Pain control

1. DILU DAVIS
IIND YEAR POSTGRADUATE
PAIN CONTROL IN
OPERATIVE DENTISTRY
1

2. • HISTORY
• INTRODUCTION
• DEFINITION
• CHANGING CONCEPTS
• NEW DIMENSIONS
• PURPOSE OF PAIN
• CLASSIFICATION
• SOMATOSENSORY SYSTEM
• NEURAL PATHWAY OF PAIN
• THEORIES OF PAIN
FLOW CHART
2

3. 3
• CAUSES OF OROFACIAL PAIN
• DIAGNOSIS OF PAIN
• ASSESSMENT OF PAIN
• FACTORS THAT INFLUENCE PAIN
• DIFFERENTIAL DIAGNOSIS OF PAIN
• METHODS TO CONTROL PAIN
• CONCLUSION
• REFERENCES

4. • Derived from Greek “Poin”; meaning “Penalty”
• Derived from Latin “Poena”; meaning “Punishment from God”
HISTORY
4

5. • Chinese : Yin and Yang : 2 opposite forces & imbalance of system
• Egyptian : Dead spirits
• Buddhist of India : Reasoned it to frustrated desire & heart is root cause
• Greek : Brain as part of sensory & motor nervous system
Early Cultural Superstitions
5

6. • Homer - Arrows Shot by the Gods
• Aristotle – distinguish five senses, considered pain to be Passion
of the Soul
• Plato – pain and pleasure arose from within and considered pain
to be an emotional experience than a localized body sensation
• Hippocrates – imbalance of body fluids
• Bible - Anguish of the Soul
• Freud - Solution to Emotional Conflicts
6

7. • Probably - most fundamental and primitive sensation
• Distributed more or less all over the body
• Protective in nature and always indicates some serious trouble in the locality, such
as a structural damage or a serious functional or metabolic derangement
INTRODUCTION
7

8. An unpleasant emotional experience associated with actual or potential
tissue damage or described in terms of such damage.
International Association for the Study of Pain (IASP) (WHO)
An unpleasant emotional experience usually initiated by noxious stimulus
and transmitted over a specialized neural network to CNS where it is
interpreted as such.
Monheim
DEFINITION
8

9. An unpleasant sensation that is perceived as arising from a specific region of the
body and is commonly produced by processes which damage or are capable of
damaging bodily tissue.
Fields
A more or less localized sensation of discomfort, distress, or agony resulting from
the stimulation of specialized nerve endings."
Dorland's Medical Dictionary
The subject’s conscious perception of modulated nociceptive impulses that generate
an unpleasant sensory and emotional experiences associated with actual of potential
tissue damage or describe in terms of such damage.
Bell
9

10. Pain is …
• protective mechanism
• localized sensation as a result of noxious stimulation
• now recognized as being more of an experience than a sensation
CHANGING CONCEPT OF PAIN
10

11. Cognitive : Subject’s ability to comprehend &
evaluate
Emotional : Represents the feeling that
regenerated
Motivational : Drive to terminate
NEW DIMENSIONS TO PAIN
11

12. • Protective mechanism for the body
• Tissue damage ignites individual’s reaction to pain stimulus
e.g. Skin ischemia - No pain - Desquamation
PURPOSE OF PAIN
12

13. Depending on experience, pain can be classified as :
1. Experimental
2. Acute
3. Chronic
CLASSIFICATION OF PAIN
13

14. Experimental
• Noxious stimuli causes a
mild uncomfortable or
painful sensation
Acute Pathological Pain
• Elicits a psychological or
behavioral reaction
• The cause of this
continuous pain is often
unknown to patient
• May create anxiety,
anger, physical gesture
• Usually alleviated with
the help of professional
care
Chronic Pathological Pain
• Complicated physical,
behavioral and
psychological problem
• Experience of persistent
pain that last many
months to years
• Little apparent cause &
not self limiting
• Pain often increases over
time & is aggravated by
many factors
• Response is persistent
anxiety, confusion, sleep
disturbances,
depression, disability
14

15. Transient Pain
• Short duration
• Severe
• Self limiting
Acute
• Associated with postoperative, post
injury
• More duration
• Requires pharmacological
assistance(analgesics)
Persistent
• Long term duration
• Eg.: Cancer & neurogenic pain
• Pharmacological assistance(analgesics) and
cognitive approach
Chronic or Disabling
• Continue beyond expectation for disease
process
• Pain and pain therapy dominate the life
• Depression, anxiety
Depending On Duration
15

16. Pain is also classified into two types :
FAST PAIN
• Felt within about 0.1 second
• Described as: sharp, pricking, acute, electric pain
• Not felt in most deeper tissue of body
SLOW PAIN
• Begins only after 1 second or more & then increases slowly over many
seconds & some times even minutes
• Slow burning, throbbing, nauseous, chronic pain
• Associated with tissue destruction
16

17. PHYSICAL CONDITIONS PSYCHOLOGIC CONDITIONS
SOMATIC PAIN
NEUROPATHIC PAIN
MOOD DISORDERS
ANXIETY DISORDERS
SOMATOFORM DISORDERS
OTHER CONDITIONS
17

18. 1. SOMATIC PAIN
• Superficial somatic pain
• Cutaneous pain
• Mucogongival pain
• Deep somatic pain
• Musculoskeletal pain
• Muscle pain
• Protective co-contraction
• Delay onset muscle soreness
• Myofascial pain
• Myospasm
• Myositis
• Temporomandibular joint pain
• Ligamentous pain
• Retrodiscal pain
• Capsular pain
• Arthritic pain
• Osseous and periosteal pain
• Soft connective tissue pain
• Periodontal dental pain
• Visceral pain
• Pulpal dental pain
• Vascular pain
• Arteritis
• Coritidynia
• Neurovascular pain
• Migraine with aura
• Migraine without aura
• Cluster headache
• Paroxysmal hemicrania
• Neurovascular variants
• Visceral mucosal pain
• Glandular, ocular and auricular pain
18

19. 2. NEUROPATHIC PAIN
• Neuropathic pain
• Episodic neuropathic pain
• Paroxysmal neuralgia
• Trigeminal neuralgia
• Glossopharyngeal neuralgia
• Geniculate neuralgia
• Superior laryngeal neuralgia
• Nervus intermedius
• Neurovascular pain
• Continuous neuropathic pain
• Neuritis
• Peripheral neuritis
• Herpes zoster
• Postherpetic neuralgia
• Deafferentation pain
• Neuroma
• Atypical odontalgia
• Sympathetically maintained pain
19

20. PSYCHOLOGIC CONDITIONS
• Mood disorders
• Depressive disorders
• Bipolar disorders
• Mood disorders due to a medical condition
• Anxiety disorders
• Generalised anxiety disorder
• Post traumatic stress disorder
• Anxiety disorders due to medical condition
• Somatoform disorders
• Undifferentiated somatic disorders
• Conversion disorders
• Pain disorders
• Hypochondriasis
• Other conditions
• Malingering
• Psychologic factors affecting a medical condition
• Personality traits or coping style
• Maladaptive health behavior
• Stress related physiologic response
• Any other mental disorders not mentioned in this
classification 20

21. 21

22. 1. Hyperreactive pulpalgia
a. Dentinal hypersensitivity
b. Hyperemia
2. Acute pulpalgia
a. Incipient
b. Moderate
c. Advanced
3. Chronic pulpalgia
a. Barodontalgia
PULPAL CAUSES OF PAIN
4. Hyperplastic pulpitis
5. Necrotic pulp
6. Internal resorption
7. Traumatic occlusion
8. Incomplete fracture
22

23. PAIN OF NON-DENTAL ORIGIN
II) NEUROVASCULAR TOOTHACHE - ASSOCIATED WITH MIGRAINE VARIANTS
CLINICAL FEATURES
1. Toothache is characterized by remission
2. Temporal behavior
3. Minor or no dental cause
I) MUSCULAR TOOTHACHE - TEMPORALIS, MASSETER
CLINICAL FEATURES
1. Constant tooth ache which is non pulsatile
2. Not responsive to local provocation of the tooth
3. Pain increases with function of involved muscle
4. LA - not effective
5. LA of involved muscle - reduces toothache
23

24. 4. Following dental treatment - pain may spread to adjacent teeth, opposing teeth or entire face
5. Associated autonomic effects - nasal congestion, lacrimation, edema of eyelids and face
III) CARDIAC TOOTHACHE
CLINICAL FEATURES
1. Aching pain is cyclic
2. Pain is increased with physical exertion and exercise
3. Toothache associated with chest pain
4. Toothache decreased with nitroglycerin tablets
5. Failure of toothache to respond to reasonable dental therapy
24

25. IV) NEUROPATHIC TOOTHACHE
CLINICAL FEATURES
1. Pain is unilateral, severe, lacerating, shock - like
2. Pain is provoked by a trigger
3. Local anesthesia at the tooth will not reduce the pain
4. Local anesthesia at the trigger will reduce the attack
V) SINUS TOOTHACHE
CLINICAL FEATURES
1. Pressure below eyes
2. Increased pain with lowering of the head
3. Increased pain with applied pressure over the sinus
4. Local anesthesia of tooth not eliminating pain
5. Diagnosis confirmed by imaging studies
25

26. 26

27. V) PSYCHOGENIC TOOTHACHE
CLINICAL FEATURES
1. Multiple teeth reported painful
2. Physiologic patterns of pain not applicable
3. Chronic pattern of pain
4. Lack of response to reasonable dental treatment
5. Not identifiable as any other pain condition
DIFFERENTIAL DIAGNOSIS
 HETEROTROPHIC REFERRED PAIN
 NEUROPATHIC PAINS
 PAINS OF CENTRAL ORIGIN
27

28. SOMATOSENSORY SYSTEM
TYPES OF SENSATIONS
• The sensations are generally classified into four types :
a) Epicretic sensations
b) Protopathic sensations
c) Deep sensations
d) Special sensations
28

29. A) Epicretic sensations
• Mild or light sensations
• These sensations are perceived more accurately
 Fine touch or tactile sensation
 Tactile localization
 Tactile discrimination
 Temperature sensation with finer range i.e., between 25 and 40°C
29

30. B) Protopathic sensations
• Crude sensations or the primitive type of sensations
 Pressure sensation
 Pain sensation
 Temperature sensation with a wider range
ie. Above 40°C and below 25°C
30

31. C) Deep sensations
Sensations arising from the deeper structures beneath the skin and the
visceral organs
 Sensation of vibration or pallesthesia
 Kinesthetic sensation or kinesthesia
 Visceral pain arising from viscera
31

32. D) Special sensations
• The special senses are :
 visual sensation
 auditory sensations
 gustatory (taste) sensation
 olfactory (smell) sensation
32

33. NEURAL PATHWAY OF PAIN
Given by Fields -1987 ; modified later by others
Fields divided the processing of pain from the stimulation of primary
afferent nociceptors to the subjective experience of pain into four steps :
•TRANSDUCTION
•TRANSMISSION
•MODULATION
•PERCEPTION
33

34. I. Transduction: process by which noxious stimuli is converted to
electrical activity in the appropriate sensory nerve endings
II. Transmission: refers to neural events that carry nociceptive input
into CNS for proper processing. In this, first and second order
neurons are involved
III. Modulation: refers to the ability of the CNS to control the pain
transmitting neurons
IV. Perception: if the nociceptive input reaches the cortex, perception
occurs. It is at this point the suffering and pain behavior begins
34

35. TRANSDUCTION
is the activation of the primary afferent nociceptor
External stimuli
• Intense thermal
• Mechanical stimuli
• Noxious chemicals
• Noxious cold
Endogenous Chemical
Substances (Inflammatory
Mediators)
• Polypeptide bradykinin (BK)
• Potassium
• Histamine
• Serotonin
• Arachidonic acid
35

36. • Activation of cutaneous C fibers causes their cell bodies to synthesize :
• Neuropeptides
• Substance P
• Calcitonin gene–related peptide (CGRP)
WHICH IS RESPONSIBLE FOR PROLONGED PAIN
36

37. NEUROTRANSMITTERS
SMALL (rapid acting)
Acetylcholine
NOREPINEPHRINE
SEROTONIN
GAMMA
AMINOBUTYRIC ACID
GLYCINE
DOPAMINE
ASPARTATE
LARGE (slow acting)
Substance P
Endorphins
37

38. Pain receptors
FIRST ORDER NEURONS
SPINAL CORD
Three classes of nociceptive afferent neurons provide the input whereby the brain perceives pain :
1. Mechanothermal afferents are primarily A∂ fibers : respond to intense thermal and mechanical stimuli
2. Poly modal afferent C fibres : conduct more slowly : respond to mechanical thermal and chemical stimuli
3. High Threshold mechanoreceptive afferents are chiefly A∂ Fiber normally respond to intense mechanical stimuli
First order neurons are the cells in the posterior nerve root ganglia
These neurons receive impulses of pain sensation from the pain receptors through their
dendrites and their axons reach the spinal cord
38

39. • The fibers of fast pain sensation are carried by A∂
afferent fibers
• After reaching the spinal cord, the fibers synapse with
marginal cells in the posterior gray horn
• The fibers transmitting impulses of slow pain belong to
C type and these fibers synapse with substantia
gelatinosa in the posterior gray horn
39

40. Sensory receptors
Spinal cord
Spinothalamic pathway
Thalamus & cortex
Muscle
1st order neuron
Dorsal root
2nd order neuron
Interneuron
3rd order neuron
40

41. There are 2 systems for processing the pain signals on their way to the brain :
1) The neospinothalamic tract for fast pain
2)The paleospinothalamic tract for slow pain
41

42. 42

43. TRANSMISSION
Refers to the process by which
peripheral nociceptive
information is relayed to the
central nervous system by
second and third order neurons
43

44. SECOND ORDER NEURONS
• From spinal cord to the thalamus
• The marginal cells and the cells of substantia gelatinosa form the second
order neurons
• Fibers from these cells ascend in the form of the LATERAL
SPINOTHALAMIC TRACT situated near the gray matter
• Fibers of marginal cells for fast pain are long. Immediately after taking
origin, the fibers cross the midline via anterior gray commissure, reach the
anterolateral white column and ascend.
• These fibers form the NEOSPINOTHALAMIC TRACT, a part of lateral
spinothalamic tract.
44

45. • The third order neurons of pain pathway are the
neurons of thalamic nucleus, reticular formation,
tectum and gray matter around aqueduct of Sylvius.
• Axons from these neurons reach the sensory area of
cerebral cortex
• Some fibers from reticular formation reach
hypothalamus
45

46. MODULATION
• Refers to mechanisms by which the
transmission of noxious information to the
brain is reduced
• Endogenous opioid system - pain modulation
46

47. Brain Opiate System
• 1965, Reynold proposed presence of morphine like substances :
• Endorphins
• Enkephalins
• Dynorphin
• Believed to cause pre and post synaptic inhibition of type C and Aδ fibres
• Serotonin and norepinephrine also play a role in descending inhibitory pathway
47

48. • Multiple areas of brain show opiate receptors
 Enkephalin - brain stem and spinal cord
 -Endorphine - hypothalamus and spinal cord
 Dynorphin - brain stem and spinal cord
Intrinsic analgesic potency similar to morphine
• Abundance of opiate receptors present in brain in Amygdala & remainder of limbic
called Emotional or Visceral Brain
• Mediates integration of sensory information pertaining to pain & emotional behavior
48

49. 49

50. • Behave like morphine & bind to opiate receptors to obtund pain like
morphine
• β endorphin - closely related to pituitary function
• The enkephalin & endorphins have antinociceptive effects
• Underlying mechanism not fully analyzed
Endorphins
β-Endorphin has approximately 80 times the analgesic potency of morphine
50

51. • Secreted by nuclei that originate in median raphe of the brain stem &
project to many areas of brain & spinal dorsal horn.
• Released when necleus raphe magnus in brain stem stimulated by
sensory input
• Released by blood platelets, synthesized in CNS
• Potentiate endorphin – analgesia
Serotonin
51

52. • The pain receptors adapt very little OR not at all
• As the pain stimulus continues, excitation of the pain fibers becomes progressively
greater
• Increase in sensitivity of pain receptors is called hyperalgesia
• Significance : keeps the person apprised of a tissue damage stimulus as long as it
persists
Nonadapting Nature Of Pain Receptors
52

53. • Pain impulses are believed to be conducted into the central nervous
system by two types of nerve fibers, which are classified by the size
and speed at which they conduct the impulse
PATHWAYS OF PAIN SENSATION
53

54. CENTER FOR PAIN SENSATION
• The center for pain sensation is in the post central gyrus of parietal
cortex.
• Fibers reaching hypothalamus are concerned with arousal mechanism
due to pain stimulus.
57

55. Referred Pain
• The pain is not felt over the area where the viscus is situated but felt
some where else
• Felt in the area where the viscus was situated in the embryonic life
e.g.
• Pain of heart - left arm, neck
• Pain of center of diaphragm - tip of shoulder
• Lower molar to ear
58

56. FEATURES OF REFERRED PAIN
Wholly spontaneous
Not accentuated by provocation of site
Ceases immediately if primary pain is arrested
Felt in superficial or deep structures
59

57. Theories Of Referred Pain
• The two most popular theories are
1) Convergence – Projection
2) Convergence - Facilitation
1. Convergence-Projection Theory:
• This is the most popular theory
• Primary afferent nociceptors from both visceral and cutaneous
neurons often converge onto the same second-order pain transmission
neuron in the spinal cord
60

58. Brain having more awareness of cutaneous than of visceral structure through past
experience, interpret the pain coming from the regions served by cutaneous afferent
fibers
EXAMPLE (Milne et al 1981)
61

59. 2. Convergence – Facilitation Theory:
•Similar to convergence – projection theory
•Believed that the internal organs were insensitive to stimuli and that
they created a irritable focus on the spinal cord leading to R.P.
•Did not hold good
62

60. Afferent fiber is bifurcated before connecting to the dorsal horn
3. Axon-Reflex
4. Thalamic Convergence
Referred pain is perceived as such due to the summation of neural
inputs in the brain
63

61. 64

62. Dental condition that causes head and neck pain
1. Hypersensitive dentin
2. Cracked tooth syndrome
3. Pulpal and periapical system
4. Barodontalgia
Oral condition that cause head and neck pain
.
1. PDL disease pain
2. TMJ disturbance
3. MPDS
4. Bruxism
5. Pain from cysts and tumour dry socket
6. Traumatic neuron
65

63. Pathway From Dental Pulp To Cortex :- (mand molar)
Once the nociceptors located in the pulp activated
the impulse is carried into the CNS by primary afferent neuron in the
mandibular branch of 5th nerve
GASSERIAN OR TRIGEMINAR GANGLION
Nucleus Caudalis
Nucleus Oralis may also play important role
Fast pain Slow pain
Thalamus Reticular formation
Sensory cortex 66

64. 67

65. THEORIES OF PAIN
69

66. • Peripheral free nerve endings mediate pain
to the central apparatus
• Direct line from receptor to the brain
• Pulling one end of the rope causes a ring on
the other end of the bell
• No morphological basis
Specificity Theory
Descartes - 1664
70

67. Intensity Theory :
Mumford & Newton-1971
• Pain is caused when nerve is stimulated beyond certain level
• Pain is non-specific sensation
• Depends on high intensity stimulation
• e.g., application of heat is pleasant ; but more heat causes burning
• Intensity of stimulation is a factor in causing pain
71

68. Protopathic & Epicritic Theory
Head & Rivers 1908
• Two groups of sensory nerves from periphery to CNS
• Protopathic – primitive, yielding diffuse impression of pain & temperature
• Epicritic- concerned with touch & small changes in temperature
• These groups do not exist
72

69. Pattern Theory
Goldscheider 1894
• Pain is produced by intense stimulation of non-specific receptors
• Pain sensation depends on spatiotemporal pattern of nerve impulse
reaching brain
• spatio-temporal:- warmth, cold, pain
(according to Weddel 1955)
• Pattern of nerve impulse entering the brain will be different for different
regions
• Designation of sensation as hot, cold, tingling etc., is somewhat arbitrary
since there are many grades in between
73

70. 74

71. GATE CONTROL THEORY Melzack & Wall 1965
75

72. 76

73. • Proposed by Ronald Melzack and Patrick Wall in 1965 & in 1982
• Described psychological mechanism by which psychological factors can
affect the experience of pain
• Neural gate can be open & close - modulate the pain
• Gates are located in spinal cord
• Allow to pass directly to the brain
• Altered prior to being forwarded to the brain (for instance, influenced by
expectations)
• Prevented from reaching the brain (eg: by hypnosis-induced anesthesia)
77

74. Although the theory may be simply stated, its ramifications are
extremely complex
Gate Control Theory postulates :
1. Information about the presence of injury is transmitted to the central nervous system
by small peripheral nerves
2. Cells in the spinal cord or nucleus of the fifth cranial nerve, which are excited by these
injury signals, are also facilitated or inhibited by other large peripheral nerves that
also carry information about innocuous events (for example, temperature or
pressure)
3. Descending control systems originating in the brain modulate the excitability of cells
that transmit information about injury
78

75. 79

76. Large-diameter fiber input has the ability to modulate synaptic transmission of
small-diameter fibers within the dorsal horn
• Large diameter fibers transmit impulses
at a greater rate of speed than do small diameter fibers
initiated by pressure, vibration, and temperature
• Small diameter fibers transmit noxious or painful sensations
• Intentional stimulation of the large fiber system results in inhibition of synaptic
transmission within the smaller, pain producing fibers
• Acupuncture and
• transcutaneous electrical nerve stimulation (TENS)
80

77. 81

78. Factors Involving In Opening & Closing Of Gate
• Amount of activity in pain fibers
• Amount of activity in other peripheral fibers
• Message that descend from brain
82

79. Factors that open the gate
• Physical conditions
o Extent of injury
o Inappropriate activity level
• Emotional conditions
o Anxiety or worry
o Tension
o Depression
• Mental conditions
o Focusing on pain
o boredom
Conditions that close the gate
• Physical conditions
 Medications
 Counter stimulation
• Emotional conditions
 Positive emotions
 Relaxations, rest
• Mental conditions
 Intense concentrations or
distraction
 Involvement and interest in life
activities
83

80. CAUSES OF OROFACIAL PAIN
1. Local Pathosis of Extracranial Structures – can arise from:
a. Tooth pulp, periodontium, periradicular structures, gingiva, mucosa
b. Salivary gland disorders – mumps , acute parotitis (children)
- mucus plug, sialolith (adults)
- Sjogren’s syndrome(inflammation)
c. Ear pain – otitis media, otitis externa, mastoiditis
84

81. d. Sinus & paranasal pain – maxillary, frontal & ethmoid sinusitis
e. Tongue
f. Eyes
g. Temporomandibular joint articular disorders – polyarthritis, disc derangements,
osteoarthritis, dislocations, fractures
85

82. 2. Intracranial causes –
a. Neoplasm
b. Aneurysm
c. Meningitis
d. Hematoma / hemorrhage
86
e. Edema
f. Abscess
g. Angioma
h. Cerebrovascular accidents
I. Venous thrombosis

83. 3. Referred pain from remote pathologic sites – can be from:
a. Heart – angina pectoris , myocardial infarction
b. Thyroid – inflammation
c. Carotid artery – inflammation , other causes
d. cervical spine – inflammation , trauma , dysfunction
e. muscles – myofascial trigger points
87

84. 4 . Neurovascular causes –
a. Migraine
b. Cluster headaches & chronic paroxysmal hemicrania
c. Headaches with vascular disorders – arteritis, hypertension
d. headaches with substance exposure or withdrawal – nitrates, alcohol, narcotics,
caffeine
e. Headaches with metabolic disorders – hypoxia, hypoglycemia, dialysis
88

85. 5. Neuropathic causes –
a. Paroxysmal
- Trigeminal neuralgia
- Glossopharyngeal neuralgia
- Nervus intermedius neuralgia
- Occipital neuralgia
- Neuroma
b. Continuous
- Postherpetic neuralgia
- Post – traumatic neuralgia
- Anesthesia dolorosa
89
6. Causalgic pain – reflex sympathetic dystrophy - arises from sympathetic nervous system

86. 7. Muscular pains –
a. Myospasm pain
b. Myositis pain
c. Local myalgia – unclassified
d. Myofascial pain
- tension – type headaches
- coexisting migraine and tension-type headaches
8. Unclassifiable pains / atypical facial pains
a . Atypical odontalgia
b. Burning mouth syndrome
90

87. HISTORY
1. Chief complaint – a) Location of Pain
b)Onset Of Pain – associated with other factors
- progression
c)Characteristics of Pain - Quality
- Behaviour
- Intensity
- Concomitant symptoms
- Flow of the pain
d)Aggravating / Alleviating Factors
e)Past Treatments
2. Past Medical History
3. Psychologic Assessment
91
DIAGNOSIS OF PAIN

88. 92
CHARACTERISTICS OF PAIN

89. CLINICAL EXAMINATION
1. General examination
• Vital Signs
• Cranial Nerve Evaluation
• Eye / Ear Evaluation
• Cervical Evaluation
• Balance Coordination
93

90. 2. Muscular examination
• Pain & Tenderness
• Trigger Points & Pain Referral
3. Masticatory Evaluation
• Range Of Mandibular Movements
• Temporomandibular Joint Evaluation
• Oral Structures ( Teeth, Periodontia, Occlusion )
4) Other Diagnostic Tests
• Thermal Test
• Pulp Vitality Test
• Imaging
• Laboratory Tests 94
MRI
CT
ULTRASOUND
SINGLE PHOTON CT
POSITRON ELECTRON
TOMOGRAPHY

91. Locating the source of pain – DIAGNOSTIC BLOCKS
LA at site of pain fails to reduce pain
LA at source of pain reduces the pain at
the source as well as the site
95

92. ASSESSMENT OF PAIN
Numerical Rating Scale 0-10 Scale
Visual Analog Scale Mark point on 10 cm line
McGill Pain Questionnaire
Pt. identifies terms describing pain
from 20 sets of words
West Haven Yale Multidimensional
Pain inventory
Language skills
52 questions assessing various aspects
of pain
Faces Scale
Pictures of Faces ranging from smiling
to crying indicating level of discomfort
96

93. 97
FACES SCALE

94. • A visual analog scale is a line that represents a continuum of a particular
experience, such as pain
• The most common form used for pain is a 10 cm line, whether horizontal
or vertical, with perpendicular stops at the ends
• The ends are anchored by “No pain” and “Worst pain imaginable”
1. Visual Analog Scale:
98

95. • Patients are asked to place a slash mark somewhere along the line to indicate
the intensity of their current pain complaint.
• For scoring purposes, a millimeter ruler is used to measure along the line and
obtain a numeric score for the pain ratings.
• Children as young as 5 years are able to use this scale.
99

96. 100

97. • It is a verbal pain scale that uses a vast array of words commonly used to
describe a pain experience.
• The words are listed in 20 different categories in order of magnitude
from least intense to most intense and are grouped according to
distinctly different qualities of pain.
• The patients are asked to circle only one word in each category that
applies to them.
2.McGill Pain Questionnaire
101

98. • First 10 categories represent different sensory descriptors that cover
various temporal, spatial, pressure, and thermal qualities of pain
• Next five categories are affective or emotional descriptors
• Category 16 is evaluative (ie, how intense is the pain experience)
• Last four categories are grouped as miscellaneous.
102

99. 103

100. • To score the questionnaire, the words in each category are given a
numeric value
• The first word in each category ranks as 1, the second as 2, etc
• The scores for each category are added up separately for the sensory,
affective, evaluative, and miscellaneous groupings
• Then the total number of words chosen is also noted
104

101. • Biological
• Genetic variations leads differences in amount & type of neurotransmitters.
• Previous pain experience
• Gender
• Cognitive
• Younger –report greater level of pain
• Older children understand the meaning of pain
• Upto 3 months- no understanding of pain but memory is present
• By 6 month respond to pain by anger
• By 20 months anger becomes more dominant
Factors That Influence Pain
105

102. • Psychologial
• Feeling of lack of control - intensify pain perception
• Sociocultural
• Difference in perception exist among different cultural group
• Parents perception & response to their child’s pain strongly influence child’s
perception & his reaction to pain
Are Indians and Females Less Tolerant to Pain? An Observational Study Using a Laboratory Pain Model
Med J Malaysia Vol 64 No 2 June 2009
106

103. Thresholds for Sensation and Pain
• Three thresholds for sensation and pain help in understanding the
experience of pain :
1. Sensory threshold
2. Pain threshold
3. Pain tolerance/response threshold
Psychologic Factors Modifying Pain
107

104. • First time the subject reports perception of any sensation is termed the
"sensory threshold."
• This is defined as the lowest level of stimuli that will cause any response
• Pain threshold : As the current is increased, the sensation becomes
stronger until the subject states that it is painful.
• Neurologically, when the summation of firing of primary afferent
nociceptive fibers reaches a certain point, pain is perceived
108

105. Pain tolerance
• If the intensity of the electrical current is increased above pain threshold, a level
of pain will be reached that the subject can no longer endure.
• At this point, the individual makes an attempt to withdraw from the stimulus.
• The range between the pain threshold and response threshold is termed a
person's tolerance to pain
109

106. 110
Differential Diagnosis of Pain

107. 112

108. SITE OF PAIN REFERRAL INVOLVED TEETH
Frontal region Maxillary incisors
Nasolabial area
Maxillary canine
Maxillary premolars
Temporal region Maxillary 2nd premolar
Below mandibular molar area Maxillary 2nd & 3rd molar
Ear Mandibular molars
114

109. Mental region Mandibular incisor , canine & premolar
Angle of mandible Mandibular first & second molar
Midramal region Mandibular second pre molar
Superior laryngeal area Mandibular 3rd molar
Maxillary premolar Maxillary canine
Maxillary molars
Maxillary canine
Mandibular premolars
Mandibular premolars
Maxillary canine
Maxillary premolars
Mandibular first premolar Mandibular first and second molar
Glick DH 1962
115

110. Pulpal And Periapical Pain
117

111. Hypothetical Mechanism For Pain In Pulp
1. Cholinergic neurotransmitters(Ach) – found in pulp
2. ANS :
The neurotransmitters elaborated by autonomic efferent in inflamed pulp
Bradykinin level during inflammation increases significantly
3. Adrenergic neurotransmitters (histamine) released from inflamed pulp
(mast cell)
118

112. 4. Prostaglandin :
• Present in inflamed tissue
• Create pain by direct irritation of nerve endings
• Alerts the sensors to kinin
• Bradykinin in minute conc. evokes pain
5. Cyclic AMP – cGMP
• Nerve stimulated – increased amount of c AMP – hyperpolarization of
nerve – decreased transmission of nerve impulse
• cGMP – depolarization of neurons – increased neuronal excitability
119

113. 6.Lowered O2 tension
• Decreased O2 tension - nerve impulses fired rapidly
• Pulpal ischemia - cell injury
• Outer membranes, subcellular mitochondria, lysosomes damaged
• Accumulation of Ca++ ions and release of enzymes that break down cell
components
• Reduced O2 tension in pulp
• Stimulation of sympathetic and parasympathetic nerves in blood vessels of
pulp, during this period generate pain
120

114. 7.Increased Intrapulpal pressure –
Inflammation
Increased temperature
Increased intrapulpal pressure
Pain
8.Specific infection of pulp and P.A. tissue
• Responsible for transmitting or modulating nerve impulses
• Therefore may be related to pain or pulpitis.
This theory is still unclear
121

115. METHODS OF PAIN CONTROL
1. Removing the cause
2. Blocking the pathway of painful impulses
3. Raising the pain threshold
4. Preventing pain by cortical depression
5. Using psychosomatic methods
122

116. Method Of Control Of Pain In Restorative Dentistry
• Gaining confidence of the patient : fear - pain
• Sharp instruments employed with skill and confidence
• Use of cooling devices
• Use of obtundents
• Preventing desiccation of the dentin
• Local anesthesia
• General anesthesia
• Newer methods of pain control
123

117. • Supra periosteal infiltration
• Regional nerve block : depositing suitable local anesthetic solution close to a main nerve
trunk preventing afferent impulses from traveling centrally beyond that point
Local Anesthesia
124

118. • Posterior superior alveolar nerve
• Anterior superior alveolar nerve
• Greater palatine
• Nasopalatine
Maxillary Anesthesia
• Inferior alveolar nerve block
• Incisive nerve block
• Mandibular block
• Vasirani Akinosi technique (closed mouth technique)
Mandibular Anesthesia
125

119. • Intra Osseous Anesthesia
• Intra Ligamentary Anesthesia
• Intra Septal Anesthesia
• Intra Pulpal Anesthesia
Additional Local Anesthetic Procedures
126

120. • Anesthetize soft tissue and bone overlying the apical region of the tooth through
local infiltration
Intraosseous injection
Intraseptal infiltration
• 27 gauge 1 inch needle
• More successful in younger patients - less density of bone
Intrapulpal injection
• Used when all other techniques have failed or during endodontic therapy as an
adjunct
• Most commonly on mandibular molars, but not exclusively
• Intense, instantaneous pain is usually felt by the patient
127

121. • Conscious sedation
• Nitrous oxide gas
General Anesthesia
128

122. • General anesthesia should not be administered in dental clinics which
are not equipped with :
• Surgical grade suction unit
• Medication kit including oxygen to tackle any anesthetic complications
• Adequate floor assistance
• Large comfortable area for recovery of the patient
• Access to medical emergency services
Precautions
129

123. • Patients with acute inflammatory lesions in which local anesthetic is likely to be effective
• Over - reactive patients
• Patients who experience repeated fainting after intra-oral injections patients who are intolerant of
drill noises
• Children who are uncooperative
• Patients who experience a hyperactive gagging reflex
• Patients with cardiovascular conditions, in whom mental stress should be avoided
• Patients with neuro/psychological disorders or emotional instability
• Patients with histories of convulsions and fits
• Patients who are handicapped with involuntary muscular movements or spasms, or who have
inability to communicate adequately
Indications
130

124. Advantages
 Practically universally accepted
 Increased safety
 Adverse reactions less frequent
 Adverse reactions less severe
Oral sedation
Disadvantages
× Slow onset of action (15 - 30) minutes
× Long duration of action (3 - 4hr)
× Inability to rapidly increase or decrease of
sedation
× Patient require escort from office
Drugs which can be used for sedation include diazepam, triazolam, zaleplon, lorazepam, and
hydroxyzine
131

125. Advantages
 Rapid onset of action
 Ability to titrate to ideal level of sedation
 Ability to rapidly increase or decrease sedation
level
 Total clinical recovery within 3 to 5 minutes
 Ability to discharge most patients without need
for adult escort
Inhalation Sedation
Disadvantages
× Cost and size of equipment
× Requirement for education in proper use of inhalation
sedation
Potential Complications:
× Chronic exposure of low level of nitrous oxide
× Abuse potential of nitrous oxide
132

126. • A favorable mental attitude may be established through suggestions of relaxation.
• Better control over patients habits such as talking, rinsing.and oral tissue tension
Hypnosis
133

127. DRUGS COMMONLY USED TO MANAGE ACUTE DENTAL PAIN
134

128. NSAIDS CONSIDERED SAFE
Paracetamol
Ibuprofen
Naproxen
Paracetamol with codeine
Dental Pain during Pregnancy
ANALGESICS TO AVOID
Aspirin
Ibuprofen
Naproxen
Codeine
ANTIBIOTICS CONSIDERED SAFE
Penicillin
Amoxicillin
Cephalexin
Clindamycin
Metronidazole
135

129. • Preoperative oral NSAID, one hour before start of treatment
• Local anesthetic of choice for pain control during surgery
• Bupivacaine or etidocaine HCL administration at END of procedure
immediately prior to dismissal of patient
• Continue oral NSAIDs on timed basis for number of days deemed
appropriate
• Postoperative telephone call evening of appointment
Pain Management Protocol
136

130. • Vibrotactile devices
• Computer controlled LA delivery system
• Jet injectors
• Safety dental syringes
• And devices for IO anaesthesia
NEWER PAIN CONTROL METHODS
137

131. 1. Vibraject : attached to normal syringe, high frequency vibration
1. DentalVibe : It is a cordless, rechargeable, hand held device that delivers
soothing, pulsed, percussive micro-oscillations to the site where an injection is
being administered
138

132. • Accupal :
• CCLAD : Incorporated computer technology to control the rate of flow of the anesthetic
solution through the needle
• WAND
• Comfort Control Syringe
139

133. •SYRIJET
•MEDJET
140

134. • Stabident system : 2 parts: a perforator, a solid needle that
perforates the cortical plate of bone with a conventional
slow-speed contra-angle handpiece, and an 8 mm long, 27-
gauge needle that is inserted into this predrilled hole for
anesthetic administration
• X-tip :Composed of a drill and guide sleeve.
• IntraFlow :
Newer Intraosseous LA
141

135. PAIN THERAPY FOR OROFACIAL PAIN
142

136. MANAGEMENT OF OROFACIAL PAIN – THERAPEUTIC MODALITIES
1. Pharmacological therapy
• Analgesic agents – NSAIDs & narcotic agents
• Anesthetic agents – topical / injectable local anesthetics
• Anti – inflammatory agents
• Anticonvulsants
• Muscle relaxants
• Antidepressants
• Anxiolytic
• Antihistamine
• Others – clonidine ; baclofen ; gabapentine ; tramadol ; NMDA
receptor antagonist
143

137. OPIOIDS
Opioid analgesics bind to opioid receptors
& causes decrease in neurotransmission
by several mechanisms
Morphine ; codeine
Pentazocine ; butorphanol
144

138. ANTIINFLAMMATORY AGENTS
Acts by preventing formation of
prostaglandin E by inhibiting the
cycloxygenase pathway
Aspirin, NSAIDs, Corticosteroids
145

139. 146

140. ANESTHETIC AGENTS
Acts by blocking conduction in the sodium (Na) channel
Uses:
a. To arrest primary pain input
b. To interrupt pain cycling
c. To resolve myofascial trigger point activity
d. To induce a sympathetic blockade in cases of :
- reflex sympathetic dystrophy
- herpes zoster
- postherpetic neuralgia
147

141. ANTICONVULSANTS
Action is by blocking sodium channel & suppressing neuronal discharge
- CARBAMAZEPINE (Tegretol)- exerts analgesic effects by central potentiation of
adrenoreceptor & by increasing the nor-adrenergic output
- PHENYTOIN SODIUM (Dilantin)
148

142. ANXIOLYTIC AGENTS
BENZODIZEPINES
BARBITURATES
Their action is on GABA – a RECEPTORS
149

143. MUSCLE RELAXANTS
Act by CNS depression
- CYCLOBENZAPRINE has anticholinergic activity & works
on the neuromuscular junction to reduce electrochemical
signals
-SUCCINYLCHOLINE CHLORIDE
-METHOCARBAMOL
150

144. ANTIDEPRESSANTS
It acts by inhibiting the reuptake & storage of Neurogenic
amines :
- SEROTONIN
- NOREPINEPHRINE
- AMITRIPTYLINE
151

145. ANTIHISTAMINES
They may have some analgesic activity by virtue of
reduction of histamine released in the area of inflammation
- DIPHENHYDRAMINE
- HYDROXYZINE
- PYRILAMINE
152

146. SURGICAL MANAGEMENT OF OROFACIAL PAIN –
TRIGEMINAL NEURALGIA
- interruption of pain pathways between center & periphery achieved
by:-
EXTRACRANIALLY :
1. Alcohol block in peripheral nerve
2. Peripheral neurectomy – supra / infra orbital
- lingual
- inferior alveolar nerve ( Ginwalla’s tech.)
3. Electrosurgery
4. Cryosurgery
5. Selective radiofrequency thermocoagulation
153

147. INTRACRANIALLY:
1. Alcohol blockade of the gasserian gangloin
2. Radio – frequency thermocoagulation of gasserian ganglion
3. Retrogasserian rhizotomy
4. Medullary tractotomy
5. Midbrain tractotomy
6. Intracranial sensory nerve root decompression
- jannetta’s approach
- dandy’s approach
154

148. OTHER ADJUVANT THERAPIES
1. Acupuncture
2. Placebos
3. Ultrasound
4. Deep heat
5. Massage
6. Hypnosis
7. Physical activity
8. Exercises
9. Counselling
155

149. 156
• WHO analgesic ladder

150. • Pain is a diagnostic challenge. A doctor should be aware of
the physiologic and psychological aspects of pain and
anxiety as it applies to the patient. There is a vast array of
diseases that manifest with painful symptoms clinically.
• Adequate clinical assessment and diagnosis are the keys to
successfully manage such painfull conditions.
CONCLUSION

151. 158
1. Bell’s orofacial pain – Jeffrey P.Okeson.
2. Pain control in dentistry – Samuel Seltzer
3. DCNA -PAIN 1978
4. Orofacial pain- J. M. Mumford
5. Relief of pain in clinical practice – Samson Lipton

152. 159
Understanding medical physiology.
- Bijlani
- 3rd edition.
Textbook of medical physiology.
- Guyton and hall
- 10th edition.
Clinical oral physiology.
- Timothy S Miles.
Essentials of oral physiology.
- Robert M Bradley.
Management of temporomandibular disorders and occlusion.
- Jeffrey P okeson
- 5th edition
Oral bioscience.
- David B Fergusion

153. 160
1. REVIEW OF MEDICAL PHYSIOLOGY- GANONG
2. CONCISE MEDICAL PHYSIOLOGY- CHAUDHRI
3. TEXT BOOK OF MEDICAL PHYSIOLOGY :GYTON AND
HALL
4. TEXT BOOK OF MEDICINE :DAVIDSON
5. TEXT BOOK OF ENDODONTICS : INGLE
6. PATHWAYS OF PULP : COHEN
7. MONEIHM’s LOCAL ANESTHESIA : C R BENNET
8. ESSENTIALS OF MEDICAL PHYSIOLOGY : K.
SEMBULINGAM

154. 161