PHYSIOLOGY OF PAIN

INTRODUCTION:

Pain, all of us have experienced this entity at some or the other phase of

life. And still it remains a vague term/ experience to be described. It is described

as sharp, burning, aching, cramping, dull or throbbing but the actual pain

experience varies greatly as a result of human emotions. The involvement of these

emotions may be the reason why the word pain has not been defined in a manner

agreeable to all.

Pain can be elicited by many means. We shall be discussing the physiology

of pain and the pain of orofacial origin. Now lets have a look at the various

definitions, of course no single definition would be accepted by all.

Dorland’s Medical Dictionary:

It is an unpleasant sensation associated with actual or potential tissue

damage and mediated by specific nerve fibre to the brain where its conscious

appreciation may be modified by various factors.

Beecher (1959) described it as a subjective matter which is difficult to

define in precise terms.

According to him, the behavioral reaction to the nociception varies from

individual to individual and also the significance of the injury to that individual.

According to his observations in 1956, it was noted that only 25% of

soldiers wounded in battle requested narcotic medications for pain relief,

compared to more than 80% of civilian patients with surgical wound of similar

magnitude.

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The wounded soldier may be relieved to be out of life threatening situation

whereas the surgical patient may be concerned about the consequences afer the

surgery.

Fields:

Defined pain as an unpleasant sensation that is perceived as arising from a

specific region of the body and is commonly produced by processes that damage

or are capable of damaging bodily tissue.

He emphasized the need to be able to localize the painful source in order to

distinguish it from psychological pain and suffering for e.g. the “pain” of a broken

heart!

Nociception – Tissue Damage:

A more complete definition is cast by the International Association for the

study of Pain (IASP) in its taxonomy of painful disorders.

It says; “Pain is an unpleasant sensory and emotional experience associated

with actual or potential tissue damage or described in terms of such damage”.

This definition emphasizes that “Pain is pain, even if a nociceptive source

is not readily identified”.

Though it is highly subjective, the pain owing to psychological causes is as

real as any pain associated with actual nociception and should be treated as such.

Monheim’s:

It is an unpleasant emotional experience usually initiated by a noxious

stimulus and transmitted over a specialized neural network to the central nervous

system where it is interpreted as such.

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Before exploring the depths of pain physiology, lets have a brief look at the

neuroanatomy and functions of the nervous system of the human body.

Primarily, the nervous system is divided into two parts:-

I) Central Nervous System

a. Brain

b. Spinal cord

II) Peripheral nervous system

a. Peripheral nerves and

b. Its ganglia

I] CNS:-

Brain is divided into cerebrum – cerebellum – mid brain – pons – medulla

continues as spinal cord.

II] PNS:-

The PNS is formed by neurons and their processes present in all the regions

of the body. This consists of cranial nerves arising from brain and spinal nerves

arising from spinal cord.

This is again divided into 2 subdivisions viz:-

a) Somatic nervous system

b) Autonomic nervous system

a) Somatic Nervous System:-

Includes the nerves supplying the skeletal muscles. Thus, the somatic

nervous system controls the movements of the body by acting on the skeletal

muscles.

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b) Autonomic Nervous System:-

It is concerned with regulation of visceral or vegetative functions. So, it is

otherwise called negative or involuntary nervous system. It consists of two

systems:

- Sympathetic division

- Parasympathetic division

Nervous System

CNS PNS

Brain

Cerebrum Somatic NS Autonomic NS

Cerebellum

Mid brain Sympathetic Parasympathetic

Pons

Medulla

Spinal cord

SPINAL CORD:

- It is the downward continuation of medulla and descends through the vertebral

canal and it ends at the lower border of the lumbar vertebra.

- Its cross section on microscopic examination shows outer white matter

consisting of tracts either sensory (ascending) or motor (descending).

- The inner grey matter looks somewhat like English alphabet H.

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Three ______ can be distinguished in it:-

i) Anterior horn, gives rise to somatic motor nerves supplying skeletal

muscles.

ii) Posterior horn, which receives the sensory nerve via the dorsal root

ganglion.

iii) Lateral horn, gives rise to sympathetic fibres only in the thoracic and

upper lumbar segments.

Formation of a mixed spinal nerve:

1) As stated just now, the axons emerge from the anterior horn cells to form

the ventral root or the motor root.

2) The sensory fibers bringing sensory information from various areas enter

the posterior horn. The nerve cell bodies of these sensory nervous are

situated little outside the spinal cord and constitute the dorsal root ganglion

(DRG). The are unipolar i.e. having are peripheral process which brings the

impulse from periphery and one central process.

3) The two roots viz, the motor and sensory, unite together, little outside the

spinal cord to form a mixed spinal nerve.

LAMINAR STRUCTURE OF SPINAL CORD:

- Concept of lamina in spinal cord was introduced by B Rexed in 1950’s.

After his work on the cats.

- General confirmation of laminar pattern in human material has been

provided by Schoenen (1973) and Schoenen and Faull (1990).

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- Based on neuronal size, shape, cytological features and density in different

region, 10 laminae have been distinguished.

- They are described in roman digits.

I to VI are found in posterior/ dorsal horn receive sensory afferent

cutaneous fibers e.g. pain, pressure, temp.

VII is found in lateral horn.

VIII & IX are found in lateral horn

X is found in centre.

Neurons:

Neuron is a structural and functional unit of the nervous system. It contains:

i) A nerve cell body or soma

ii) Its processes

i. Dendrite (endron-branch of a tree)

ii. Axon

All neurons contain one and only one axon but dendrite(s) may be absent,

one or many. In fact, in a given neuron, hundreds of dendrites may be present.

The axon carries the impulse from the soma to the other direction whereas a

dendrite brings impulse from a distance towards the soma.

Structure of Myelinated Nerve Fiber:

- The axons are sheathed by the tubula sheath called myelin sheath which is

surrounded by cells known as Schwan cells.

- Under the light microscopes, the axon shows constricted areas at regular

intervals known as the ‘nodes of Ranvier’.

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- Outside the axoplasm lies the myelin sheath. Outside the myelin sheath, the

external most sheath called Neurilemma exists.

- The myelin sheath is made up of lipid materials and in particular is rich in

sphingomyelin.

- Myelin has a whitish appearance. Great majority of n-fibers in our body are

myelinated nerves. The white matters of the brain or spinal cord or

preganglionic autonomic fibers look white because they are myelinated

fibers.

Non-myelinated nerve fibers:

- These fibers are smaller in diameter as there is no myelin sheath.

Importance of Myelin Sheath:

- Propagation of action potential (that is the wave of excitation is very fast in

myelinated nerve fiber but slow in the non-myelinated ones.

- This faster rate of conduction is because the salutatory conduction is

possible only in amyelinated nerve fiber but not in a non-myelinated fiber.

- To understand why so, we need to understand the action potential and the

basic properties of nerve fiber that is; excitability and conductivity.

Excitability:

Now, to understand this, we need to know the resting membrane potential

and action potential.

- There are plenty of ions present in the intra cellular fluid and the extra

cellular fluid. Cations are in excess just outside the resting cells. Cations are

positively charged particles. While just inside the membrane, anions

(negatively charged particles) are in excess.

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- Therefore if two electrodes are placed on a membrane of a resting cell, one

just outside it and another one just inside it and they be connected with a

suitable galvanometer, the galvanometer will record a potential difference.

So the potential difference across the cell membrane while the cell is at rest

will be known as ‘resting membrane potential’ (RMP).

- The potential difference is zero when the cell is in a resting state as the

concentration of anions and cations is equal across the cells membrane.

- This is called the ‘polarized state’ of the cell.

- On the other hand, when the cell is stimulated and becomes ‘active’, the

picture changes as follows: at the spot where the stimulus is applied, the

‘polarity is reversed’ i.e. inside becomes positive (in respect to outside) and

outside becomes negative.

- In other words, the spot at which the stimulus is applied, there is potential

difference between the external and internal surfaces of the membrane.

- This is known as the action potential.

Conductibility:

The conduction of an impulse by a nerve depends on the electrical potential

that exists across the nerve membrane. Although an electrical potential exists

across the membrane of most cells in the body, the nerve cell, being excitable,

possesses the ability of transmitting or conducting impulses along its length. This

phenomenon is brought about by the flow of current across the membrane during

the transition of the nerve from the resting to the active state.

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Depolarization:

When a stimulus of sufficient intensity to create an impulse is applied to the

nerve, the membrane is activated by an alteration in its permeability that permits

sodium to increase its rate of diffusion through the membrane into the nerve cell.

It appears that initiation of changes in membrane permeability to sodium

occurs as a result of displacement of calcium ions from a phospholipids binding

site. The marked increase in the diffusion of sodium into the cell is followed by

the passage of potassium out of the cell. This action is said to abolish the resting

potential and depolarize the membrane.

As a nerve is stimulated, there is a rapid (0.1 to 0.2 m sec) passage of

sodium into the cell and a lower (1 to 2 m sec) passage of potassium out of it. The

alteration in the permeability of the cell membrane that is initiated after an

adequate stimulus is applied is believed to be the result of the liberation of a

transmitter substance, acetylcholine at the site of stimulation.

All or none law:

- If a weak stimulus is applied, that will be no depolarization.

- Once the strength of the stimulus is adequate an action potential will

develop.

- However, supra adequate strong stimulus will no initiate a stronger action

potential. This is known as all or none law.

The passage of the impulse or the speed of action potential is the result of a

continuing stimulation or chain reaction. In larger myelinated nerves, the

stimulation takes place only at the nodes, with the impulse conducted along the

nerve fiber from node to node by its own energy.

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The jumping of impulse from node to node through the surrounding

interstitial tissue is called salutatory conduction which explains the greater rate of

speed at which the impulses are conducted in myelinated fibers.

Repolarization:

Following depolarization the permeability of the nerve membrane again

decreases while the high permeability to potassium is restored. Potassium moves

freely out of the cell, thereby restoring the original electromechanical equilibrium

and resting potential.

Synapses and Neurotransmitters:

Definition:-

Synapse is the junctional region between two neurons where information

from neuron is transmitted or relayed to another neuron, but there is no

protoplasmic connection between the two neurons.

The neurotransmitters are the chemicals secreted by nerve terminals. After

being released, they bind with their receptors situated at the effector – now the

effector is stimulated to activity. Acetylcholine is such neurotransmitter, there are

many other NTs secreted at various junctions in the body which we shall discuss

later.

CLASSIFICATION OF NERVE FIBERS:

A] Depending upon the structure:

1) Myeinated nerve fibers: They are covered by myelin sheath. E.g. as

fibers.

2) Non-myelinated nerve fibers:- They do not have myelin sheath. E.g. C

fibers.

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B] Depending upon the distribution:

1) Somatic nerve fibers: Supply the skeletal muscles of the body.

2) Visceral or autonomic nerve fibers: Supply the various internal organs of

the body.

C] Depending upon the source of origin:-

1) Cranial nerves:- Nerve fibers arising from brain are called cranial nerves.

13 pairs.

2) Spinal nerve:- Nerve fibers arising from spinal cord are called spinal

nerves.

D] Depending upon the Function:-

1) Motor nerve fibers:- Carry motor impulses from central nervous system to

different parts of body also called efferent fibers.

2) Sensory nerve fibers:- Carry sensory impulses from different parts of the

body to the central nervous system. Also known as afferent fibers.

E] Depending upon the neurotransmitters:-

1) Adrenergic nerve fibers:- Secrete noradrenaline

2) Chlinergic nerve fibers:- Secrete acetyl choline

F] Depending upon the diameter and conduction:

Type A fibers are typical myelinated fibers of spinal nerves. Type C fibers

are the small, unmyelinated fibers that conduct impulses at low velocities. C.fibers

constitute more than half of the sensory fibers in most peripheral nerves as well as

all the postganglionic autonomic fibers.

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The thing to be noted among these fibers is that, a few large fibers can

transmit impulses at velocities as great as 120 m/sec – a distance in 1 sec that is

longer than a football field.

On the other hand, the smallest fibers transmit impulses as slowly as 0.5

m/sec, requiring about 2 sec to go from the big toe to the spinal cord.

G] Alternate classification used by sensory physiology:-

Certain techniques have made it possible to separate A fibers into 2

subgroups but they cannot distinguish easily between A and A fiber.

Therefore, the following classification is used by sensory physiologists.

Group 1a: Fibers from the annulosiral endings of muscle spindles (average about

17 diameter these are A type fibers in general classification).

Group Ib: Fibers from the Golgi tendon organs (average about 16 diameter,

these also are 2 type A fibers).

Group II: Fibers from most discrete cutaneous tactile receptors and from the

flower-spray endings of the muscle spindles (average about 8 in diameter these

are and type A fibers in the general classification).

Group III: Fibers carrying temperature, crude touch and pricking pain sensations

(about 3 diameter they are -type A fibers in the general (classification).

Group IV: Unmyelinated fibers carrying pain, itch, temperature, crude touch

sensations (0.5 – 2 diameter, they are called type C fibers in general

classification).

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THE NEUROPHYSIOLOGY OF PAIN:

Purpose of pain:

Pain is unpleasant sensation no doubt, but on the whole it is usually

beneficial to the man (or animal). It’s a kind of alarm which warns us about the

presence of the injurious agent and that is why we seek removal of the injurious

agent by appropriate measure.

For e.g. In leprosy, the pain sensation in the affected region may be lost,

resulting in ignoring small cuts/ sores etc. Ultimately, the unattended wound may

enlarge and lead to much crippling deformities. However, in some cases, the

presence of pain may be a mere annoyance to the patient. For e.g. pain in incurable

forms of cancers or trigeminal neuralgia, only adds up to the misery of the patient.

Characteristics of Pain:

1. Threshold and intensity:-

If the intensity of the stimulus is below threshold (sub threshold), pain is

not felt. As the intensity increases more and more, pain is felt more and more

according to the Weber-Fechner’s law, which is as follows:

Suppose the intensity of the stimulus on a receptor is 10 (arbitary units) and

the sense perceived is 1 (arbitary unit) (i.e. a tenfold increment) the perception of

intensity will be only doubled, not tenfold because log of 100 is 2. Similarly, a 100

fold increase in stimulus intensity will increase the perception intensity only

threefold (log10 1000 = 3).

Mathematically it can be expressed as,

R = 2 log S

Where, R = intensity of the reaction (sense perceived)

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2 = a constant and

S = intensity of the stimulus

However, if mind is destracted, the threshold of pain increases. Severe

excitement and emotion can altogether abolish even a severe pain (endogenous

pain inhibiting system, explained later).

2) Adaptation:-

Pain receptors show no adaptation and so the pain continues as long as the

receptors continue to be stimulated.

3) Localisation of Pain:

Pain sensation is somewhat poorly localized. However, superficial pain is

comparatively better localized than deep pain visceral pain is usually referred.

4) Emotional Accompaniment:-

Pain sensations are commonly accompanied by emotions. These emotions

as a rule, are unpleasant.

5) Influence of the rate of damage on the intensity of pain:

If the rate of tissue injury (extent of damage per unit time) is high, intensity

of pain is also high and vice versa. Therefore, a very slowly growing tissue

damaging agent (e.g. Cancer at early stage) may not produce any pain at all.

6) Fast and slow pain:-

After receiving a nociceptive stimulus, two types of nerve fibers are

stimulated viz A and C.

Studies done by Dr. Narthi et al (1992) say that the sensation evoked by

stimulation of human teeth vary according to the type of stimuli applied. The pain

response produced is a 2 phase response, where the initial momentary sharp pain

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to external stimulus is generated by A fibers, because of their peripheral

location, low threshold of excitability and greater conduction speed.

On the other hand, continuous, constant or throbbing pain is a result of

sustained smaller C.fiber activity, they have much higher threshold of excitability.

As fibers can be stimulated without injuring the tissue, whereas C.fiber

stimulation is associated with tissue damage and inflammatory process.

Response of A and C fibers to special stimulus:

Differences in excitation of A and C fibers:

Receptors:

They may be considered as structures which catch the sensory stimulus.

From the receptors, emerge the afferent sensory which eventually reaches the

CNS.

These receptors are the first structures in the sensory path. Also called ‘end

organs’. “Base nerve endings” are the receptors of pain.

Pain receptors are also called “Nociceptors”.

They are specific to a certain kind of stimulus for e.g. a bare nerve ending,

a nociceptor will not be stimulated by light etc.

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CLASSIFICATION OF PAIN:

1) According to Site:

Pain

Somatic Visceral (from viscera)

e.g. angina pectoris / peptic ulcer/ renal colic etc.

Superficial Deep (from skin and subcutaneous From (muscles, bones, joints, tissue. E.g. superficial cuts/ fascia, periosteum)

burns etc. e.g. Fracture, slipped intervertebraldisc, arthritis etc.

II) According to Type:

Nociceptive Pain Neuropathic Pain

1) Caused by irritation to special nerve

endings (nociceptors).

1) Caused by dysfunction or damage to

the nervous system.

2) Associated with events such as

burning the hand, twisting the ankle etc.

2) Associated with evens such as injury,

disease, or trauma confined to a small

area due to an infection or a surgery.

3) Felt as dull or sharp aching pain and

mild to severe in nature.

3)Felt as sharp, intense and constant in

nature.

4) Typically controlled by removing the

irritation or medical treatment.

Responds well to mild pain medications

like NSAIDs or other drug therapies.

4) Responds poorly to standard pain

therapies such as mild analgesics and

other pain medications.

5) E.g. Sprained ankle (temporary)

cancer or arthritis – chronic.

5) Trigeminal neuralgia.

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PROCESSING OF PAIN:

Now, we know the anatomical and physiological components contributing

to the pain phenomenon, lets put them all together to understand processing of

pain.

Acute Pain Pathways:

The body has specialized neurons that respond only to noxious stimuli.

These neurons are called primary afferent nociceptors and are made up of small

diameter thinly myelinated. As and unmyelinatd C.fibers they synapse in the

substantia gelatinosa of the dorsal horn of the spinal cord with neurons known as

second order pain transmission neurons. From here these signals are transmitted

along specialized pathways (Spinothalamic and reticulothalamic tracts) to the

medial and lateral regions of the thalamus. Perception of nociception may occur in

the thalamus and cortex, but the exact location is unknown and the contribution of

the cortex to pain perception is controversial.

Fields divided processing of pain from the stimulation of primary afferent

nociceptors to the subjective experience of pain into 4 steps:

- Transduction

- Transmission

- Modulation and

- Perception

1) Transduction:

- Is the activation of the primary afferent nociceptor.

- These are activated by intense thermal and mechanical stimuli, noxious

chemicals and noxious cold.

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- They are also activated by stimulation from endogenous algesic chemical

substances (inflammatory mediator) produced by body in response to tissue

injury.

- Damaged tissue or blood cells release the polypeotide bradykinin (BK),

potassium, histamine, serotonin and arachidonic acid.

- Arachidonic acid is processed by two different enzyme systems to produce

prostaglandins and leukotrienes which along with BK act as inflammatory

mediators.

- Bradykinin acts synergistically with these other chemicals to increase

plasma extravasation and produce edema.

- Plasma extravasation, in turn, replenishes the supply of inflammatory

chemical mediators, whereas prostaglandins stimulate the primary afferent

nociceptor directly.

- The leukotrienes contribute indirectly by causing polymorphonuclear

neutrophil leukocytes to release another chemical, which in turn, stimulates

the nociceptor.

- In addition to sending nociceptive impulses to synapse in the dorsal horn of

the spinal cord, activation of cutaneous C.fibers causes their cell bodies to

synthesize neuropeptides, substance P and calcitonin gene related peptide.

- These neuropeptides are then antidromically transported along axon

branches to the periphery by an axon transport system where they induce

further plasma extravasation and increased inflammation.

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- The release of these algogenic substances at the peripheral axon injury site

produces the flare commonly seen around an injury site and is referred to as

neurogenic inflammation or the axon reflex.

2) Transmission:-

Refers to the process by which peripheral nocicpetive information is

relayed to the central nervous system.

A and C fibers from tooth / pulp

Synapse with the

2nd order pain transmission neurons

Through anterior and lateral spinothalamic tracts

Reaches thalamus

Through thalamocortical tract

Reach the

Post Central gyrus of cerebral cortex

- The lateral spinothalamic tract tansmits fast and direct sharp pain.

- The anterior spiothalamic tract transmits slow and indirect dull pain.

3) Modulation:

Refers to mechanisms by which the transmission of noxious information to

the brain is reduced. In the past, only midline structures such as the periaqueductal

gray and nucleus raphe magnus were known to be involved in descending

nociceptive modulation.

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Now many sites previously thought to be primarily involved in

cardiovascular function and autonomic regulation (e.g. nucleus tractus soliterius,

etc.) have also been shown to play a role in pain modulation.

The ascending nocicpetive signal that synapses in the midbrain area,

activates the release of norepinephrine and serotonin – two of the main

neurotransmitters involved in the descending inhibitory pathways.

The system works as follows:-

A bunch of descending fibers arise from periaqueductal gray

relay in magnus raphe nucleus situated in the midline at the junction of pons and

medulla

The next order neuron terminate at Substantia Gelatinosa situated at the tip of the

posterior horn of spinal cord

- Recall the first order neuron which carries pain from the periphery,

depicted as afferent pain carrying neuron, terminates at Substantia

gelatinosa.

- From there, the 2nd order neuron emerges which constitutes the

spinothalamic tract to terminate in the thalamus.

- The neurotransmitter at the synapse between terminal part of APC and

beginning of _____ is substance P.

- When the descending pain inhibiting system is stimulated, the terminal part

of DPI releases some endogenous opoid peptides as neurotransmitters at

substantia gelatinosa.

These endogenous opoid peptides cause inhibition of substance p.

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transmission block of pain sensation results

No pain is felt

When the DPI fibers are stimulated?

Ans: 1) When the limbic systemic stimulated. It is the seat of emotion. Fibers from

limbic system supply the periaquiductal gray.

2) Auto feedback – when spinothalamic tract is stimulated, collateral from the

tract can stimulate the descending pain inhibition system.

Acupuncture:

The Chinese have been practicing acupuncture since ancient times.

Recently it’s gaining popularity across the world. The procedure consists of

introducing sharp needle in selected spots such introductions cause local pain

which probably activates enkephalinergic and serotonergic pathways that descend

from brain stem to the dorsal horn of spinal cord. As a result an already existing

pain disappears.

THE DUAL NATURE OF PAIN:

All the pain transmission theories propose the dual nature of pain. It is the

pain perception and pain reaction.

As we just discussed,

Pain perception is the physioanatomical process whereby an impulse is

generated following application of adequate stimulus and is transmitted to

CNS. This aspect of pain is remarkably similar in all individuals.

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Pain reaction is a psychophysiological process that represents the individual’s

over manifestation of the unpleasant perception process that just occurred. This

phenomenon varies markedly from individual to individual.

If pain is to be controlled, both aspects of its nature must be considered.

Methods of pain control:

1. Removing the cause

2. Blocking the pathway of painful impulses Pain perception

3. Raising the pain threshold Affects Both

4. Preventing pain reaction by cortical depression Affects pain reaction

5. Using psychosomatic methods Patient counseling

Theories Explaining the Mechanism of Pain Transmission:

A) Specificity theory

B) Pattern theory

C) Gate control theory

a) Specificity theory:-

- Advanced by von-Frey 1894

- States that different sensory fibers mediate different sensory modalities

such as pain, heat, cold, touch and pressure.

- Free nerve endings were implicated as pain receptors. A pain center was

thought to exist within the brain, which was responsible for all overt

manifestations of the unpleasant experience.

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b) Pattern theory:-

- It suggested that particular pattern of nerve impulses that evoke pain are

produced by the summation of sensory input within the dorsal horn of the

spinal column.

- Pain results when the total output of the cells exceeds a critical level. E.g.

touch +pressure + heat might add up in such a manner that pain was the

modality experienced.

c) Gate control theory:-

- Proposed by Melrak and Wall in 1965

- According to this theory 2 factors control pain transmission

o Exhibition or stimulation of SG

o Endogenous pain inhibiting system which we discussed

a) Inhibition or stimulation of substantia gelatinosa:-

- Present in dorsal horn

- Contains small neurons with short ________

T-cells:-

- Present in lamina IV

- Adjacent to SG

- Larger than SG cells

- Form spinothalamic tract

Dendrites of T-cell synapse with SG cells.

Axons of large diameter fiber follows the same path.

SG cells send branches to synapse with incoming axion entering T-cell pool.

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The only activity that SG cells do is to send inhibitory impulses to the T-cells,

preventing pain propagation.

Large fibers Only excite SG cells (A , A , A )

Thus it sends inhibitory impulses to T cells

Gate closed (no pain)

Small fibers Only inhibit SG cells (As & c)

Thus stop SG cells to send inhibitory response to T-cells

Gate open (pain felt)

Referred Pain:

Pain arising from deep tissues, muscles, ligaments, joints and viscera is

often perceived at a site distant from the actual nociceptive source. Thus, pain of

angina pectoris is often felt in the left arm or jaw.

Referred pain presents a diagnostic dilemma. If left unrecognized, it may

misguide the clinician to believe that the patient is having psychogenic pain.

The mechanism of pain is still somewhat enigmatic. The two most popular

theories are:-

1) Convergence projection theory &

2) Convergence facilitation theory

1) Convergence Projection theory:-

- This is the most popular theory

- Primary nociceptors from both visceral and cutaneous neurons often

converge onto the same second order pain transmission neuron in the spinal

cord.

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- The brain has no way of knowing the actual source and mistakenly

projects the sensation to the somatic structure.

2) Convergence facilitation theory:-

- It is similar to convergence projection theory except that nociceptive input

from deeper structures causes the resting activity of the 2nd order pain

transmission neuron in the spinal cord to increase or be ‘facilitated’.

- The resting activity is normally created by impulses from the cutaneous

afferents. Facilitation from deeper nociceptive impulses cause pain to be

perceived in the area that creates normal, resting background activity.

- This theory tries to incorporate the clinical observation, that blocking

sensory input from the reference area, with either local anaesthetic or cold

can sometimes reduce perceived pain.

- This is particularly true with referred pain from myofascial trigger points

for which application of a vapor coolant spray is actually a popular and

effective modality of pain control.

CONCLUSION:

Physiology of pain is a complex phenomenon and inspite of lots of

advances in research, it still remains to be understood thoroughly. The knowledge

of the physiology of pain helps the clinician in understanding the probable origin

of pain and cure it appropriately.

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