminal buttons

• Synaptic knob

• End-feet

• Axon telodendria.

Dendrite spines - present on dendrite in

cerebral and cerebellum cortex.

Basket cells- Sometimes form a basket

around postsynaptic cell in

cerebellum & autonomic ganglia

Wavy or coiled with free endings without the knob :

-inhibitory function

Each neuron divide to form 2000 synapse

Covered by presynaptic membrane which contain

synaptic

vesicles:

Types of synaptic vesicle:

1. Small,clear:

Acetylcholine, glycine, GABA or glutamate.

2. Small, dense core:

Catecholamines

3. Large,dense core:

Neuropeptides

RECYCLING OF VESICLES

Small vesicles gets recycled after use

Regulated by

V-snare protein Synaptobrevin : Vesicle membrane

T-share protein Syntaxin : Neuron membrane.

seminar\Neural Synapse.flv

ANATOMY OF CHEMICAL SYNAPSE:

POSTSYNAPTIC AXON TERMINAL:

Covered by postsynaptic membrane

Contain large number of receptor protein

molecule

These molecule has two components:

Receptor molecule

Binding component

Bind to neurotransmitter

Ion channe

l

Second messenger

ION CHANNEL:

Allow passage of specific ion

through the membrane.

Rapid action

Two type:

Cation channel: Lined by negative ions Allow passage of cations like Na, K and Ca

Anion channel: Lined by positive ions Allow passage of anions like Cl.

“SECOND MESSENGER” system:

Prolonged affect

G-Protein (Most common )

Have 3 component:

alpha, beta and gamma.

EFFECTS OF ACTIVATOR α COMPONENT

Opening of specific ion channels

Activation of cAMP or cGMP

Activation of some intracellular enzyme

Activation of gene transcription.

POST SYNAPTIC DENSITY:

Ordered complex of Specific receptors, Binding proteins, &

Enzymes induced by postsynaptic effect.

SYNAPTIC CLEFT :

Space between Pre & Postsynaptic neuron

200-400 angstroms wide

Contain cholinesterase.

CONJOINT SYNAPSE:

Have both Electrical and Chemical synapse propeties

FUNCTIONS OF SYNAPSE:

To transmit the impulse from one neuron to

another neuron or muscle.

Both excitatory and inhibitory action

EXCITATORY FUNCTION-

EPSP ( EXCITATORY POST SYNAPTIC POTENTIAL):

Graded potential

Initial depolarizing response.

Begin 0.5 Ms after afferent impulse enters.

Reaches peak 1-1.5 ms later, then declines exponentially.

Increases excitability of neuron

Confined to only synapse.

EPSP produced by all the active knob summate.

Clinical significance of EPSP:

If strong enough, can produce action potential

Arrival of Action potential in Axon terminal

Opening of calcium channels

Influx of calcium ions

Opening of vesicles and release of Ach

Passage of Ach through synaptic cleft

Formation of Ach-Receptor complex

Opening of sodium channels

Development of EPSP

Opening of sodium in initial segment of axon

Development of action potential

Spread of action potential

INHIBITORY FUNCTION:

Three types :

Post synaptic / Direct inhibition

Pre synaptic / Direct Inhibition

Renshaw cell inhibition

Transmitter-receptor complex formation

Opening of ligand gated K & Cl channel instead of Na channel

Hyperpolarization

Inhibit synapse transmission.

IPSP( Inhibitory Postsynaptic Potential)

POSTSYNAPTIC INHIBITION:

Due to release of an inhibitory neurotransmitter.

Ex: GABA, Dopamine, glycine

Mechanism of action:

Causes development of IPSP( Inhibitory Postsynaptic Potential)

 PRE SYNAPTIC INHIBITION/INDIRECT INHIBITION;

Failure of presynaptic axon terminal to release

the excitatory neurotransmitter substance

RENSHAW CELL INHIBITION:  

Renshaw are small motor neuron present in anterior gray

horn of spinal cord.

Collateral fibre : Some of the fibre terminate on renshaw

cell

instead of leaving spinal cord.

Sends inhibitory impulse to motor neuron.

SLOW POSTSYNAPTIC POTENTIALS:

Slow EPSP (due to decrease in K+ concentration)

IPSP (due to increase in K+ concentration)

Seen in autonomic ganglia, cardiac and smooth

muscle and cortical neurons.

Latency period : 100-500 ms and last several seconds

PROPERTIES OF SYNAPSE:

ONE WAY CONDUCTION:

Impulse are transmitted only in 1 direction in chemical synapse

(BELL-MAGENDIE LAW)

An impulse conducted antidromically

Dies out after at cell body of neuron,

Prevented by one way gate at synapse as chemical mediators

are present only in presynaptic nerve terminal

SYNAPTIC DELAY:

Occur during the transmission of impulse through the synapse.

Occur due to time taken for

Release of neurotransmitter

Passage of neurotransmitter

Action of neurotransmitter on receptor

Action of receptor

Inward diffusion of Na

Normal duration : 0.3-0.5 ms

Clinical significance:

Helps to find out if the reflex pathway

is monosynaptic or polysynaptic.

FATIGUE:

Occurs during continous activity

Occurs due to

exhaustion or partial exhaustion of neurotransmitter store

Destroyed by acetylcholinesterase

New acetylcholine is not synthesized

Progressive inactivation of receptor

Slow development of abnormal concentration of ions

inside postsynaptic neuronal cell.

CONVERGENCE AND DIVERGENCE:

Anatomic substrates for Facilitation ,

Occlusion and Reverberation.

Convergence-

Many presynaptic neurons terminate

on a single postsynaptic neuron.

Can be from single or multiple source.

Divergence:

One presynaptic neuron terminate

on many postsynaptic neuron.

Can be amplifying type or

the one diverging into multiple tracts.

SUMMATION :

Fusion of effects of progressive increase in the EPSP

leading to facilitation of response. It is of two types;

1. Spatial summation:

Many presynaptic terminals are stimulated simultaneously

2. Temporal summation:

One nerve fibre stimulated repeatedly

NEUROTRANMITTERS:

More than 50 types have been reported

Two types-Small molecule, and larger molecule

1. Small molecule:

Rapidly acting transmitters:

Causes acute response of nervous system.

Ex:Transmission of sensory signals

TYPES:

Class I- Acetylcholine

Class II- Amines (Norepinephrine,, epinephrine dopamine,

serotonin,histamine)

Class III-Aminoacids ( GABA, Glycine, Glutamate, Aspartate)

Class IV-Nitric oxide(NO)

Synthesized in cytosol of presynaptic terminal

Absorbed by active transport into the Synaptic vesicles

1 vesicle contain - 2000 to 10,000 acetylcholine molecule

Continuously recycled.

2. Large molecule, slowly acting transmitters:

These are neuropeptide

Ribosomes.

Two changes occur in golgi bodies:

Split enzymatically

Packaged into minute transmitter vesicles

Released into cytoplasm

Axoplasmic streaming

More potent

Prolonged actions

PROPERTIES OF NERVE FIBRE:

1. EXCITABILITY

2. CONDUCTIVITY

1.EXCITABILITY:

Nerve fibre have low threshold than other cells.

Two types of response :

Action potential / Nerve impulse

Electrotonic potential / Local response / Graded potential

IONIC BASIS OF ELECTRICAL EVENTS:

RESTING MEMBRANE POTENTIAL

-70 mV.

Maintained mainly by :

Sodium Potassium pump:

Selective permeability of membrane

Leak channels

SODIUM POTASSIUM PUMP

  Na and K are actively transported

in opposite direction

3 Na out and 2 K in

Uses energy from ATP

Highly concentrated in :

Initial segment,

First node of ranvier,

Sensory neurons.

SELECTIVE PERMEABILITY OF MEMBRANE: 

Depend on gated channels

Only specific ion can pass through

LEAK CHANNELS:

Na and K both ion can diffuse back by leak channels.

seminar\Resting Membrane Potential.flv

ACTION POTENTIAL:

Series of electrical events that occur in nerve

membrane when nerve fibre is activated

Rapid & Small changes

Occur in two phases – Depoarization and repolarization

Studied in motor neuron and anterior horn of spinal cord.

Begins in initial segment of the axon

Recorded using Electronic amplifier & Cathode ray

oscilloscope (CRO).

Following action potential curve is obtained.

2. LATENT PERIOD:

Isopotential interval

Follows stimulus artifact

Ends with the start of action potential

Time taken : site of stimulation to recording electode.

Last for 0.5-1 ms

1. STIMULUS ARTIFACT:

Slight irregular deflection of baseline

Last for a very short period of time.

Leakage of current from stimulated

electrode to recording electode.  

4. OVERSHOOT:

From firing level curve reaches isoelectric potential rapidly ,

then shoots up beyond it till +35 mV

3. FIRING LEVEL:

Depolarization starts after latent period

Very slow for about 15mv,

then increases suddenly

Firing level :

Point at which the depolarization increases

suddenly

6. SPIKE POTENTIAL:

Rapid rise in depolarization and rapid fall in

repolarization

Rate of repolarization decreases when it is

almost

70 % completed.

Last for 0.4 ms

5. REPOLARIZATION:

Starts when depolarization is completed

Initially it is rapid later it become slow

7. AFTER DEPOLARIZATION / NEGATIVE AFTER POTENTIAL:

Slow repolarization

Follows rapid fall in repolarization.

Last for 2-4 mS

8. AFTER HYPERPOLARIZATION / POSITIVE AFTER POTENTIAL:After reaching the resting level, it becomes more negative beyond resting level.

Last for 40 Ms

On repeated conduction, changes in Afterpolarization

may occur without changes in the rest of the action potential.

MONOPHASIC ACTION POTENTIAL:

Electric potential recorded with

one electrode on surface & one inside the nerve fibre.

BIPHASIC ACTION POTENTIAL:

Both electrode on surface

ACTION POTENTIAL (ionic basis)

Onset of depolarization : Slow influx of Na

Spike potential : Rapid opening & rapid closing

of voltage gated Na channel

Repolarization : K channel start opening

Hyperpolarization : K channel remain open for long time

seminar\Action Potenital.flv

GRADED POTENTIAL: 

Mild local change in membrane potential when stimulated.

Develop in

Receptor

Synapse

Neuromuscular junction

2. CONDUCTIVITY:

Transmiting the impulse from area of stimulation

to the other tissue.

Constant amplitude and velocity.

Unidirectional

In experimental condition : Either direction.

Myelinated fibre :

50 times faster

Because of saltatory conduction

( depolarization jumps from one node to another node)

seminar\Action potential propagation in an unmyelinated axon.flv

seminar\Saltatory Conduction.flv

REFRACTORY PERIOD

Period at which nerve doesnot give response to a stimulus.

Two types-

1. Absolute refractory period:

Nerve doesnot show any response at all

2. Relative refractory period:

Nerve fibre shows response ,

if strength of stimulus is increased to maximum.

ADAPTATION:

Also called desensitization

Decline in discharge of sensory impulses when receptor

is stimulated continuously

Partial or complete.

Two types: Tonic and Phasic

1. Tonic receptors-

Slowly adapting receptors

Detect continous stimulus strength

Ex: Musle spindle, Pain and Chemoreceptors.

2. Phasic /Rate/Movement receptors-

Rapidly adapting receptors

Detect change in stimulus strength

Ex:Touch and pressure receptors

ALL OR NONE LAW:

When a nerve is stimulated by a stimulus either it gives

maximum response or doesnot give response at all.

ACTION POTENTIAL GRADED POTENTIAL

Propagative Non-propagative

Long distance signal Short distance signal

Both depolarization and repolarization

Only depolarization and hyperpolarization

Obey all or none law Does not obey

Summation not possible Possible

Has refractory period No refractory period

COMPARISON OF ACTION POTENTIAL AND GRADED POTENTIAL

TRANSMISSION AND PROCESSING OF

SIGNALS IN NEURONAL POOL

NEURONAL POOL:

Collection of few or vast number of neurons.

STIMULATORY FIELD :

Neuronal area stimulated by a nerve fibre.

EXCITATORY / SUPRATHRESHOLD STIMULUS:

Stimulus which causes a neuron to discharge

SUBTHRESHOLD STIMULUS :

Stimulus itself doesnot cause a neuron to discharge

Make neuron more susceptible to other incoming signal

ZONES OF A NEURONAL POOL:

Discharge/excited/liminal zone: in centre

Facilitated/subthreshold or subliminal zone:

Present around the discharge zone.

Inhibitory zone

AFTERDISCHARGE

Prolongation of a signal by a neuronal pool.

Can occur due to:

Long acting synaptic transmitter

Reverberatory (oscillatory circuit)

REVERBERATORY (OSCILLATORY CIRCUIT):

Caused by positive feedback

Can involve single neuron with a collateral nerve

or many parallel fibres

Fatigue

CONTINOUS SIGNAL OUTPUT

Occur because of:

Continous intrinsic neuronal excitability.

Reverberatory circuit.

RHYTHMICAL SIGNAL OUTPUT

Result from reverberating circuit or sequential

reverberating circuits.

Ex: Walking movement, respiratory signal

RECEPTORS Sensory nerve endings terminate in the periphery as bare

unmyelinated endings or in specialized capsulated structures.

Act like a transducer ,convert Stimuli into Action potential.

Five Types :

a) Mechanoreceptor

b) Thermo receptor

c) Nociceptor

d) Electromagnetic receptor

e) Chemoreceptor

PROPERTIES OF RECEPTORS:

SPECIFICITY OF RESPONSE-

Also called doctrine of specific nerve energie/ Muller’s law

This specificity of nerve fibre for transmitting only one

modality of sensation is called the labeled line principle.

WEBER FECHNER LAW:

Change in response of a receptor is directly proportional to

logarithmic increase in intensity of stimulus.

RECEPTOR POTENTIAL:

Studies in pacinian corpuscles

It is a nonpropagated potential

Develop when a receptor is stimulated

Maximum amplitude reached is 100 mV

Amplitude increases rapidly first then progressively

slowly

Frequency increases in proportion to receptor

potential

Pressure stimulus

Compression & elongation of pacinian corpuscle

Deformation of centre core fibre

Opening of mechanically gated Na channel

Na ions into the core fibre

Receptor potential

LOCAL CIRCUIT

Spread of local circuit to first node of ranvier

Opening of voltage gated Na channel

Generation of Action potential

SEQUENCE OF EVENTS

IN

DEVELOPMENT

OF

RECEPTOR POTENTIAL

FACTORS AFFECTING NEURONAL GROWTH:

NEUROTROPHINS :

Proteins necessary for Development, survival

and growth of neuron.

Can derive from :

Organ they innervate

Schwann

Astrocyte

Cell or the nerve itself

Can undergo anterograde or retrograde transport

FOUR ESTABLISHED NEUROTROPHINS AND

THEIR RECEPTORS ARE:NEUROTROPHIN RECEPTOR

Nerve growth factor ( NGF) Trk A

Brain derived neurotrophic factor (BDNF)

Trk B

Neurotrophin 3 ( NT-3) Trk C

Neurotrophin 4/5 ( NT-4/5) Trk B

p75 NTR : One low affinity NGF receptor.

OTHER FACTORS AFFECTING NEURONAL GROWTH

CNTF ( ciliary neurotrophic factor) :

GDNF (glial cell derived neurotrophic factor)

LIF (leukemia growth factor)

IGF-I (insulin like growth factor I)

TGF (transforming growth factor)

FGF (fibroblast growth factor)

PDGF (platelet derived growth factor)

APPLIED SCIENCE :

1. CLINICAL SIGNIFICANCE OF SYNAPTIC INHIBITION:

Poison like strychnine block inhibitory function

Tonic muscle spasm

Parkinsonism : inhibitory system is impaired

Rigidity

2. FEW TOXIN EXERT THEIR ACTION BY BLOCKING NEUROTRANSMITTER RELEASE:

Tetanus toxin:

Block Presynaptic transmitter release in CNS

spastic paralysis

Botulinum toxin :

Block release of acetylcholine

Flaccid paralysis

Local injection are used

In facial muscles to remove wrinkles

3. LOSS OF MYELIN

Delayed or blocked conduction.

Ex: multiple sclerosis

4. CAFFEINE, THEOPHYLLINE AND THEOBROMINE Reduces threshold.

Increases neuronal excitability

5. EFFECT OF ALKALOSIS AND ACIDOSIS

Alkalosis increased neuronal excitability

Ex: overbreathing precipitate epileptic attack.

Acidosis decreases neuronal excitability:

Ex: Coma in diabetic or uremic acidosis

6. EFFECT OF PRESSURE:

Loss of conduction in large fibre

Small pain fibres not effected

Ex: Saturday night or Sunday morning paralysis.

7. EFFECT OF LOCAL ANAESTHESIA:

Exert their effect at nerve membrane.

Occur during the depolarization phase of the action potential.

Many theories have been proposed to explain the mechanism

of action of local anesthetics.

Acetylcholine theory

Surface charge theory

Membrane expansion theory

Calcium displacement theory

Specific receptor theory

(Most accepted theory)

Displacement of calcium ion from the sodium channel receptors site

Binding of the local anesthetic molecule to "this receptor site

Blockade of the sodium channel

Decrease in sodium conductance

Depression of the rate of electrical depolarization

Failure to achieve the threshold potential level

Lack of development of propagated action potential

Conduction blockade

Seminar \ lidocaine in action 2.flv

CLASSIFICATION OF LOCAL ANESTHETIC ON THE BSIS OF SITE OF ACTION:

CLASS DEFINITION CHEMICAL SUBSTANCE

A RECEPTOR SITE ON EXTERNAL

SURFACE OF NERVE MEMBRANE

BIOTOXIN

B RECEPTOR SITE ON INTERNAL

SURFACE OF NERVE MEMBRANE

QUATERNARY

AMMONIUM ANALOGUES

OF LIDOCAINE

C RECEPTOR INDEPENDENT

CHEMICAL MECHANISM

BENZOCAINE

D BOTH RECEPTOR & RECEPTOR

INDEPENDENT

MOST CLINICALLY USED

L.A.AGENTS

1. Inadequate pulpal anesthesia develop sometime in the

presence of subjective symptoms of adequate soft tissue

anesthesia

Cutaneous afferents are smaller than pulp afferents

and

thus more susceptible to the local anesthetic.2. Even in case of excellent pain control patient sometimes feel

pressure because

Mechanoreceptors pain fibres are relatively large

and frequently not affected by anaesthetic

Group C pain fibre are effected before group A touch Fibre

FEW CLINICAL ASPECTS OF LOCAL ANAESTHESIA

3. Molars are anesthetized much earlier than the incisors

because fibers near the surface of the nerve innervate

more proximal regions,whereas fibers in the core bundles

innervate the more distal points of nerve distribution

4. Recovery is usually a slower process than induction because

the local anesthetic is bound to the drug receptor site in the

Na channel and hence released more slowly than it is absorbed.

Increasing lipid solubility

Faster nerve penetration

Rapid action.

5. EFFECT OF LIPID SOLUBILITY

6. EFFECT OF INFLAMMATION

Reduced affect seen because of :

Increased ionised form

Some inflammatory exudate lowers the response threshold

Dialated vessels : Rapid uptake of anaesthetic molecule

ALTERNATIVE :

Inject in a distant site

Inject large amount of anaesthetic

Histamine blockers as anaesthetic

General anaesthesia

Alternative method of pain control:

Electronic Dental Anaesthesia (TENS)

Hypnosis

NERVE GAS:

ORGANOPHOSPHORUS COMPOUNDS

(TABUN, SARIN, AND SOMAN)

Developed by Germany during as a weapon of chemical warfare

during World war II but not used

VX

Produced in huge quantities by the U.S & Soviet union

 during the Cold War of 1993.

stockpiling and use during war are now banned by the

  Chemical Weapons Convention of 1993.

Affects the transmission of nerve impulses through the

  nervous system.

A single droplet of VX or Sarin, if inhaled or in contact

with the skin, can be absorbed into the bloodstream

and

paralyze the nervous system, leading to respiratory

failure

and immediate death

TOKYO TUBE ATTACK

NERVE CONDUCTION STUDY (NCS)

Nerve conduction study (NCS) :

A test commonly used to evaluate the function,

especially the ability of electrical conduction, of the motor

and sensory nerves of the human body.

Nerve conduction velocity (NCV) :

Common measurement made during this test.

Normal conduction velocity is 50 to 60 mps (approx)

Related to the diameter of nerve and myelination

Patient may lie down or sit during the test.

Patch-like 2 electrodes are affixed on the skin at various nerve locations.

A probe emits a very low electrical impulse.

Speed of the Recorded on a moitor

PROCEDURE:

USES OF NCS

Localize site of pain

Nerve damage from herniated discs.

Diagnose Peripheral neuropathy.

Diagnose Focal neuropathy (carpal tunnel syndrome).

Myopathy.

Diseases of neuromuscular junction ( mythenia gravis).

Symptoms indicative of nerve damage as numbness,

weakness.

Differentiation between local or diffuse disease process

Prognosis of nerve injury.

-

INTERPRETATION OF NCS:

Slowing of the NCV indicates there is damage to the myelin.

Example:

Carpal tunnel syndrome:Focal compression of median nerve at wrist

Slowing across the wrist for the motor and sensory latencies

Generalized diseased of nerves, or generalized peripheral neuropathy.

Slowing of all nerve conductions

CONCLUSION:

Neuron are the electrically active and excitable cells forming

the building blocks of a system, which control all the other

systems of the body. Hence to better understand the

mastermind behind all the activities carried out by the complex

body, it is must to have a firm knowledge of its structure,

physiology and clinical implications.

REFERENCES

Guyton -Textbook of medical physiology--11th edition

William F Ganong - Review of medical physiology -

21st edition

K.Sembulingam-Essentials of Medical Physiology,

5th edition

Monheim’s Local anesthetic and pain control.

Malamed- Handbook of local anaesthesia.