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. ow lets have a loo! at the various
definitions, of course no single definition would be accepted by all.
Dorlands Medical Dictionar:
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.
"eecher #$%&%' described it as a sub(ective 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 in(ury to that individual.
According to his observations in $%&), it was noted that only *&+ of
soldiers wounded in battle re,uested narcotic medications for pain relief,
compared to more than -.+ of civilian patients with surgical wound of similar
magnitude.
$
The wounded soldier may be relieved to be out of life threatening situation
whereas the surgical patient may be concerned about the conse,uences afer the
surgery.
Fields:
/efined 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.
0e emphasi1ed the need to be able to locali1e the painful source in order to
distinguish it from psychological pain and suffering for e.g. the 2pain3 of a bro!en
heart4
Nocice!tion " Tiss#e Da$a%e:
A more complete definition is cast by the International Association for the
study of Pain #IA5P' in its taxonomy of painful disorders.
It says6 2Pain is an unpleasant sensory and emotional experience associated
with actual or potential tissue damage or described in terms of such damage3.
This definition emphasi1es that 2Pain is pain, even if a nociceptive source
is not readily identified3.
Though it is highly sub(ective, the pain owing to psychological causes is as
real as any pain associated with actual nociception and should be treated as such.
Mon&ei$s:
It is an unpleasant emotional experience usually initiated by a noxious
stimulus and transmitted over a speciali1ed neural networ! to the central nervous
system where it is interpreted as such.
*
"efore exploring the depths of pain physiology, lets have a brief loo! at the
neuroanatomy and functions of the nervous system of the human body.
Primarily, the nervous system is divided into two parts78
I' 9entral ervous 5ystem
a. "rain
b. 5pinal cord
II' Peripheral nervous system
a. Peripheral nerves and
b. Its ganglia
I: 9578
"rain is divided into cerebrum ; cerebellum ; mid brain ; pons ; medulla
continues as spinal cord.
II: P578
The P5 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 * subdivisions vi178
a' 5omatic nervous system
b' Autonomic nervous system
a' 5omatic ervous 5ystem78
Includes the nerves supplying the s!eletal muscles. Thus, the somatic
nervous system controls the movements of the body by acting on the s!eletal
muscles.
<
b' Autonomic ervous 5ystem78
It is concerned with regulation of visceral or vegetative functions. 5o, it is
otherwise called negative or involuntary nervous system. It consists of two
systems7
8 5ympathetic division
8 Parasympathetic division
ervous 5ystem
95 P5
"rain
9erebrum 5omatic 5 Autonomic 5
9erebellum
=id brain 5ympathetic Parasympathetic
Pons
=edulla
5pinal cord
SPINAL CORD:
8 It is the downward continuation of medulla and descends through the vertebral
canal and it ends at the lower border of the lumbar vertebra.
8 Its cross section on microscopic examination shows outer white matter
consisting of tracts either sensory #ascending' or motor #descending'.
8 The inner grey matter loo!s somewhat li!e >nglish alphabet 0.
?
Three @@@@@@ can be distinguished in it78
i' Anterior horn, gives rise to somatic motor nerves supplying s!eletal
muscles.
ii' Posterior horn, which receives the sensory nerve via the dorsal root
ganglion.
iii' Aateral horn, gives rise to sympathetic fibres only in the thoracic and
upper lumbar segments.
For$ation o' a $i(ed s!inal ner)e:
$' As stated (ust now, the axons emerge from the anterior horn cells to form
the ventral root or the motor root.
*' 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
#/BC'. The are unipolar i.e. having are peripheral process which brings the
impulse from periphery and one central process.
<' The two roots vi1, the motor and sensory, unite together, little outside the
spinal cord to form a mixed spinal nerve.
LAMINAR STRUCTUR* OF SPINAL CORD:
8 9oncept of lamina in spinal cord was introduced by " Bexed in $%&.Ds.
After his wor! on the cats.
8 Ceneral confirmation of laminar pattern in human material has been
provided by 5choenen #$%E<' and 5choenen and Faull #$%%.'.
&
8 "ased on neuronal si1e, shape, cytological features and density in different
region, $. laminae have been distinguished.
8 They are described in roman digits.
I to GI are found in posterior/ dorsal horn receive sensory afferent
cutaneous fibers e.g. pain, pressure, temp.
GII is found in lateral horn.
GIII H II are found in lateral horn
I is found in centre.
Ne#rons:
euron is a structural and functional unit of the nervous system. It contains7
i' A nerve cell body or soma
ii' Its processes
i. /endrite #endron8branch of a tree'
ii. Axon
All neurons contain one and only one axon but dendrite#s' may be absent,
one or many. In fact, in a given neuron, hundreds of dendrites may be present.
The axon carries the impulse from the soma to the other direction whereas a
dendrite brings impulse from a distance towards the soma.
Str#ct#re o' Melinated Ner)e Fi+er:
8 The axons are sheathed by the tubula sheath called myelin sheath which is
surrounded by cells !nown as 5chwan cells.
8 Jnder the light microscopes, the axon shows constricted areas at regular
intervals !nown as the Knodes of BanvierD.
)
8 Lutside the axoplasm lies the myelin sheath. Lutside the myelin sheath, the
external most sheath called eurilemma exists.
8 The myelin sheath is made up of lipid materials and in particular is rich in
sphingomyelin.
8 =yelin has a whitish appearance. Creat ma(ority of n8fibers in our body are
myelinated nerves. The white matters of the brain or spinal cord or
preganglionic autonomic fibers loo! white because they are myelinated
fibers.
Non,$elinated ner)e 'i+ers:
8 These fibers are smaller in diameter as there is no myelin sheath.
I$!ortance o' Melin S&eat&:
8 Propagation of action potential #that is the wave of excitation is very fast in
myelinated nerve fiber but slow in the non8myelinated ones.
8 This faster rate of conduction is because the salutatory conduction is
possible only in amyelinated nerve fiber but not in a non8myelinated fiber.
8 To understand why so, we need to understand the action potential and the
basic properties of nerve fiber that is6 excitability and conductivity.
*(cita+ilit:
ow, to understand this, we need to !now the resting membrane potential
and action potential.
8 There are plenty of ions present in the intra cellular fluid and the extra
cellular fluid. 9ations are in excess (ust outside the resting cells. 9ations are
positively charged particles. While (ust inside the membrane, anions
#negatively charged particles' are in excess.
E
8 Therefore if two electrodes are placed on a membrane of a resting cell, one
(ust outside it and another one (ust inside it and they be connected with a
suitable galvanometer, the galvanometer will record a potential difference.
5o the potential difference across the cell membrane while the cell is at rest
will be !nown as Kresting membrane potentialD #B=P'.
8 The potential difference is 1ero when the cell is in a resting state as the
concentration of anions and cations is e,ual across the cells membrane.
8 This is called the Kpolari1ed stateD of the cell.
8 Ln the other hand, when the cell is stimulated and becomes KactiveD, the
picture changes as follows7 at the spot where the stimulus is applied, the
Kpolarity is reversedD i.e. inside becomes positive #in respect to outside' and
outside becomes negative.
8 In other words, the spot at which the stimulus is applied, there is potential
difference between the external and internal surfaces of the membrane.
8 This is !nown as the action potential.
Cond#cti+ilit:
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.
-
De!olari-ation:
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 mar!ed 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 depolari1e the membrane.
As a nerve is stimulated, there is a rapid #..$ to ..* m sec' passage of
sodium into the cell and a lower #$ to * m sec' passage of potassium out of it. The
alteration in the permeability of the cell membrane that is initiated after an
ade,uate 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 la.:
8 If a wea! stimulus is applied, that will be no depolari1ation.
8 Lnce the strength of the stimulus is ade,uate an action potential will
develop.
8 0owever, supra ade,uate strong stimulus will no initiate a stronger action
potential. This is !nown 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 ta!es place only at the nodes, with the impulse conducted along the
nerve fiber from node to node by its own energy.
%
The (umping 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.
Re!olari-ation:
Following depolari1ation 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 e,uilibrium
and resting potential.
Sna!ses and Ne#rotrans$itters:
/efinition78
5ynapse is the (unctional 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 Ts secreted at various (unctions in the body which we shall discuss
later.
CLASSIFICATION OF N*R/* FI0*RS:
A: /epending upon the structure7
$' =yeinated nerve fibers7 They are covered by myelin sheath. >.g. as
fibers.
*' on8myelinated nerve fibers78 They do not have myelin sheath. >.g. 9
fibers.
$.
": /epending upon the distribution7
$' 5omatic nerve fibers7 5upply the s!eletal muscles of the body.
*' Gisceral or autonomic nerve fibers7 5upply the various internal organs of
the body.
9: /epending upon the source of origin78
$' 9ranial nerves78 erve fibers arising from brain are called cranial nerves.
$< pairs.
*' 5pinal nerve78 erve fibers arising from spinal cord are called spinal
nerves.
/: /epending upon the Function78
$' =otor nerve fibers78 9arry motor impulses from central nervous system to
different parts of body also called efferent fibers.
*' 5ensory nerve fibers78 9arry sensory impulses from different parts of the
body to the central nervous system. Also !nown as afferent fibers.
>: /epending upon the neurotransmitters78
$' Adrenergic nerve fibers78 5ecrete noradrenaline
*' 9hlinergic nerve fibers78 5ecrete acetyl choline
F: /epending upon the diameter and conduction7
Type A fibers are typical myelinated fibers of spinal nerves. Type 9 fibers
are the small, unmyelinated fibers that conduct impulses at low velocities. 9.fibers
constitute more than half of the sensory fibers in most peripheral nerves as well as
all the postganglionic autonomic fibers.
$$
The thing to be noted among these fibers is that, a few large fibers can
transmit impulses at velocities as great as $*. m/sec ; a distance in $ sec that is
longer than a football field.
Ln the other hand, the smallest fibers transmit impulses as slowly as ..&
m/sec, re,uiring about * sec to go from the big toe to the spinal cord.
C: Alternate classification used by sensory physiology78
9ertain techni,ues have made it possible to separate A fibers into *
subgroups but they cannot distinguish easily between A and A fiber. Therefore,
the following classification is used by sensory physiologists.
Croup $a7 Fibers from the annulosiral endings of muscle spindles #average about
$E diameter these are A type fibers in general classification'.
Croup Ib7 Fibers from the Colgi tendon organs #average about $) diameter,
these also are * type A fibers'.
Croup II7 Fibers from most discrete cutaneous tactile receptors and from the
flower8spray endings of the muscle spindles #average about - in diameter these
are and type A fibers in the general classification'.
Croup III7 Fibers carrying temperature, crude touch and pric!ing pain sensations
#about < diameter they are 8type A fibers in the general #classification'.
Croup IG7 Jnmyelinated fibers carrying pain, itch, temperature, crude touch
sensations #..& ; * diameter, they are called type 9 fibers in general
classification'.
$*
TH* N*UROPHYSIOLOGY OF PAIN:
P#r!ose o' !ain:
Pain is unpleasant sensation no doubt, but on the whole it is usually
beneficial to the man #or animal'. ItDs a !ind of alarm which warns us about the
presence of the in(urious agent and that is why we see! removal of the in(urious
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. Jltimately, the unattended wound may
enlarge and lead to much crippling deformities. 0owever, 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.
C&aracteristics o' Pain:
12 T&res&old and intensit:,
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 Weber8FechnerDs law, which is as follows7
5uppose the intensity of the stimulus on a receptor is $. #arbitary units' and
the sense perceived is $ #arbitary unit' #i.e. a tenfold increment' the perception of
intensity will be only doubled, not tenfold because log of $.. is *. 5imilarly, a $..
fold increase in stimulus intensity will increase the perception intensity only
threefold #log$. $... M <'.
=athematically it can be expressed as,
B M * log 5
Where, B M intensity of the reaction #sense perceived'
$<
* M a constant and
5 M intensity of the stimulus
0owever, if mind is destracted, the threshold of pain increases. 5evere
excitement and emotion can altogether abolish even a severe pain #endogenous
pain inhibiting system, explained later'.
34 Ada!tation:,
Pain receptors show no adaptation and so the pain continues as long as the
receptors continue to be stimulated.
54 Localisation o' Pain:
Pain sensation is somewhat poorly locali1ed. 0owever, superficial pain is
comparatively better locali1ed than deep pain visceral pain is usually referred.
64 *$otional Acco$!ani$ent:,
Pain sensations are commonly accompanied by emotions. These emotions
as a rule, are unpleasant.
74 In'l#ence o' t&e rate o' da$a%e on t&e intensit o' !ain:
If the rate of tissue in(ury #extent of damage per unit time' is high, intensity
of pain is also high and vice versa. Therefore, a very slowly growing tissue
damaging agent #e.g. 9ancer at early stage' may not produce any pain at all.
84 Fast and slo. !ain:,
After receiving a nociceptive stimulus, two types of nerve fibers are
stimulated vi1 A and 9.
5tudies done by /r. arthi et al #$%%*' say that the sensation evo!ed by
stimulation of human teeth vary according to the type of stimuli applied. The pain
$?
response produced is a * phase response, where the initial momentary sharp pain
to external stimulus is generated by A fibers, because of their peripheral location,
low threshold of excitability and greater conduction speed.
Ln the other hand, continuous, constant or throbbing pain is a result of
sustained smaller 9.fiber activity, they have much higher threshold of excitability.
As fibers can be stimulated without in(uring the tissue, whereas 9.fiber
stimulation is associated with tissue damage and inflammatory process.
Res!onse o' A and C 'i+ers to s!ecial sti$#l#s:
Di''erences in e(citation o' A and C 'i+ers:
Rece!tors:
They may be considered as structures which catch the sensory stimulus.
From the receptors, emerge the afferent sensory which eventually reaches the
95.
These receptors are the first structures in the sensory path. Also called Kend
organsD. 2"ase nerve endings3 are the receptors of pain.
Pain receptors are also called 2ociceptors3.
They are specific to a certain !ind of stimulus for e.g. a bare nerve ending,
a nociceptor will not be stimulated by light etc.
$&
CLASSIFICATION OF PAIN:
$' According to 5ite7
Pain
5omatic Gisceral
#from viscera'
e.g. angina pectoris / peptic
ulcer/ renal colic etc.
5uperficial /eep
#from s!in and subcutaneous From #muscles, bones, (oints,
tissue. >.g. superficial cuts/ fascia, periosteum'
burns etc. e.g. Fracture, slipped intervertebral
disc, arthritis etc.
II' According to Type7
ociceptive Pain europathic Pain
$' 9aused by irritation to special nerve
endings #nociceptors'.
$' 9aused by dysfunction or damage to
the nervous system.
*' Associated with events such as
burning the hand, twisting the an!le etc.
*' Associated with evens such as in(ury,
disease, or trauma confined to a small
area due to an infection or a surgery.
<' Felt as dull or sharp aching pain and
mild to severe in nature.
<'Felt as sharp, intense and constant in
nature.
?' Typically controlled by removing the
irritation or medical treatment.
Besponds well to mild pain medications
li!e 5AI/s or other drug therapies.
?' Besponds poorly to standard pain
therapies such as mild analgesics and
other pain medications.
&' >.g. 5prained an!le #temporary'
cancer or arthritis ; chronic.
&' Trigeminal neuralgia.
PROC*SSING OF PAIN:
$)
ow, we !now the anatomical and physiological components contributing
to the pain phenomenon, lets put them all together to understand processing of
pain.
Ac#te Pain Pat&.as:
The body has speciali1ed 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 9.fibers they synapse in the
substantia gelatinosa of the dorsal horn of the spinal cord with neurons !nown as
second order pain transmission neurons. From here these signals are transmitted
along speciali1ed pathways #5pinothalamic 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 un!nown 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 sub(ective experience of pain into ? steps7
8 Transduction
8 Transmission
8 =odulation and
8 Perception
14 Transd#ction:
8 Is the activation of the primary afferent nociceptor.
8 These are activated by intense thermal and mechanical stimuli, noxious
chemicals and noxious cold.
$E
8 They are also activated by stimulation from endogenous algesic chemical
substances #inflammatory mediator' produced by body in response to tissue
in(ury.
8 /amaged tissue or blood cells release the polypeotide brady!inin #"N',
potassium, histamine, serotonin and arachidonic acid.
8 Arachidonic acid is processed by two different en1yme systems to produce
prostaglandins and leu!otrienes which along with "N act as inflammatory
mediators.
8 "rady!inin acts synergistically with these other chemicals to increase
plasma extravasation and produce edema.
8 Plasma extravasation, in turn, replenishes the supply of inflammatory
chemical mediators, whereas prostaglandins stimulate the primary afferent
nociceptor directly.
8 The leu!otrienes contribute indirectly by causing polymorphonuclear
neutrophil leu!ocytes to release another chemical, which in turn, stimulates
the nociceptor.
8 In addition to sending nociceptive impulses to synapse in the dorsal horn of
the spinal cord, activation of cutaneous 9.fibers causes their cell bodies to
synthesi1e neuropeptides, substance P and calcitonin gene related peptide.
8 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.
$-
8 The release of these algogenic substances at the peripheral axon in(ury site
produces the flare commonly seen around an in(ury site and is referred to as
neurogenic inflammation or the axon reflex.
34 Trans$ission:,
Befers to the process by which peripheral nocicpetive information is
relayed to the central nervous system.
A and 9 fibers from tooth / pulp
5ynapse with the
*
nd
order pain transmission neurons
Through anterior and lateral spinothalamic tracts
Beaches thalamus
Through thalamocortical tract
Beach the
Post 9entral gyrus of cerebral cortex
8 The lateral spinothalamic tract tansmits fast and direct sharp pain.
8 The anterior spiothalamic tract transmits slow and indirect dull pain.
54 Mod#lation:
Befers to mechanisms by which the transmission of noxious information to
the brain is reduced. In the past, only midline structures such as the peria,ueductal
gray and nucleus raphe magnus were !nown to be involved in descending
nociceptive modulation.
$%
ow 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 wor!s as follows78
A bunch of descending fibers arise from peria,ueductal gray

relay in magnus raphe nucleus situated in the midline at the (unction of pons and
medulla

The next order neuron terminate at 5ubstantia Celatinosa situated at the tip of the
posterior horn of spinal cord
8 Becall the first order neuron which carries pain from the periphery, depicted
as afferent pain carrying neuron, terminates at 5ubstantia gelatinosa.
8 From there, the *
nd
order neuron emerges which constitutes the
spinothalamic tract to terminate in the thalamus.
8 The neurotransmitter at the synapse between terminal part of AP9 and
beginning of @@@@@ is substance P.
8 When the descending pain inhibiting system is stimulated, the terminal part
of /PI releases some endogenous opoid peptides as neurotransmitters at
substantia gelatinosa.

These endogenous opoid peptides cause inhibition of substance p.

*.
transmission bloc! of pain sensation results

o pain is felt
When the /PI fibers are stimulatedO
Ans7 $' When the limbic systemic stimulated. It is the seat of emotion. Fibers from
limbic system supply the peria,uiductal gray.
*' Auto feedbac! ; when spinothalamic tract is stimulated, collateral from the tract
can stimulate the descending pain inhibition system.
Ac#!#nct#re:
The 9hinese have been practicing acupuncture since ancient times.
Becently itDs gaining popularity across the world. The procedure consists of
introducing sharp needle in selected spots such introductions cause local pain
which probably activates en!ephalinergic and serotonergic pathways that descend
from brain stem to the dorsal horn of spinal cord. As a result an already existing
pain disappears.
TH* DUAL NATUR* OF PAIN:
All the pain transmission theories propose the dual nature of pain. It is the
pain perception and pain reaction.
As we (ust discussed,
Pain perception is the physioanatomical process whereby an impulse is
generated following application of ade,uate stimulus and is transmitted to
95. This aspect of pain is remar!ably similar in all individuals.
*$
Pain reaction is a psychophysiological process that represents the individualDs
over manifestation of the unpleasant perception process that (ust occurred. This
phenomenon varies mar!edly from individual to individual.
If pain is to be controlled, both aspects of its nature must be considered.
Met&ods o' !ain control:
$. Bemoving the cause
*. "loc!ing the pathway of painful impulses Pain perception
<. Baising the pain threshold Affects "oth
?. Preventing pain reaction by cortical depression Affects pain reaction
&. Jsing psychosomatic methods Patient counseling
T&eories *(!lainin% t&e Mec&anis$ o' Pain Trans$ission:
A' 5pecificity theory
"' Pattern theory
9' Cate control theory
a' 5pecificity theory78
8 Advanced by von8Frey $-%?
8 5tates that different sensory fibers mediate different sensory modalities
such as pain, heat, cold, touch and pressure.
8 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.
**
b' Pattern theory78
8 It suggested that particular pattern of nerve impulses that evo!e pain are
produced by the summation of sensory input within the dorsal horn of the
spinal column.
8 Pain results when the total output of the cells exceeds a critical level. >.g.
touch Ppressure P heat might add up in such a manner that pain was the
modality experienced.
c' Cate control theory78
8 Proposed by =elra! and Wall in $%)&
8 According to this theory * factors control pain transmission
o >xhibition or stimulation of 5C
o >ndogenous pain inhibiting system which we discussed
a' Inhibition or stimulation of substantia gelatinosa78
8 Present in dorsal horn
8 9ontains small neurons with short @@@@@@@@
T8cells78
8 Present in lamina IG
8 Ad(acent to 5C
8 Aarger than 5C cells
8 Form spinothalamic tract
/endrites of T8cell synapse with 5C cells.
Axons of large diameter fiber follows the same path.
5C cells send branches to synapse with incoming axion entering T8cell pool.
*<
The only activity that 5C cells do is to send inhibitory impulses to the T8cells,
preventing pain propagation.
Aarge fibers Lnly excite 5C cells
#A , A , A '
Thus it sends inhibitory impulses to T cells

Cate closed #no pain'

5mall fibers Lnly inhibit 5C cells
#As H c'
Thus stop 5C cells to send inhibitory response to T8cells

Cate open #pain felt'

Re'erred Pain:
Pain arising from deep tissues, muscles, ligaments, (oints 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 (aw.
Beferred pain presents a diagnostic dilemma. If left unrecogni1ed, 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 are78
$' 9onvergence pro(ection theory H
*' 9onvergence facilitation theory
$' 9onvergence Pro(ection theory78
8 This is the most popular theory
8 Primary nociceptors from both visceral and cutaneous neurons often
converge onto the same second order pain transmission neuron in the spinal
cord.
*?
8 The brain has no way of !nowing the actual source and mista!enly
pro(ects the sensation to the somatic structure.
*' 9onvergence facilitation theory78
8 It is similar to convergence pro(ection theory except that nociceptive input
from deeper structures causes the resting activity of the *
nd
order pain
transmission neuron in the spinal cord to increase or be KfacilitatedD.
8 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 bac!ground activity.
8 This theory tries to incorporate the clinical observation, that bloc!ing
sensory input from the reference area, with either local anaesthetic or cold
can sometimes reduce perceived pain.
8 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 !nowledge
of the physiology of pain helps the clinician in understanding the probable origin
of pain and cure it appropriately.
*&