An unpleasant sensory & emotional experience associated with actual or potential tissue damage, or described in terms of damage

2. CONTENTS
• Introduction
• Definitions
• History
• Glossary
• Basic structure of a Neuron
• Stimulus and Receptors
• Dental and Pulpal pain
• Neurotransmitters

3. • Theories of Pain
• Fields subjective experience of Pain
• Pathways of Pain
• Pain modulation
• Classification of Pain
• Physiological pain vs Clinical pain
• Referred Pain
• Phantom Pain
• Summary
• References

4. • Pain is almost UNIVERSAL experience
• The mechanisms involved in pain sensation have been the object
of considerable attention by neurophysiologists , physicians and
pain’s unhappy victims
• Pain is difficult to define ,for pain is a SUBJECTIVE sensation
INTRODUCTION

5. • An unpleasant sensory & emotional experience associated with actual or
potential tissue damage, or described in terms of damage
IASP definition, Burket’s Oral Medicine 11th ed.
• The subject’s conscious perception of modulated nociceptive impulses that
generate an unpleasant sensory & emotional experience associated with actual
or potential tissue damage, or described in terms of such damage
Bell’s Orofacial Pain 5th ed.
DEFINITIONS

6. • Pain is defined as an “unpleasant emotional experience usually initiated by a
noxious stimulus and transmitted over a specialized neural network to the
central nervous system where it is interpreted as such”.
Monhem’s Local anesthesia & pain control in
dental practice. 7th ed

7. • A more or less localized sensation of discomfort ,distress, or agony resulting
from the stimulation of specialize nerve endings.
Dorland’s Medical Dictionary
• An unpleasant sensation that is perceived as arising from a specific region of
the body and is commonly produced by process that damage or are capable of
damaging bodily tissue.
Fields

8. HISTORY
• Derived from Latin word - “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

9. • 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.

10. • Use of Willow bark & leaves by Hippocrates: Salicylic acid in
willow plant of genus Salix is the active ingredient of ASPIRIN
• Coca cola was initially sold as a cure for pain: concept of using
cocaine as a pain reliever.

11. • Queen Victoria was the first one to have anaesthesia for pain control
during childbirth
 chloroform was used

12. GLOSSARY OF PAIN
Merskey H, Bogduk N. 1994 Classifcation of Chronic Pain. IASP Press Seattle, WA

13. Merskey H, Bogduk N. 1994 Classifcation of Chronic Pain. IASP Press Seattle, WA

14. Merskey H, Bogduk N. 1994 Classifcation of Chronic Pain. IASP Press Seattle, WA

15. Merskey H, Bogduk N. 1994 Classifcation of Chronic Pain. IASP Press Seattle, WA

16. Merskey H, Bogduk N. 1994 Classifcation of Chronic Pain. IASP Press Seattle, WA

17. BASIC STRUCTURE OF NEURON
Neurone transmits messages from the brain to a muscle or gland.
A sensory neuron is similar to a motor neuron except it has one long dendron
and is designed to bring impulses to the brain.

18. STIMULUS
• A variety of stimuli are responsible for evoking pain.
• These are ……….
Mechanical tissue destruction
High tempt.
Low Ph
Chemical mediators
Hyper-osmotic solutions

19. • Sherrington  all the stimuli capable of evoking pain are
NOXIOUS as they are associated with actual or potential tissue
injury.
• He postulated the existence of sensory receptors that sensed
noxious agents (NOCICEPTORS)
• Hence perception of the pain also referred to as NOCICEPTION

20. RECEPTORS
FREE NERVE ENDINGS
C-FIBERSA-DELTA
FIBERS

21. After receiving a nociceptive stimulus, two types of nerve
fibers are stimulated.
A-d fibers ‘C’ fibers
Thick & finely myelinated. The thin & non myelinated.
Fast rate of conduction (15-
20m/s).
Slower rate of conduction
(0.5-2m/s).
Sensation due to the
stimulation of A-d fibers is
felt earlier than ‘C’ fibers.
Sensation due to the
stimulation of ‘C’ fibers is
felt after a long interval.
They conduct impulses to
laminae I & V fibers.
They conduct impulses to
laminae I & II of substantia
gelatinosa

22. Dental and pulpal pain

25. NEUROTRANSMITTERS
• Neurochemicals that transmit
impulses across synaptic cleft
• Types:
• Small rapid-acting molecules
• Larger slower-acting molecules

26. 26
ACETYLCHOLINE
- Most common
- Excitatory effect on
postsynaptic neuron
NOREPINEPHERINE
- Excitatory
neurotransmitter
GLUTAMATE
- An amino acid
- Excitatory effect
ASPARTATE
- An amino acid
- Excitation
SEROTONIN
- A monoamine
released by platelets
- Algogenic agent
- Analgesic effect
GABA
- Inhibitory effect on
postsynaptic neuron
GLYCINE
- Inhibitory transmittor
DOPAMINE
- Inhibitory effect
HISTAMINE
- Vasodilator
- Contraction of smooth
muscle
RAPID-ACTING (SMALL MOLECULE)
NEUROTRANSMITTERS

27. 27
SUBSTANCE P
• Released at central
terminals of primary
nociceptive neurons
• Acts as transport
substance
• Excitatory
neurotransmitter
• Action: rapid & short-
lived
ENDORPHINS
• Bind to morphine
receptors to obtund
pain
• Long lasting
• Antinociceptive
property
BRADYKININ
• Algogenic agent
• Excites all types of
receptors
SLOW-ACTING (LARGE MOLECULE)
NEUROTRANSMITTERS

29. SPECIFICITY THEORY
DESCARTES 1664, MULER 1840
pain occurs due to stimulation of specific pain receptors
(nociceptors) with transmission by nerves directly to the
brain .
pain is purely an afferent sensory experience.

30. • PATTERN THEORY
GOLDSCHEIDER IN 1894 stimulus intensity and
central summation are critical determinants of pain
particular patterns of nerve impulses that evoke pain are
produced by summation of sensory input within the dorsal
horn of spinal cord
pain results when total output of the cells exceeds a critical
level….
for eg. touch+pressure+heat might add up in such a manner
that pain is the modality experienced

31. GATE CONTROL THEORY:
Ronald Melzack and Patrick Wall proposed that a gating mechanism
exists within the dorsal horn of the spinal cord.

32. Small nerve fibers (pain
receptors) and large nerve
fibers ("normal" receptors)
synapse on projection cells
(P), which go up the
spinothalamic tract to the
brain, and inhibitory
interneurons (I) within the
dorsal horn.

33. The interplay among these
connections determines when
painful stimuli reaches brain
When no input comes in, the
inhibitory neuron prevents the
projection neuron from sending
signals to the brain (gate is closed).

34. • Normal somatosensory input
happens when there is more
large-fiber stimulation (or
only large-fiber stimulation).
• Both the inhibitory neuron
and the projection neuron are
stimulated, but the inhibitory
neuron prevents the
projection neuron from
sending signals to the brain
(gate is closed).

35. • Nociception when there is
more small-fiber stimulation or
only small-fiber stimulation.
• This inactivates the inhibitory
neuron, and the projection neuron
sends signals to the brain
informing it of pain (gate is
open).
One byproduct of gate control theory was
the introduction of Transcutaneous electrical
nerve stimulation (TENS) as a therapeutic
modality.

36. Descending pathways
from the brain close the
gate by inhibiting the
projector neurons and
diminishing pain
perception.

37.  FIELDS has described that the subjective experience
of pain arises by 4 distinct process:
* Transduction
* Transmission
* Modulation
* Perception

38.  TRANSDUCTION:
Process by which noxious stimuli lead to electrical
activity in sensory nerve endings.
There are specialized sensory receptors distributed all over
the body which respond to physical & chemical stimuli.
- Extroceptors
- Proprioseptors
- Interoseptors

39. • Extroceptors
are sensory receptors that are stimulated by the immediate external
environment.
These receptors provide information from the skin and mucosa.
Egs
1. Merkel’s corpuscles : tactile receptors in the submucosa of the
tongue and oral mucosa.
2. Meissner’s corpuscles : tactile receptors in skin
3. Ruffini’s corpuscles : pressure and warmth receptors
4. Krause’s corpuscles or end bulbs : cold receptors
5. Free nerve endings : perceives superficial pain and touch

40. • Proprioseptors
are sensory receptors that provide information from the
musculoskeletal structures concerning the presence, position and
movement of the body.
Egs
1. Pacinian corpuscles : receptors concerned in the preception of
pressure
2. Periodontal mechanoreceptors : responds to biomechanical stimuli
3. Free nerve endings : perceive deep somatic pain and other
sensation.

41. • Interoseptors
are sensory receptors that are located in and transmit impulses from the
viscera (supply system) of the body.
Sensation from these receptors are involved in the involuntary
functioning of the body.
Egs
1. Pacinian corpuscles : receptors concerned in the preception of
pressure.
2. Free nerve endings : perceive visceral pain and other sensation.

42. • TRANSMISSION:
neural events that carry the nociceptive input into the CNS
1) Peripheral Sensory Nerve : Primary afferent neuron- carries
nociceptive input from the sensory organ (receptors) into the
spinal cord.
2) Second Order Neuron- carries input to the higher centers
through spinal cord.
3) Third Order Neuron- Interaction of neurons between the
thalamus cortex and the limbic system as the nociceptive
input reaches these higher centers.

43.  MODULATION:
- Ability of the CNS to control the pain transmitting neurons.
- Several areas of brain & cortex have been identified that can
either enhance or reduce nociceptive input.
 PERCEPTION:
Reaching of the nociceptive input to the cortex is perception
It is at this level suffering & pain behavior begins.

45. THE SPINAL CORD
• Traditionally it was thought that most pain fibers entered the
dorsal root of the spinal cord (the "sensory" root) and then
synapse in the dorsal part of the spinal gray matter, before
passing the message up through the spinothalamic tract.
• It is now known that this is a gross oversimplification. In
fact, anything up to 40% of sensory fibers enter in the
ventral root!
• Histological the gray matter of the spinal cord is divided into
ten 'laminae.by REXED

46. PATHWAYS OF PAIN SENSATION
Dorsal column medial leminiscal systemconveys touch, vibration and
other non noscious stimuli ( not considered a pain pathway)
Ventrolateral system  conveys noxious stimuli
Main ascending spinal pathways involved with relaying noxious stimuli
to brain
spinothalamic
spinohypothalamic
spinoreticular
spinomesenchephallic

47. PATHWAY OF PAIN SENSATION FROM VISCERA AND FACE
Thoracic&abdominal sympathetic nerves(thoracolumbar)
Oesophagus, trachea, larynx  vagus& gloss pharyngeal nerves
Face trigeminal nerve
Pelvic  sacral parasympathetic nerve.

48. DUAL TRANSMISSION OF PAIN TO CNS
• All pain receptors are free nerve endings these endings use
two separate pathways for transmitting pain signals into CNS
• Two types of pathways are
1. A fast-sharp pain pathway
( neospinothalamic)
2. A slow-chronic pain Pathway
(paleospinothalamic)

49. NEOSPINOTHALAMIC TRACT
• A-delta fibers…mainly
mechanical and acute
• Terminate in lamina I
(lamina marginalis) of the
posterior dorsal horns.
• Excite second order neurons
of neospinothalamic tract
giving rise to long fibers that
cross to opposite side through
the anterior grey commissure
and then pass upward to the
brain stem in anteriolateral
columns

50. • TERMINATION- in the reticular areas of the brain stem, but
most pass all the way to thalamus, terminating in the ventro-
basal complex along with dorsal column- medial lemniscal
tract for tactile sensation.
• LOCALIZATION.- more exactly than slow pain
• NEUROTRANSMITTER- glutamate

51. PALEOSPINOTHALAMIC TRACT
• c-fibers but to some extent
by a-delta fibers also.
• Peripheral fibers terminate
in laminae II and III of the
dorsal horns(SUBSTANTIA
GELATINOSA).
• Then the signal pass through
short fibers in dorsal horns
and enter laminae V

52. • long axon arise & cross the anterior commissure to the
opposite side of the cord, then upward to the brain in the
anteriolateral pathway.
• NEUROTRANSMITTER – mainly substance-p and
glutamate.
• Action of glutamate last for few milliseconds giving a faster
pain or the 1st pain sensation
• Conversely sub-p is released slowly giving rise to more
lagging or the 2nd pain sensation

53. • TERMINATION- only 1/10th to 1/4th of the fibers pass all
the way to the thalamus ,instead they terminate in one of the
following areas….
1. Reticular nuclei of medulla , pons and mesencephlon.
2. The tectal area
3. Periaqueductal gray region
• LOCALIZATION- is poor,
This is due to multisynaptic and diffuse connectivity of this
pathway.

54. PAIN MODULATION
• The degree to which a person
reacts to pain varies
tremendously.
• This results from capability of
the brain to suppress inputs of
pain signals to the nervous
system by activating a pain
control system c/a
ANALGESIA SYSTEM OR
THE DECENDING
CONTROL PATHWAY

55. • This system consists of 3
components
1. The preaqueductal gray
(PAG)and preventicular
areas
2. The raphe magnus
nucleus (RM)and
3. The nucleus reticularis
paragigantocellular

56. • Electrical stimulation either in PAG(preaqueductal grey) or
RM(raphe magnus) can completely suppress strong pain
signals entering by way of dorsal horns
• neurotransmitters …enkephalins and serotonin
• produce both pre and post synaptic inhibition of incoming C
and A-delta fibers
• Pre-synaptic inhibition….by blocking Ca- channels thus
preventing the release of neurotransmitters

57. ROLE OF OPIATE SYSTEM IN
MODULATION OF PAIN
• Morphine –derivative of opium causes analgesia by binding
to the specific sites called the opiate receptors at the synapses
of nociceptive pathways.
• This decreases nociceptive excitability, thus reducing the
sensation of pain.

58. • Several such peptides are produced by the neurons that bind to
the opiate receptor called the OPIATE PEPTIDES or
ENDORPHINS (Endogenous Morphine Like Substances)
• Biologically active endorphins identified are…
Beta-endorphin. gamma-endorphin, dynorphin, leu-enkephalin,
met-enkephalin.
• Produce both pre and post synaptic inhibition

59. • Nerve arising from
PAG(preaquieductal grey)
area secrete endorphins
synapse with neuron in
Raphe Magnus.
• The neurons arising from
RM(Raphe Magnus)
terminate dorsal horn
serotonin which causes
local neurons to secrete
endorphins thus causing the
inhibition of pain

62. CLASSIFICATION OF PAIN
• Nociceptive – somatic and visceral
• Neuropathic
• Psychogenic

63. NOCICEPTIVE PAIN
• Somatic
• Activation of receptors in deep tissues
• Aching, throbbing, gnawing
• Opioid sensitive
• Visceral
• Injury to sympathetically innervated organs abdominal
organs –
• described as deep, colicky, paroxysmal

64. • NEUROPATHIC PAIN
• Injury to element of nervous system
• Neuropathic Pain Presentations
• Sensory loss
• Sympathetic dysfunction
• Hyperalgesia – increased response to a stimulus that is
normally painful
• Allodynia – Pain caused by a stimulus that does not normally
provoke pain
• Dysesthetic pain
• Burning
• Tingling
• Numbing
• Squeezing
• Pressing

65. PSYCHOGENIC PAIN
• Controversy surrounding labeling pain as
wholly psychogenic
• Anxiety
• Depression
• Anger
• Irritability, frustration

66. PHYSIOLOGICAL V CLINICAL PAIN
• Physiological pain
• Pain can be differentiated from touch
• protective function
• warns of potential damage
• transient
• well localized
• a defined stimulus response pattern

67. Clinical pain (pathological pain)
• elicited by A-delta as well as C fibers
• associated with inflammation, neuropathy
• associated with peripheral and central sensitization
• pain outlasts duration of the stimulus
• pain sensed in non-injured areas

68. Referred Pain
• DEFINITION: The pain sensation produced in some parts of the
body is felt in other structures away from the place of pain
development. It is called referred pain.
 Deep and some visceral pain are referred to other areas
 Superficial pain not reffered.

69. TRIGGER POINTS
• Regional myogenous pain condition characterized by local areas of firm,
hypersensitive bands of muscle tissue known as trigger points.
• Trigger points are clinically identified as specific hypersensitive areas within
muscle tissue
• Active trigger points represent source of deep pain & produce referred pain
• If active referring trigger points are provoked
• Referral pain will be increased

70. • MASSETER:
• Superficial layer refer to: post mandibular &
maxillary teeth, jaw, face.
• Common complaint: tooth ache
70
SOME TRIGGER POINTS AND THEIR REFERRAL
PAIN

71. • TEMPORALIS:
• All maxillary teeth
• Upper face
71

72. • LATERALPTERYGOID:
• TMJ area
• Zygomatic area
72

73. PHANTOM PAIN
• In general, Assume some one’s left superior extremity has been
amputated at the level of middle of the arm.
• If now the exposed central stump of the nerve fibers be irritated,
the fibers supposed to be coming from the fingers (which no longer
exist now) may be irritated, and the subject feels as if the sensation
is coming form the fingers (which no longer exist), thus he /she
develops pain called the PHANTOM PAIN and the limb is called
the PHANTOM LIMB

74. • In the dental literature, phantom pain felt in the tooth has been
called atypical odontalgia.
• By definition atypical odontalgia means “ toothache of unusual
cause”.
• Eg. Atypical odontalgia associated with neurogenic inflammation
leading to secondary hyperalgesia.

75. Summary
• Pain is both a sensory and emotional experience, and patients past experiences,
fears and anxieties can play an important role.
• Pain transmission is a result of complex peripheral and central processes. These
processes can be modulated at different levels.
• Pain perception is a result of the balance between facilitatory and inhibitory
interactions.
• Current areas of interest in pain research include investigating the effect of mood
on pain processing in the brain and looking for novel drugs to block channels
involved in pain transmission.

76. REFERENCES
1. Orofacial pain- okeson
2. Textbook of physiology- a k jain
3. Textbook of medical physiology – guyton 11th edition
4. Textbook of local anaesthesia-monheims
5. International association for the study of pain:
http://www.Iasppain.Org/content/navigationmenu/generalresourcelinks/paindef
initions/default.Htm
6. Temporomandibular Disorders & Orofacial Pain. DCNA 2007; 51 (1)
7. Merskey H, Bogduk N. 1994 Classifcation of Chronic Pain. IASP Press
Seattle, WA
8. Medical problems in Dentistry. Scully & Cawson. 5th ed.

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