PAIN AND PAIN

PATHWAYS

Presented by:
Dr. Dhwani Gohil
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"I don't accept the maxim 'there's no

gain without pain', physical or
emotional. I believe it is possible to
develop and grow with joy rather than
grief. However, when the pain comes
my way, I try to get the most growth
out of it." ~Alexa McLaughlin
2

CONTENTS
Introduction
Definition
History
Incidence
Related Terms
Characteristics of pain
Classification
Pain receptors
Neural pain pathways
Sensory neurons
Peripheral mechanism of injury induced pain
Theories of pain
Pain pathways
Dual pain pathway
Pain pathway of Maxillofacial Region
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 Modulation of pain
Factors affecting pain
Visceral pain
Referred pain
Phantom limb pain
Inhibition of pain
Diagnosis
Treatment
Conclusion
References

INTRODUCTION
Pain is a sensory experience of special significance to physicians and
basic scientists.
Pain is the commonest symptom which physicians are called upon to
treat.
Apart from its obvious applied value, study of physiology of pain has
taught us a lot about neural function in general.
Pain is an intensely subjective experience, and is therefore difficult to
describe.

 But it has two features which are nearly universal. First, it is an

unpleasant experience; and secondly, it is evoked by a stimulus which is
actually or potentially damaging to living tissues.
That is why, although it is unpleasant, pain serves a protective function
by making us aware of actual or impending damage to the body.
Like all sensory experiences, pain has two components, the first
component is the awareness of a painful stimulus and the second is the
emotional impact (or effect) evoked by the experience.

 While the awareness is localized to the area stimulated, the experience involves the
whole being.
That is why even when only a finger is hurt, the whole person suffers.
The two components of pain also imply that the same painful experience may
evoke widely different degrees of suffering in different persons, and even in the
same person under different circumstances.
From a physiological point of view, there are two types of pain. One, fast pain, is
conducted by faster conducting myelinated fibers, is well localized, and is sharp or
pricking in character. The other, slow pain is conducted by slower conducting
unmyelinated fibers, is poorly localized, and is burning or dull and aching in
character.

DEFINITION OF PAIN
The International Association for the Study of Pain
Pain is "an unpleasant sensory and emotional experience
associated with actual or potential tissue damage, or described in
terms of such damage"
Monheim : An unpleasant emotional experience usually
initiated by noxious stimulus and transmitted over a specialized
neural network to the CNS where it is interpreted as such.

HISTORY
Derived from Latin -Poena meaning punishment from God.
Homer thought pain was due to arrows shot by God.
Aristotle, who probably was the first to distinguish five physical senses
considered pain to the passion of the soul that somehow resulted from
the intensification of other sensory experience.

 Plato contented, pain and pleasure arose from within the body,
an idea that perhaps gave birth to the concept that pain is an
emotional experience more than a localized body disturbance.
The Bible makes reference to pain not only in relationship to
injury and illness but also an anguish of the soul.

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INCIDENCE OF PAIN
According to Cohen It was found that 21.8% of
adult in the United States experience orofacial
pain symptoms within 6 months of study.
The most common pain was toothache, which
was estimated to have occurred in 12.3% of the
population

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RELATED TERMS
Allodynia
Hyperalgesia & hypoalgesia
Hyperesthesia & hypoesthesia
Hyperpathia
Causalgia
Neuralgia

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CHARECTERISTICS OF PAIN
1. Threshold and Intensity
. If the intensity of the stimulus is below the threshold (sub-threshold)
pain is not felt. As the intensity increases more and more, pain is felt
more and more according to the Weber-Fechners law. This law
ensures that while our body can perceive pain due to low intensity
stimulus, a severe crushing injury will not cause death due to pain
sensation, yet as stimulus increases, sense of perception also
increases.

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2. Adaptation Pain receptors show no adaptation and so the pain

continues as long as receptors continue to be stimulated.
3. Localization of pain - Pain sensation is somewhat poorly localized.
However superficial pain is comparatively better localized than deep
pain.
4. Influence of the rate of damage on intensity of pain
If the rate of tissue injury (extent of damage per unit time) is high,
intensity of pain is also high.

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CLASSIFICATION OF PAIN
PAIN

Somatic
(somasthetic)

Superficial (from skin &

subcutaneous tissue) e.g.
superficial cuts/burns, etc.

Visceral (from viscera)

e.g. angina pectoris,
peptic ulcer, intestinal
colic, renal colic, etc.
Deep (from
muscles/bones/fascia/periosteum)
e.g. fractures/arthritis/fibrositis,
rupture of muscle belly
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 Fast pain within 0.1 sec

Slow pain after 1 sec or more : Associated with tissue destruction
PRACTICAL CLINICAL CLASSIFICATION OF CARNIO FACIAL PAIN

General
Classification

Origin of Pain

Quality of Pain

Extra cranial
Structure

Craniofacial region

Varies

Referred pain from

remote pathologic
sites

Distant organs and

structures

Aching and
pressing

Intracranial
pathosis

Brain and related

structures

Varies

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Neurovascular

Blood Vessels

Throbbing,
pulsing or
pounding

Neuropathic

Sensory nervous
system

Shooting, sharp,
burning pain

Causalgic

Sympathetic
nervous system

Burning

Muscular

Muscles

Deep aching, tight

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It can be also classified as :Typical Pain Disorders

Periodontalgia
Neuralgic (trigeminal neuralgia)
Vascular (migraine, cluster
headache)
Otic (Otitis media)
Sinus (Sinusitis)
Heart (cariogenic jaw pain)
Salivary gland Disorder
Musculo skeletal disorder

Atypical Pain Disorders

Causalgia
Reflex sympathetic dystrophy
Atypical facial pain
Phantom tooth pain
Neuralgia including
cavitational osteonecrosis

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PAIN RECEPTORS

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 Sensory Receptors :
Sensory input from various external stimuli is thought to be received by
specific peripheral receptors that act as transducers and transmit by nerve
action potentials along specific nerve pathways toward the central nervous
system.
Termed firstorder afferents, these peripheral terminals of afferent nerve
fibers differ in the form of energy to which they respond at their respective
lowest stimulus intensity, that is, are differentially sensitive.
The impulse interpreted is nociceptive (causing pain) if it exceeds the pain
threshold, that is, the intensity of the stimulus is so great that the receptor is no
longer differentially sensitive.

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SENSORY RECEPTORS
SENSES

GENERAL

SOMATIC

SUPERFICIAL
Touch-pressure
Thermal
Pain

SPECIAL

VISCERAL

DEEP

Pain
Baroreception
Chemoreception

Pain
Proprioception

Visual
Audition
Olfaction
Gustation

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 Cutaneous Receptors:
The perception of different kinds of sensation has demonstrated the existence of sensory
spots in the skin. These sensory spots are thought to contain receptors which are
distinguished by the form of stimulus that excites them and their location within the skin,
and are distinguished morphologically as corpuscular and noncorpuscular.
The pacinian corpuscles, in particular, are highly sensitive mechanoreceptors which
respond to rapid mechanical changes, and are especially responsive to vibration. Other
mechanoreceptors are the Meissner corpuscles, Golgi Mazzoni corpuscles, Ruffinis
ending and Krause bulb.
Although, electron microscopy has defined the presence of many receptors structurally,
functionally three categories of cutaneous receptors are thought to exist:
mechanoreceptors, thermo receptors, and nociceptors.

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NOCICEPTORS
A nerve ending that responds to noxious stimuli that can actually or
potentially produce tissue damage.
Free nerve endings i.e., they are not enclosed in a capsule. The receptors for
fast pain are sensitive to mechanical or thermal stimuli of noxious strength.
The receptors for slow pain are sensitive not only to noxious mechanical and
thermal stimuli but also to a wide variety of chemicals associated with
inflammation.

These substances include histamine, serotonin, bradykinin,

acetylcholine, potassium ions and hydrogen ions. It is possible that
noxious mechanical and thermal stimuli also act through the release of
some of these chemicals.

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 Since pain receptors respond to a wide variety of stimuli, they

are called polymodal.

Types of nociceptors :
A Mechanical Nociceptors
C Polymodal Nociceptors
C fibre mechanical nociceptors
High threshold cold nociceptors

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Mechanoreceptors
Mechanoreceptors, which respond to tactile non painful stimuli, can be
assessed psychophysically by the ability of a human subject to discriminate
whether application of a two blunt-point stimuli is perceived as one or two
points.
These receptors are divided into two functional groups (rapidly or slowly
adapting) depending on their response during stimuli.
Rapidly adapting mechanoreceptors respond at the onset and offset of the
stimuli, while slowly adapting mechanoreceptors respond throughout the
stimuli duration.

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Mechanoreceptors can be divided into those expressed in:

Hairy skin (hair follicle receptors):
Low threshold, rapidly adapting.
Three major subtypes: down, guard, tylotrich.
Glabrous (hairless) skin:
Small receptive fields.
Two major subtypes: Meisseners capsule (rapidly adapting) and Merkels
disc (slowly adapting).

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 Proprioception (limb position sense), which refers tooth position

and movement of the limbs (kinaesthesia), is determined by
mechanoreceptors located in skin, joint capsules and muscle
spindles.
The CNS integrates information received from these receptors,
while keeping track of previous motor responses that initiated limb
movement a process known as efferent copy or corollary
discharge (reviewed by Matthews, 1982).

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C fibre mechano heat sensitive

nociceptors

These fibres are considered polymodal, as they respond to mechanical,

heat, cold and chemical stimuli.
Their monotonic increase in activity evokes a burning pain sensation at
the thermal threshold in humans (4149C).
CMH responses are affected by stimuli history and are subject to
fatigue and sensitization modulation.

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A-fibre mechano-heat-sensitive nociceptors

Activation of these receptors is interpreted as sharp prickling or aching pain.
Owing to their relatively rapid conduction velocities (536 m/s), they are
responsible for first pain. Two subclasses of AMHs exist: types I and II.
Type I fibres respond to high magnitude heat, mechanical and chemical stimuli
and are termed polymodal AMHs. They are found in both hairy and glabrous
skin.
Type II nociceptors are found exclusively in hairy skin. They are mechanically
insensitive and respond to thermal stimulation in much the same way as CMHs
(early peak and slowly adapting response) and are ideally suited to signal the first
pain response.

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Deep tissue nociceptors

Unlike cutaneous pain, deep pain is diffuse and difficult to localize, with no
discernable fast (first pain) and slow (second pain) components. In many cases
deep tissue pain is associated with autonomic reflexes (e.g. sweating,
hypertension and tachypnoea).

Units that do not respond to mechanical stimuli have been termed silent
nociceptors. Silent nociceptors are also present within the viscera.
Silent visceral afferents fail to respond to innocuous or noxious stimuli,
but become responsive under inflammatory conditions.
Visceral afferents are mostly polymodal C- and A-fibres.

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Summary of receptor types

A - fibres

A - fibres

C- fibres

Threshold

Low

Medium

High

Axon diameter

6-14m

1-6m

0.2-1m

Myelination

Yes

Thinly

No

Velocity

36-90

5-36

0.2-1

Receptor types

Mechanoreceptor

Mechano/Nocice
ptor

Nociceptor

Receptive field

Small

Small

Large

Quality

Touch

Sharp/first pain

Dull/second pain

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NEURAL PAIN PATHWAYS

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 Nociception is the neural mechanism by which an individual detects the presence of a potentially
tissue harming stimulus. There is no implication of (or requirement for) awareness of this stimulus.
The nociceptive mechanism (prior to the perceptive event) consists of a multitude of events as
follows:
Transduction:
This is the conversion of one form of energy to another. It occurs at a variety of stages along the
nociceptive pathway from:
Stimulus events to chemical tissue events.
Chemical tissue and synaptic cleft events to
- Electrical events in neurones.
Electrical events in neurones to chemical events at synapses.

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 Transmission:
Electrical events are transmitted along neuronal pathways, while
molecules in the synaptic cleft transmit information from one cell
surface to another.
Modulation:
The adjustment of events, by up- or down regulation. This can
occur at all levels of the nociceptive pathway, from tissue, through
primary (1) afferent neurone and dorsal horn, to higher brain
centres.

Thus, the pain pathway as described by Descartes has had to

be adapted with time.

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SENSORY NEURONS

First Order

Second Order

Third Order

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First Order Neuron

Each sensory receptor is attached to a first order primary afferent neuron that
carries the impulses to the CNS.
The axons of these first-order neurons are found to have varying thickness. It
has long been known that a relationship exists between the diameter of nerve
fibers and their conduction velocities. The larger fibers conduct impulses more
rapidly than smaller fibers.
A general classification of neurons divides the larger fibers from the smaller
ones.

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Type A fibers
Alpha fibers: size - 13 to 20 m, velocity - 70 to 120 m/ s.
Beta fibers: size 6 to 13 m, velocity 40 to 70 m/s.
Gamma fibers: size 3 to 8 m, velocity 15 to 40 m/s.
Delta fibers: size 1 to 5 m, velocity 5 to 15 m/s.

Type C fibers
Size 0.5 to 1 m, velocity 0.5 to 2 m/s.

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Second Order Neuron

The primary afferent neuron carries impulse into the CNS and
synapses with the second-order neuron.
This second-order neuron is sometimes called a transmission
neuron since it transfers the impulse on to the higher centers.
The synapse of the primary afferent and the second-order neuron
occurs in the dorsal horn of the spinal cord.

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Third Order Neuron

Cell bodies of third order neurons of the nociception-relaying
pathway are housed in: the ventral posterior lateral, the ventral
posterior inferior, and the intralaminar thalamic nuclei
Third order neuron fibers from the thalamus relay thermal sensory
information to the somesthetic cortex.

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PERIPHERAL MECHANISMS OF INJURY

INDUCED OR INFLAMMATORY PAIN
Nociceptor activation is dynamically modulated by the magnitude of stimuli.
Therefore, it is not surprising that supra-threshold or tissue-damaging stimuli alter
subsequent nociceptor responses.
Overt tissue damage, or inflammation, causes the sensation of pain.
The most common symptom of on-going or chronic pain states is tenderness of
the affected area. This tenderness, or lowered threshold for stimulation-induced
pain is termed hyperalgesia.

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Hyperalgesia, or lowered-threshold to thermal and mechanical stimuli, occurs at

the site of trauma (primary hyperalgesia).
Uninjured tissue around this area also becomes sensitized, but to mechanical
stimuli only (secondary hyperalgesia or allodynia).
Peripheral sensitization mediates primary hyperalgesia to thermal stimuli.
Campbell and Meyer illustrated that CMHs become sensitized to burn injuries in
hairy skin, but fail to do so in glabrous skin, where AMH become sensitized for
heat hyperalgesia.

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Sensitization of nociceptors:
inflammation
Tissue injury results in complex sequelae procured in part by the recruitment of
inflammatory mediators. The inflammatory reaction rapidly proceeds in order to remove
and repair damaged tissue after injury. Pain develops in order to protect the organism from
further damage. The affected area typically becomes:
Red (rubor).
Hot (calor): as a result of increased blood flow.
Swollen (tumor): due to vascular permeability.
Functionally compromised (function lasea).
Painful (dolor): as a result of activation and sensitization of primary afferent nerve fibres.

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Sensitization occurs due to the release of chemical inflammatory

mediators from damaged cells.
A number of mediators directly activate nociceptors, while nonnociceptive afferents remain unaffected.
Others act on local microvasculature causing the release of further
chemical mediators from mast cells and basophils, which then attract
additional leucocytes to the site of inflammation.

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NEUROCHEMISTRY OF
NOCICEPTIVE PAIN
The peripheral nociceptor can be activated by thermal, mechanical, and chemicals
stimulation.
When thermal and mechanical stimulation produce nociceptive input, the reason for
the pain is usually apparent.
There are a variety of compounds that can accumulate near the nociceptor
following tissue injury that can be responsible for maintaining nociceptive input.
There are at least three sources of these compounds: the damaged cells themselves,
secondary to plasma extravasation and lymphocyte migration, or the nociceptor
itself.

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Damage to tissue cells produces leakage of intracellular contents. Among the

substances released by tissue damage are potassium and histamine, both of
which either activate or sensitize the nociceptor.
These substances have been documented to excite polymodal nociceptors and
produce pain when injected into skin. Other compounds such as acetylcholine,
serotonin, and ATP maybe released by tissue damage and are known to either
activate or sensitize nociceptors.
Bradykinin one of the most potent pain producing substances that appears in
injured tissue. Bradykinin is an endogenous polypeptide consisting of a chain of
nine amino acids.

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Released as part of an inflammatory reaction, it is a powerful vasodilator and

causes increased capillary permeability.
Bradykinin requires the presence of prostaglandins act. It is also released
during ischemic episodes. Polymodal nociceptors can be activated by
bradykinin and they then can become sensitized to thermal stimuli.
Another group of compounds that synthesize the regions of tissue damage are
the metabolic products of arachidonic acid. These compounds are considered
inflammatory mediators and include both prostaglandins and leukotrienes.

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Prostaglandin E2 is metabolized from arachidonic acid through the action of

cyclo oxygenase. This occurs in conjunction with an inflammatory process.
Prostaglandins do not seem to be algogenic substances per se. They sensitize
nociceptive nerve endings to different type stimuli, thus lowering their pain
thresholds to all kinds of stimulation.
Prostaglandins are required for bradykinin to act, bradykinin in turn stimulates
the release of prostaglandins.
The two are therefore naturally potentiating.

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In addition to the chemical mediators that are released from damaged cells
or synthesized in the region of damage, the nociceptors themselves can
release substances that enhance nociception.
One such substance is substance P. and, when stimulated, can release this
potent excitatory neurotransmitter into the extra cellular space.
Substance P is a very strong vasodilator and produces edema. Substance P
also causes release of histamine from mast cells, which is an excitatory
neurotransmitter and also causes vasodilatation and edema.

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THEORIES OF PAIN

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It is often assumed that pain is a warning that damage has

occurred. But this is not strictly true.
Because pain may occur when there is no obvious disease as in
primary neuralgias and many diseases does not cause pain, at least
in the early stages.
So these are various theories being put forward on how nerve
impulses give rise to sensation of pain.

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INTENSITY THEORY
According to this view, pain is produced when any sensory nerve is stimulated
beyond a certain level.
In other words pain is supposed to be a non-specific sensation and depends
only on high intensity stimulation.
But the trigeminal system provides an example against this theory. In case of
trigeminal neuralgia the patient can suffer excruciating pain from a stimulus
no greater than a gentle touch provided it is applied to a trigger zone.
Although, the intensity theory is not accepted, it remains true to say that
intensity of stimulation is a factor in causing pain.

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 Specificity Theory (Johannes Muller, 1842):

According to this view, pain is a specific modality equivalent to vision and hearing
etc.
Just as there are Meissner corpuscles for the sensation of touch, Ruffini end organs
supposedly for warmth and Krause end organs supposedly for cold, so also pain is
mediated by free nerve endings.
Certain psychophysical studies have been regarded as supporting specificity
theory. Specialization is known to exist in nervous system and there are well
known tracts.
But concept of specific nerve ending is no long tenable. The Krause and Ruffini
endings are absent from the dermis of about all hairy skin, so it is certain that these
structures cannot be receptors for cold and warmth.

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 Protopathic and Epicritic theory:

Head and Rivers (1908) postulated the existence of two cutaneous sensory
nerves extending from the periphery to the CNS.
The protopathic system is primitive, yielding diffuse impression of pain,
including extremes of temperature and is upgraded.
The epicritic system is concerned with tough discrimination and small changes
in temperature and is phylogenetically a more recent acquisition .

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Pattern theory (Goldscheider, 1894):

This theory states that pain sensation depends upon spatio temporal pattern
of nerve impulses reaching the brain.
According to Woddell (1962) warmth, cold and pain are words used to
describe reproducible spatio temporal pattern, or codes of neural activity
evoked from skin by changes in environment.
The precise pattern of nerve impulse entering the CNS will be different for
different regions and will vary from person to person because of normal
anatomical variations.

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 Gate Control Theory

This theory proposed by Melzack and Wall in 1965 and recently reevaluated is receiving considerable attention.
This theory of pain takes into account the relative in put of neural
impulses along large and small fibers, the small nerve fibers reach the
dorsal horn of spinal cord and relay impulses to further cells which
transmit them to higher levels.
The large nerve fibers have collateral branches, which carry impulses to
substantia gelatinosa where they stimulate secondary neurons.

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The substantia gelatinosa cells terminate on the smaller nerve fibers just as the
latter are about to synapse, thus reducing activity, the result is, ongoing activity
is reduced or stopped gate is closed.
The theory also proposes that large diameter fiber input has ability to modulate
synaptic transmission of small diameter fibers within the dorsal horn.
Large diameter fibers transmit signals that are initiated by pressure, vibration
and temperature; small diameter fibers transmit painful sensations.
Activation of large fiber system inhibits small fiber synaptic transmission,
which closes the gate to central progression of impulse carried by small fibers.

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PAIN PATHWAYS

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From the site of pain generation, i.e. from the periphery, the pain senses are
carried by A & C fibres.
Their cell bodies are situated in the dorsal root ganglion.
The central processes of the neuron, lying in the sensory root of the spinal
nerve enter the dorsal horn to terminate in the SGR ( Substantia gelatinosa
Rolandi), situated in the tip of dorsal horn.
From the SGR, next order ( i.e. 2nd order) neuron arises, crosses to the opposite
side, then moves up through the white matter of spinal cord to reach the brain.

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i)

Most of these 2nd order neurons travel up as spinothalamic tract (STT), then
ultimately terminate in the proper area of thalamus, from these specific nuclei
of thalamus, next order neurons arise to terminate on the cerebral cortex, at
areas SI & SII as well as cingulate gyrus (which is the key area for production
of some emotions).

) At SGR, there is a synapse between 1st order & 2nd order neuron. Also there is
synapse of 2nd & 3rd order neuron at thalamus.
) The NT (neurotransmitter ) at the synapse between A fiber & 2 nd order
neuron at SGR is glutamate while the NT between C fiber & 2nd order neuron
(slow pain) at SGR is substance P.

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Other 2nd order neurons, from SGR also are known, & they also cross to the
opposite side to reach different areas of brain.
The tip of dorsal horn, particularly the SGR plays a key role in modification of
pain perception. It is called a gate. As a gate can be shut/ partially opened/ fully
opened to control incoming traffic, so also behaves the SGR controlling the
incoming traffic of pain.

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Dual Pain Pathways in Cord & Brainstem

Neospinothalamic Tract for Fast Pain
The fast type A() pain fibers transmit mainly mechanical and
acute thermal pain.
They terminate mainly in lamina I at the dorsal horn and these
excite second order neurons of the neospinothalamic tract.

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Paleospinothalamic tract for Slow Pain

This pathway transmits pain mainly from peripheral slow chronic Type
C pain fibers.
In this pathway, the peripheral fibers terminate almost entirely in
lamina II and III of dorsal horns of spinal cord, together called as
substantia gelatinosa.

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Axons of secondary neurons emerge from the spinal nucleus, cross the
midline and ascend to join fibers of mesencephalic nucleus to form
trigeminal lemniscus or spinothalamic tract of 5th nerve.
These tracts continue upward and terminate in the postero ventral
nucleus of thalamus. From here it is transmitted to posterocentral
convolutions of cortex.

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Pain pathway of Maxillofacial Region

5th cranial nerve or trigeminal nerve is principal sensory nerve of head region.
Any stimulus in area of trigeminal nerve is first received by both myelinated
and non-myelinated fibers, and conducted as an impulse along afferent fibers of
ophthalmic, maxillary and mandibular branches into semilunar or gasserian
ganglion.
Pain impulse descends from the pons by spinal tract fibers of trigeminal nerve
through the medulla.

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FAST PAIN & SLOW PAIN

Fast Pain
Also known as Sharp pain, pricking pain or acute pain.
Easily localized.
Not felt in the deep visceral organs.
Slow Pain
Also known throbbing pain, aching pain or chronic pain.
It can occur both in skin and in almost any deep tissue or organ.

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The three main types of stimuli for pain are mechanical, thermal and chemical.
Fast pain is elicited by mechanical and thermal types of stimuli, whereas slow
pain can be elicited by all three types.
Some of the chemicals that excite the chemical type of pain are bradykinin,
serotonin, histamine, potassium ions, acids, acetylcholine and substance P and
also prostaglandin.
Chemical substances are especially important in stimulating the slow, suffering
type of pain that occurs after tissue injury.

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MODULATION OF PAIN

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 Noxious stimuli of comparable intensity may produce varying

degrees of pain in the same individual under different
circumstances.
For example, an injury acquired by an athlete in the sports field or
by a soldier in the battlefield is less painful than a comparable
injury suffered in a road accident.
In other words, pain can be modulated.

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In the 1960s neurophysiological studies provided evidence that the ascending

output from the DH of the spinal cord following somatosensory stimulation
depended on the pattern of activity in different classes of 1 sensory neurones.
Melzack and Wall proposed the gate control theory of pain.
It suggested that activity in low-threshold, myelinated 1 afferents would
decrease the response of DH projection neurones to nociceptive input (from
unmyelinated afferents). Although there has been controversy over the exact
neural substrates involved, the gate control theory revolutionized thinking
regarding pain mechanisms.

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Pain is not the inevitable consequence of activation of a specific pain

pathway beginning at the C-fibre and ending at the cerebral cortex.
Its perception is a result of the complex processing of patterns of activity
within the somatosensory system.

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FACTORS AFFECTING PAIN

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1. Emotional status:
The pain threshold depends greatly on attitude towards the procedure. In
case of emotionally unstable and anxiety patient the pain threshold is low
but reaction is high.
2. Fatigue:
Pain reaction threshold is high in subjects who has good night sleep and
relaxed, then those persons who are tired.

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3. Age :
Older individuals tend to tolerate pain and thus have higher pain reaction
threshold than young individuals. Perhaps their philosophy of living or
the realization that unpleasant experiences are a part of life may account
for this fact.
4. Racial and nationally characteristics:
It has been said that racial characteristics are reflected in the pain. The
Caucasian and Negro races have little or no variation in the pain reaction
threshold.

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The Latin Americans and Southern Europeans are more emotional than North
Americans or Northern Europeans may be in warmer climates tend to have lower
pain reaction threshold.
5. Sex :
Men have higher pain threshold than women. This may be a reflection of mans
desire to maintain his feeling of superiority and this is exhibited in his pre
determined effort to tolerate pain.
6. Fear and apprehension:
Most cases pain threshold is lowered as fear and apprehension increases.
Individuals who are extremely fearful tend to magnify their experiences.

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VISCERAL PAIN

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A striking characteristic of the brain is that although it receives and processes

nociceptive information, the brain itself has no sensation of pain.
The internal (visceral) organs themselves have no pain receptors, pain receptors
are present embedded in the walls of the arteries serving these organs.
Visceral pain is characterized as diffuse and poorly localized and is often
referred to and felt in another somatic structure distant or near the source of
visceral pain.
Nociceptive signals from the viscera generally follow the same pathway as
signals arising from somatic structures.

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 General visceral afferent nociceptive information from visceral structures

of the trunk is carried mostly by type C, A, or A fibers.
Visceral pain signals relayed to the primary somatosensory cortex may be
associated with referred pain to a somatic structure.
In addition to projections to the somatosensory cortex, recent studies
indicate that nociceptive signals are also relayed to the anterior cingulate
and anterior insular cortices, two cortical areas implicated in the
processing of visceral pain.

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REFFERED PAIN

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 Pain occurring in a visceral structure is usually not felt in the viscus

itself but on the surface of the body or in some other somatic
structure that may be located quite some distance away. Such type of
pain is said to be referred pain.
It is commonly observed in all type of deep pain both visceral and
somatic pain e.g. the pain of angina pectoris is often felt in the left
arm or the jaw and diaphragmatic pain is often felt in the shoulder
or neck.

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It is not accentuated by provocation of the site where the pain is felt, it is

accentuated only by manipulation of the primary pain source.
It is dependent on continuance of the primary initiating pain, it ceases
immediately if the primary pain is arrested or interrupted.
Anesthesia of the structure where the referred pain is felt does not arrest the
pain. It should be noted that although the primary initiating pain is of the deep
visceral type, the secondary referred pain may be felt in either deep or
superficial structures.

82

 The two most popular theories explaining mechanism

of referred pain are
Convergence Projection Theory

Convergence Facilitation Theory

83

Convergence-Projection Theory
The sympathetic afferent fibers carrying the pain sensation emerges
from the viscus and via dorsal root ganglion ends in the posterior horn
of the spinal cord.
Afferent somatic nerve, emerging from the pain receptor, of the
corresponding dermatome of the viscus, enters the same segment and
terminates on the very same cell where sympathetic nerve is
terminating i.e. these two different neurons converge on the same next
order neuron.

84

Therefore when the next order neuron is stimulated the impulse

reaches the brain and person feels pain, but he feels as if the pain is
coming from the dermatome.

85

Convergence Facilitation Theory

According to this theory, nociceptive input from the deeper structure
causes the resting activity of the second order neurons pain
transmission in the spinal cores to increase or be facilitated.
The resting activity is normally created by impulses from the
cutaneous afferents, facilitation from deeper nociceptors causes the
pain to perceived in the area that creates the normal, resting
background activity.

86

 The theory tries to incorporate the clinical observation that

blocking sensory input from the reference area with either L.A.
or cold, can sometimes reduce the perceived pain e.g. in
myofacial pain, application of a vapocoolant spray is actually a
popular and effective modality used for pain control.

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Subliminal Fringe Effect

The afferent sympathetic nerve bringing pain sensation from the viscus
terminate on the second order neuron, but at the same time it also via
collateral, stimulate another second order neuron.
This second order neuron is synapsed with somatic neuron of the
corresponding dermatome.
Therefore, when the pain is felt by the patient, he feel as if the pain is
coming from the corresponding dermatome.

88

Dermatome Rule
When pain is referred, it is usually to a structure that
developed from the same embryonic segment or dermatome
as the structure in which the pain originate. This is called
dermatome rule e.g. during embryonic development the
diaphragm migrates from neck region to the adult location
between the chest and abdomen and take its nerve supply,
the phrenic nerve with it.
One third of the fibers in the phrenic nerve are afferent
and they enter the spinal cord at the level of IInd to IV the
cervical segments, the same location at which afferents
from the tip of the shoulder enter.

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Referred pain does not occur haphazardly but in fact follows three clinical rules,
1) Referred pain frequently occurs within a single nerve root, passing from one
branch to another. E.g.. Mandibular molar presenting with a source of pain will
commonly refer pain to a maxillary molar. This is fairly common occurrence
with dental pain. Generally, if the pain is referred to another distribution of the
same nerve, it does so in a laminated manner. This lamination follows
dermatomes. Trigeminal lamination patterns are determined by the manner in
which the primary afferent neurons enter in the spinal tract nucleus. According
to Kunc, the location of the trigeminal nociceptive terminals within the nucleus
caudalis is as follows:

90

a) Fibers from parts near the saggital midline of the face terminate highest in
the nucleus (cephlad).
b) Fibers from parts located more laterally terminate lowest in the nucleus
(cauded).
c) The intermediate fibers terminate intermediately in the nucleus.
This grouping of the terminals of the primary trigeminal neurons should
influence the location of clinical effects of central excitation, a molar tooth
projects dorsal to canine projects dorsal to an incisor, which confirms the
vertical lamination just cited. This means incisors refer to incisors, premolars to
premolars, and molars to molars on the same side of the mouth. In other words,
molars do not refer pain to incisors or incisors to molars.

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2) The referred pain in the trigeminal area rarely crosses the midline
unless, it originates at the midline. For example, pain in the right
temporomandibular joint will not likely cross over to the left side of the
face nor will right molar pain refer to a left molar. This is not true in the
cervicospinal region or below, cervicospinal pain can be referred across
the midline, although it normally stays on the same side as the source.

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3) If referred pain is felt outside the nerve that mediates the pain, it
is generally felt cephalad to the nerve (upward, toward the head)
and not caudally. Clinically this means that deep pain felt in the
sacral area maybe referred to the lumbar area, as well as lumbar to
thoracic, thoracic to cervical, and cervical to trigeminal.

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PHANTOM LIMB PAIN

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Individuals who have had a limb amputated may experience pain or

tingling sensations that feel as if they were coming from the
amputated limb, just as if that limb were still present.
Although the mechanism of phantom limb pain is not understood, the
following two possible explanations are offered.
1) If a sensory pathway is activated anywhere along its course, nerve
impulses are generated that travel to the CNS where they initiate
neural activity. This neural activity ultimately creates sensations
that feel as though they originated in the nonexistent limb.

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2) Another possibility is that since there is no touch, pressure, or

proprioceptive information transmitted to the CNS from the peripheral
processes of the sensory neurons that initially innervated the
amputated limb, there are no impulses from touch fibers to attenuate
the relaying of nociceptive impulses to the nociceptive pathways,
enhancing nociceptive transmission and pain sensation. Since
nociception is not as localized, cortical areas corresponding to the
phantom limb will be activated.

96

INHIBITION OF PAIN

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Pain sensations may be controlled by interrupting the pain impulse between

receptor and interpretation centers of brain.
This may be done chemically, surgically or by other means.
Most pain sensations respond to pain reducing drugs/analgesics which in
general act to inhibit nerve impulse conduction at synapses.
Occasionally however, pain may be controlled only by surgery. The purpose
of surgical treatment is to interrupt the pain impulse somewhere between
receptors and innervation centers of brain, by severing the sensory nerve, its
spinal root or certain tracts in spinal cord or brain.

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 Sympathectomy excision of portion of neural tissue from

autonomic nervous system.
Cordotomy severing of spinal cord tract, usually the lateral
spinothalamic.
Rhizotomy cutting of sensory nerve roots.
Prefrontal lobotomy destruction of tracts that connect the
thalamus with prefrontal and frontal lobes of cerebral cortex.

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Newer Approaches
Transcutaneous Neural Stimulation (TNS)
With TNS, cutaneous bipolar surface electrodes are placed in the painful
body regions and low voltage electric currents are passed.
Best results have been obtained when intense stimulation is maintained for
at least an hour daily for more than 3 weeks.
TNS portable units are in wider spread use in pain clinics throughout the
world and has been proved most effective against neuropathic pain.

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Acupuncture (ACUS = NEEDLE, PUNGERE = STING)

Method of inhibiting pain impulses.
Acupuncture theory is based on an invisible system of communication between various organs
of the body that is distinct from circulatory, nervous and endocrine system.
Needles are inserted through selected areas of skin and then twirled.
After 20-30 minutes, pain is deadened for 6-8 hours
Location of needle insertion depends on part of body acupuncturist wishes to anesthetize.
Example : to pull a tooth a needle is inserted in the web between thumb and index finger.
For tonsillectomy, a needle is inserted approximately 5 cm (2) above the wrist.

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Pain Inhibiting Mechanism

It can be Endogenous
Exogenous

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 Endogenous Method of Controlling Pain Includes 1) Removing the cause: It is a desirable methods. It is imperative that any
removal leave no permanent environmental changes in tissue, since this
condition would then be able to create the impulse, even though the original
causative factor had been eliminated.
2) Blocking the pathways of painful Impulses
)This can be done by injecting drug possessing local analgesic property in
proximity to the nerve involved.
) Thus preventing those particular fibers from conducting any impulses centrally
beyond that point. These two method act by altering pain perception.

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3) Raising the pain threshold :

Raising pain threshold depends on the pharmacological activity of drugs
possessing analgesic properties.
These drugs raise pain threshold and therefore alter pain reaction, conceptually
there are two components of pain
(a) Nociceptive
(b) Affective component.
The path of nociceptive component is spinothalamic tract Thalamus. This
component is purely physical component of pain.

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4) Affective Component

It is the psychological component associated with pain. The path is that some
fibers from STT to thalamus terminate in some intermediate stations in the
reticular formation of brain stem and are called spinoreticular thalamic system.
Non-narcotic analgesic like aspirin can inhibit the nociceptive but not the
affective component of pain whereas opioid (Morphine) inhibit affective as well
as nociceptive components of the pain. They act centrally at cortical and sub
cortical centers, to change patient mind and his reaction towards pain

105

5) Preventing pain reaction by cortical depression

Eliminating pain by cortical depression is by the use of general
anesthesia.

6) Using Psychosomatic Method

This method affects both pain perception and pain reaction. It include
audio analgesia

106

Diagnosis based on specific questions and tests

Questions asked-two type

General questions

Specific questions

107

 Some general questions areWhat can I do for you?

Pt give response in three waysHistorical, Diagnostic & Factual

What sort of pain are you having ?

Varied response affected by
Physical, psychological, social factors

108

 Do you have any reaction to hot cold and

sweetness-?
This questions differentiate between the dental pain or pain
due to non dental causes & we have to analyze the responses
and have to get an impression of the severity of the response.

109

Pain to sweetness
Pain to cold
Pain on application of cold but relieved by hot
Delayed response to heat
Unexplained sensitivity to cold in posterior teeth
Root filled teeth sensitive to cold
Pain on biting-vital posterior teeth
Pain on biting-vital anterior teeth
Pain on eating

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Pain relieved by placing hand on the side of the face

Pain on ascent or descent
Pain ass. with exertion or after exertion
Pain on swallowing
Bilateral pain
Pain on waking in the morning
Pain in the afternoon or evening
Pain at a particular time each day
Pain when the Pt goes out in the cold

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 SITE OF PAIN
Observation of the manner in which the Pt uses their hands and fingers while
describing the pain provide information About the origin of pain
Placing a fingernail between the tooth
Moving a fingernail on the tooth
Holding one tooth
Placing a finger over the apex of the tooth
Pressing over the gingival margin
Holding or moving several teeth
Pressing over the zygoma

112

Pressing under the maxilla

Pressing on side of maxilla with rotary movement or pressing on the body of
mandible with finger in motion
Using more than one finger for describing the pain
Bilateral pain
Pain on percussion of more than one tooth

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 OTHER QUESTIONS ARE

When did the pain start?
Where did the pain start ?
Does any thing relieve the pain?
Have you been able to sleep?

114

PULPAL PAIN
It is the most commonly experienced pain in and near the oral cavity.
Pulpal pain can be diagnosed based on clinical signs and symptoms
Histological finding.
Clinically pulp is referred as healthy, reversible pulpitis, irreversible pulpitis.
Histological as acute, chronic & hyperplastic.

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HYPEREMIA
The increased pressure against the sensory nerve endings in the pulp might
well produce the sensation of pain. Application of cold produce a sharp
hypersensitive response and heat produce true transient hyperemia and a dull
pain.

An assessment of pain intensity at the time of stimulation, dental history& a

thorough dental examination allow the clinician to differentiate among the
normal pulp, dentin hypersensitivity, and the reversible inflamed pulp.

116

Hyperactive pulpalgia :- It is characterized by a short, sharp, shock

pain is felt as a sensation of sudden shock. It is never spontaneous.

Dentin Hypersensitivity :- Pain arise in response to thermal,

chemical, tactile or osmotic stimuli and is not caused by any other
dental defect or pathology. This pain is explained by, hydrodynamic
theory postulated by Brannstrom.

117

Characteristic features of irreversible pulp condition are :

Hyperalgesia in the initial stage
Dull throbbing ache in the later stage
Lingering pain on application of stimuli
Pain is spontaneous
Cause referred pain in other areas
Relief is provided by cold

118

Acute Pulpalgia :- Pain is nagging or boring pain which may at first be

localized but finally becomes diffuse or referred to another area in mild
pulpalgia but in advanced lesion, pain is excruciating and relieved by cold.
Chronic Pulpalgia :- Mild pain that is quite diffuse and is difficult to locate
source of pain. It is likely to cause referred pain which is also mild.
Hyperactive pulpitis :- Pain or slight discomfort from food coming against
the tooth or on taking extreme of hot & cold.

119

Internal desorption :
Pain is mild and at tolerable level and closely resemble chronic
pulpalgia.

Incomplete fracture or split tooth :

Pain range from those of constant unexplained hyper sensitive pulp to
constant unexplained toothache. The most frequent complaint is that of
a tooth painful to bite on, with occasional mild ache.

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PERIODONTAL PAIN
Localized, deep throbbing pain
Involving inflammation of PDL around one or more teeth
Mobility
Localized bleeding
Presence of pocket
In radiograph loss of bone is there
Pain last for hour or day
Involve tooth is tender on percussion
If pain involve multiple teeth including opposing teeth then occlusal trauma
should considered

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Periradicular pain
Acute apical periodontitis
The pain has been described as constant, gnawing, throbbing and pounding.
Tooth is tender and slightly elevated in its socket. The pain is most persistent,
lasting 24 hours a day.
Acute apical abscess
Pain is similar to AAP but somewhat lower in intensity. Involved tooth is
painful to movement or mastication

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 Chronic apical periodontitis :

It is seldom painful.
Chronic apical abcess/suppurative apical periodontitis :
It is generally symptoms free. When draining fistula is closed, discomfort ensue.

Periodontal lesion pain :

Acute gingival or periodontal abscess
Tooth is painful to bite on and is not so deep seated or throbbing as that of apical
abscess.
Pain is spontaneous
Associated localized swelling is there
Presence of deep PDL pocket is there.

123

Pericoronitis : Severe radiating pain in posterior mouth region

and inability to comfortably close or open
mandible.
Tissue distal to erupting molar is most painful to
touch.

124

EAR PAIN
Odontogenic infection of posterior teeth may refer pain to the ear/TMJ area.
Similarly middle ear infection/otitis media/mastoiditis may be confused with
odontogenic pain. In otitis media pain is acute, severe, throbbing and
exacerbate on lowering the head. Pain may be referred to tooth, TMJ, tonsils,
tongue, throat, trachea and thyroid.
It is unlikely for the middle ear infection/otitis media/mastoiditis pain to be
exclusively expressed as jaw pain.

125

SINUS & PARANASAL PAIN

In acute maxillary sinusitis pain may be stabbing, with severe aching pressure. Pain is
frequently referred upward under the orbit and downward over the maxillary posterior
teeth. Pain is referred in all the teeth in the quadrant and exacerbated when head is
placed below the knee

In chronic sinusitis there is dull constant pain. The location of these symptoms may vary
from the maxilla and maxillary teeth in maxillary sinusitis, to the upper orbit and frontal
process in frontal sinusitis and at the junction of the hard and soft palate, occipital and
mastoid process in sphenoid sinusitis.

126

TEMPOROMANDIBULAR JOINT
ARTICULAR DISORDERS
Capsulitis and Synovitis

Chief complaint is continuous pain over the joint aggravated

by function. Swelling may be evident and patient may
complaint of acute malocclusion, restricted mouth opening
and teeth pain.

127

Internal Derangement :
It includes meniscus displacement, formation of intra articular adhesion and
various forms of arthritis.
There occur limited jaw opening, deviation on opening, joint clicking, crepitus
and pain directly localized to the joint area in front of the tragus of the ear.
The pain is dull, boring ache but may be more acute when exacerbated by wide
mouth opening. The symptoms become progressively worse and the degree of
pain increase.
TMJ pain is often referred into temple, cheek and posterior dental area of the
maxilla and mandible.

128

NEUROPATHIC PAIN
It results from an abnormality in one or more components of the nervous
system i.e. peripheral, central or autonomous. They are characterized as :Do not require presence of noxious stimuli in contrast to somatic pain which
does.
Pain manifestation are usually maintained by neuroplasticity that is change in
nervous pathway carrying pain.
When neuroplasticity is prolonged it result in a state of chronic or
pathophysiologic pain.

129

Hyper excitability of IInd order neuron i.e. central sensitization

Allodynia
Hyperalgesia
Pain is bright, stimulating and burning
Pain that is relatively unresponsive to low doses of narcotic analgesic

130

Neuralgias
Trigeminal Neuralgia
Etiology:
Precise cause is unknown. Evidence indicates it may be due to vascular
compression of gasserian ganglion, viral infection of neuron or nerve
sheath may be there.
It primarily involves either maxillary or the mandibular division but
sometimes it may involve ophthalmic division. Pain is severe and
lancinating, shooting into the bone and teeth.

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Electric like quality of pain is unique and is rarely encountered in

odontogenic infections.
The pain episode last only second at a time. Although paroxysms
may occur in rapid succession.
A trigger zone exists somewhere on the facial skin or occasionally
in the oral cavity.

132

Treatment:
It is essential to establish diagnosis and avoid any invasive procedure.
Carbamazipine (Tegretol)
Peripheral neurectomy
Rhizotomy
Alcohol injection
Cryotherapy

133

Radiofrequency lesioning
Laser therapy
Surgical decompression
Trans cutaneous ganglionic neurolysis

134

Post herpetic Neuralgia

This disease represent a recrudescence of a latent virus located in sensory
ganglion. The painful lesions of shingles cause a deep, boring ache involving
not only the superficial mucosal and cutaneous tissues but also the maxillary
and mandibular bones. Occurrence of prodromal pain obscure the diagnosis.
Prodromal pain is acute and electric like and the pain associated with
vesicular eruption is deep and boring. Once the vesicles clear, the residual
pain is of burning quality and chronic. The quality of pain may be confused
with odontogenic pain but the history of vesicular eruption is sufficient to
make a diagnosis

135

Treatment of post herpetic neuralgia:

TENS

Anti seizure drugs

Analgesics

Topical preparation

Refer to neurologist

136

 Glosso Pharyngeal Neuralgia :

It include unilateral rarely bilateral stabbing pain in the
lateral posterior pharyngeal and tonsilar area, the base of
the tongue, down in to the throat, the Eustachian tube or ear
and down the neck. Sometimes the pain radiates into vagus
region and may be associated with salivation, flushing,
sweating, tinnitus, cardiac arrhythmias, hypertension,
vertigo or syncope.

137

Eagles Syndrome :
It is similar to those of gloss pharyngeal neuralgia
but involve compression of the area of IXth nerve by
a calcified elongation of styloid process of the
temporal bone.
Precipitating factors include fast rotation of head,
swallowing, pharyngeal motion from talking and
chewing.

138

Vasogenic craniofacial pain

In general pain is deep, throbbing, pulsing or pounding quality, occasionally sharp and with an
aching and burning background.

Migraine
Classic migraine headache begin as ache but usually develops in to pain of a throbbing,
pulsating or bating nature. One episode can last for several hrs to a day.
Somatosensory areas are most common field and consist of dysesthesias that start in one hand
and spread up to involve the ipsilateral side of the face, nose and mouth. The headache itself is
predominantly unilateral in the frontal, temporal, or retro bulbar areas, although it may occur in
the face or in a single tooth.

139

Cluster headache (Sphenopalatine neuralgia)

It can be classified as:
CLASSIC and CHRONIC TYPE

CLASSIC type affect patient mostly in spring season.

CHRONIC type occurs through out the year.
It is often mistaken for acute pulpitis of maxillary posterior
teeth.

140

CLUSTER HEADACHE
It has temporal pattern. Tend to occur in Clusters a series of one to
eight 20-180 minute attack/day lasting for several week or months.
The pain is a severe, unilateral, continuous intense ache or burning that
often occur at night.
The most common sites are either around and behind the eye radiating
to the forehead and temple, infraorbitaly into maxilla and occasionally
into the teeth and rarely to the lower jaw and neck.

141

 Treatment
Use of oxygen at the time of attack relieves pain and used for
diagnosis of pain.
Ergotamine tartarate may cause vasoconstriction and
contraindicated in hypertensive patient.
CCBs like Nifedipine prevents pain paroxysms.
Corticosteroids alleviating pain and preventing pain
occurrence.

142

MYOFACIAL PAIN
The most common form of musculoskeletal pain affecting the head, neck and
face.
The main characteristic features are ->
Myofacial trigger point
Muscle affected have a reduced active range of movement
Referred pain in reproducible patterns remote from the site of the rigger point.
A jump sing and verbal response or reflex reaction occur on palpation of the
trigger point
Pain is deep, dull aching and provocable.

143

ATYPICAL ODONTALGIA
The most likely mechanism involved in atypical odontalgia (AO) is related to
deafferentation following injury to a nerve. Deafferentation refer to the partial
or total loss of an afferent nerve supply from a particular area, following
trauma during dental procedure. Nerve damage is reversible in most patient but
in some patient (3%).
It is permanent. Pain may not appear for week, month or even a year after the
procedure. It has been hypothesized that there is genetic predisposition towards
pain in these patients.
Involvement of sympathetic nervous system (SMP) in AO has been suggested.

144

Characteristics of pain in atypical odontalgia are:

Chronic aching pain
Pt feel it as deep within the bone & it is hard to localize.
In many Pt symptoms appears to wonder from site to site.
Intensity of pain also varies.

145

PAIN PATHWAYS AND MEDICATIONS

Pain Pathways

Medications

Peripherally (at the nociceptor)

Cannabinoids, NSAIDs, Opioids, Tramadol,

Vanilloid receptor antagonists (i.e., capsaicin)

Peripherally
(along the nociceptive nerve)

Local anaesthetics, Anticonvulsants (except

the gabapentinoids)

Centrally
(various parts of the brain)

Acetaminophen, Anticonvulsants (except the

gabapentinoids), Cannabinoids, Opioids,
Tramadol

Descending inhibitory pathway

in the spinal cord

Cannabinoids, Opioids, Tramadol, Tricyclic

antidepressants, SNRIs

Dorsal horn of the spinal cord

Anticonvulsants, Cannabinoids,
Gabapentinoids, NMDA receptor
antagonists, Opioids, Tramadol, Tricyclic
antidepressants, SNRIs
146

CONCLUSION
Pain is bad, but not feeling pain can be worse.
Individuals with a congenital absence of pain receptors are
extremely rare but not unknown. Such individuals are very poor
at avoiding accidental injuries, and often inflict mutilating
injuries on themselves.
As a result, their life span is usually short. thus pain, although
unpleasant, is a protective sensation with enormous survival
value. Pain is a multidimensional experience involving both the
sensation evolved by noxious stimuli but also the relation to it.
The sensation of pain therefore depends in part on the patient
past experience, personality and level of anxiety.
147

 Every day patient seeks care for the reduction or

elimination of pain.
Nothing is more satisfying to the clinician than the
successful elimination of pain.
The most important part of managing pain is
understanding the problem and cause of pain.
It is only through proper diagnosis that appropriate
therapy can be selected.

148

REFRENCES

149

1. Bell`s Orofacial pain, 5th edition, Jeffrey P. Okeson.

2. Text book of Medical Physiology, 2nd edition, Chaudhari.
3. Text book of Medical Physiology, 10th edition, Arther C Gyton.
4. Dental Clinics of North America 1978: 22 (1); 1-61.
5. Text book of Oral medicine- 10th edition, Burketts.
6. Gray's Anatomy 38th Edition, Churchill Eivingstone.
7. Understanding Medical physiology- 3rd edition, R L Bijlani.
8. Core Topics in Pain Anita Holdcroft, Sian Jagger.

150

9. Pain Wikipedia, the free encyclopedia

10. Rolf-Detlef Treede. Neurophysiological studies of pain pathways in
peripheral and central nervous system disorders. J Neurol (2003) 250 :
11521161.
11. Ascending Sensory Pathways, Chapter 10.
12. Pain pathway & Medications Painexplained.ca, The Canadian
Pain Society.

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