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 Peripheral nervous system Autonomic nervous system Somatic nervous system

Brain

Spinal cord

Sympathetic division

Parasympathetic division

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:

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)

FunctionForms 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)

NEUROGLIA IN PNS:
1. SCHWANN CELLS:

Major glial cell in PNS Function: Myelination: Single neuron Nerve regeneration 2.Satellite cells: Provide support to neuron. Regulate chemical environment of ECF around neuron

ORGANIZATION OF NERVE:
ENDONEURIUM PERINEURIUM EPINEURIUM SUROUND EACH AXON SURROUN FASICULUS 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

6. On the basis of diameter and conduction speed: (Erlanger & Grasser classification)
CLASS OF NERVE FIBER A A A A B DIAMETER OF FIBER VELOCITY OF IDENTITY OF NERVES /THIN OR THICK(MU) CONDUCTION (M/SEC) 12-22 12-6 6-3 5-2 Less than 2 120-70 70-30 30-15 30-12 10-3 Motor & proprioceptive Afferents for touch Motor for intrafusal muscle fibers of the spindle Afferents for thermal senses Preganglion fibers of the autonomic system

1.5-0.3

2-.05

Afferents for pain, post ganglionic sympathetic

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

NUMBER Ia Ib

ORIGIN Muscle spindle, annulo-spiral ending Golgi tendon organ

FIBRE TYPE A A

II
III

Muscle spindle, flower-spray ending, touch, pressure

Pain and cold receptors, Some touch receptors

A
A

IV

Pain, temperature, and other receptors

Dorsal root C

8. On the basis of sensitivity to hypoxia and anaesthesia

SUSCEPTIBILITY MOST SUSCEPTIBLE HYPOXIA PRESSURE LOCAL ANAESTHESIA B A C

INTERMEDIAT E A B B

LEAST SUSCEPTIBLE C C 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

Ionophor component Passes neurotransmitter inside the postsynaptic axon

Ion channel

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

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 FUNCTIONEPSP ( 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

POSTSYNAPTIC INHIBITION:
Due to release of an inhibitory neurotransmitter. Ex: GABA, Dopamine, glycine Mechanism of action: Causes development of IPSP( Inhibitory Postsynaptic Potential)
Transmitter-receptor complex formation Opening of ligand gated K & Cl channel instead of Na channel

Hyperpolarization
Inhibit synapse transmission.
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.

ConvergenceMany 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.

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. 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

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

4. OVERSHOOT: From firing level curve reaches isoelectric potential rapidly , then shoots up beyond it till +35 mV

5. REPOLARIZATION: Starts when depolarization is completed Initially it is rapid later it become slow

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

7. AFTER DEPOLARIZATION /
Slow repolarization

NEGATIVE AFTER POTENTIAL:

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)

seminar\Action Potenital.flv

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

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.

COMPARISON OF ACTION POTENTIAL AND GRADED POTENTIAL

ACTION POTENTIAL Propagative Long distance signal Both depolarization and repolarization Obey all or none law Summation not possible Has refractory period GRADED POTENTIAL Non-propagative Short distance signal Only depolarization and hyperpolarization Does not obey Possible No refractory period

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/ Mullers 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

SEQUENCE OF EVENTS IN DEVELOPMENT OF RECEPTOR POTENTIAL

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

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)

Brain derived neurotrophic factor (BDNF) Neurotrophin 3 ( NT-3) Neurotrophin 4/5 ( NT-4/5)

Trk A
Trk B

Trk C 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 A DEFINITION RECEPTOR SITE ON EXTERNAL SURFACE OF NERVE MEMBRANE B RECEPTOR SITE ON INTERNAL SURFACE OF NERVE MEMBRANE QUATERNARY AMMONIUM ANALOGUES OF LIDOCAINE CHEMICAL SUBSTANCE BIOTOXIN

RECEPTOR INDEPENDENT
CHEMICAL MECHANISM

BENZOCAINE

BOTH RECEPTOR & RECEPTOR

MOST CLINICALLY

INDEPENDENT

USED L.A.AGENTS

FEW CLINICAL ASPECTS OF LOCAL ANAESTHESIA

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

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.

5. EFFECT OF LIPID SOLUBILITY
Increasing lipid solubility Faster nerve penetration

Rapid action.

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

PROCEDURE:
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

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 Monheims Local anesthetic and pain control. Malamed- Handbook of local anaesthesia.