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Pain control in operative dentistry


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Pain control

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Pain control in operative dentistry

  4. 4. • Derived from Greek “Poin”; meaning “Penalty” • Derived from Latin “Poena”; meaning “Punishment from God” HISTORY 4
  5. 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. 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. 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. 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. 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. 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. 11. Cognitive : Subject’s ability to comprehend & evaluate Emotional : Represents the feeling that regenerated Motivational : Drive to terminate NEW DIMENSIONS TO PAIN 11
  12. 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. 13. Depending on experience, pain can be classified as : 1. Experimental 2. Acute 3. Chronic CLASSIFICATION OF PAIN 13
  14. 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. 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. 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
  18. 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. 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. 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. 21
  22. 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. 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. 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. 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. 26
  27. 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. 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. 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. 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. 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. 32. D) Special sensations • The special senses are :  visual sensation  auditory sensations  gustatory (taste) sensation  olfactory (smell) sensation 32
  33. 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. 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. 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. 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
  38. 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. 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. 40. Sensory receptors Spinal cord Spinothalamic pathway Thalamus & cortex Muscle 1st order neuron Dorsal root 2nd order neuron Interneuron 3rd order neuron 40
  41. 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. 42
  43. 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. 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. 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. 46. MODULATION • Refers to mechanisms by which the transmission of noxious information to the brain is reduced • Endogenous opioid system - pain modulation 46
  47. 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. 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. 49
  50. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 61. 64
  62. 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. 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. 64. 67
  65. 65. THEORIES OF PAIN 69
  66. 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. 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. 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. 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. 70. 74
  71. 71. GATE CONTROL THEORY Melzack & Wall 1965 75
  72. 72. 76
  73. 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. 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. 75. 79
  76. 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. 77. 81
  78. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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
  89. 89. CLINICAL EXAMINATION 1. General examination • Vital Signs • Cranial Nerve Evaluation • Eye / Ear Evaluation • Cervical Evaluation • Balance Coordination 93
  90. 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. 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. 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. 93. 97 FACES SCALE
  94. 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. 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. 96. 100
  97. 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. 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. 99. 103
  100. 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. 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. 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. 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. 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. 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. 106. 110 Differential Diagnosis of Pain
  107. 107. 112
  108. 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. 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. 110. Pulpal And Periapical Pain 117
  111. 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. 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. 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. 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. 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. 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. 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. 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. 119. • Intra Osseous Anesthesia • Intra Ligamentary Anesthesia • Intra Septal Anesthesia • Intra Pulpal Anesthesia Additional Local Anesthetic Procedures 126
  120. 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. 121. • Conscious sedation • Nitrous oxide gas General Anesthesia 128
  122. 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. 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. 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. 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. 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
  128. 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. 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. 130. • Vibrotactile devices • Computer controlled LA delivery system • Jet injectors • Safety dental syringes • And devices for IO anaesthesia NEWER PAIN CONTROL METHODS 137
  131. 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. 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. 133. •SYRIJET •MEDJET 140
  134. 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
  136. 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. 137. OPIOIDS Opioid analgesics bind to opioid receptors & causes decrease in neurotransmission by several mechanisms Morphine ; codeine Pentazocine ; butorphanol 144
  138. 138. ANTIINFLAMMATORY AGENTS Acts by preventing formation of prostaglandin E by inhibiting the cycloxygenase pathway Aspirin, NSAIDs, Corticosteroids 145
  139. 139. 146
  140. 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. 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
  143. 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. 144. ANTIDEPRESSANTS It acts by inhibiting the reuptake & storage of Neurogenic amines : - SEROTONIN - NOREPINEPHRINE - AMITRIPTYLINE 151
  145. 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. 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. 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. 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. 149. 156 • WHO analgesic ladder
  150. 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. 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. 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
  154. 154. 161