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.
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