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- 1. PRESENTED BY, Dr. Sumit Rajewar BDS, MDS (Pedodontics and Preventive Dentistry)
- 2. CONTENTS Introduction Benefits of pain sensations History Definition Characteristics of pain Classification Components of pain Pain receptors Neural pain pathways Sensory neurons Peripheral mechanism of injury induced pain Pain pathways Theories of pain
- 3. Visceral pain Referred pain tooth pulp pain Pain assessment visual analogue scale Applied physiology Conclusion References
- 4. INTRODUCTION Pain is defined as unpleasant and emotional experience associated with or without actual tissue damage. Pain sensation is describe in many ways like sharp, pricking, electrical, dull ache, shooting, cutting, stabbing etc. As such, pain is typically associated with noxious stimuli, events that are potentially or actually damaging to tissue.
- 5. Benefits of pain sensation 1) Pain gives us warning signal about the problems. It also create awareness of injury. 2) Pain prevents further damage by causing reflex withdrawal of the body from source of injury. 3) Pain urges the person to take proper treatment to prevent major damage.
- 6. History Latin word ‘poena’ – punishment from God. Aristotle - first to distinguish 5 physical senses and considered pain to be the ‘passion of the soul’ Plato – contented pain and pleasure arose from within the body. The Bible – reference to pain not only in relationship to injury or illness but also anguish of soul.
- 7. Pain is, moreover, viewed either as a normal reaction to an abnormal stimulus or as an abnormal response to a normally harmless stimulus (Rasmussen, 1965). pain is a relative and subjective human experience, but it may be accompanied by objectively discernible phenomena, such as tachycardia, arterial hypertension, hyperpnoea and vocalization, and a major purpose of somatic pain seems to be, indirectly, that of inducing tissue repair (Lim & Guzman, 1968)
- 8. The pain threshold of the skin of a human subject, determined by electrical stimulation, is almost the same throughout the body, but the face and neck exhibit the relatively lowest values (Notermans, 1966). There is no appreciable difference between the threshold values of the right and left side of the human body, nor any diurnal variation (Notermans, 1966)., Age and sex do not seem to influence the pain threshold (Hardy, Wolff & Goodell, 1943), but the pain tolerance of females may be lower than that of males, (Notermans & Tophoff, 1967).
- 10. An unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage. - IASP 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. - Monheim DEFINITION
- 11. CHARACTERSTICS OF PAIN 1. Threshold and Intensity If the intensity of the stimulus is below the threshold (sub-threshold) pain is not felt. As the intensity increases more and more, pain is felt more and more according to the Weber-Fechner’s law. (This law ensures that while our body can perceive pain due to low intensity stimulus, a severe crushing injury will not cause death due to pain sensation, yet as stimulus increases, sense of perception also increases.)
- 12. 2. Adaptation – Pain receptors show no adaptation and so the pain continues as long as receptors continue to be stimulated. 3. Localization of pain - Pain sensation is somewhat poorly localized. However superficial pain is comparatively better localized than deep pain. 4. Influence of the rate of damage on intensity of pain If the rate of tissue injury (extent of damage per unit time) is high, intensity of pain is also high.
- 13. CLASSIFICATION OF PAIN Deep (from muscles/bones/fascia /periosteum) e.g. fractures/arthritis /fibrositis, rupture of muscle belly PAIN Somatic (somasthetic Visceral (from viscera) e.g. angina pectoris, peptic ulcer, intestinal colic, renal colic, etc Superficial (from skin & subcutaneous tissue) e.g. superficial cuts/burns, etc
- 14. OROFACIAL PAIN CLASSIFICATIONOROFACIAL PAIN CLASSIFICATION (OKESON)(OKESON) AXIS I (physical conditions) 1. Somatic pain A. Superficial Somatic pain a. Cutaneous pain b. Mucogingival B. Deep Somatic Pain a. Muscle pain b. TMJ pain c. Osseous pain d. Periodontal pain 2. Visceral pain a. Pulpal pain b. Vascular pain c. Neurovascular pain d. Visceral mucosal pain e. Glandular, ocular, auricular pain AXIS II (psychologic conditions) 1. Mood disorders 2. Anxiety disorders 3. Somatoform disorders 4. Other conditions a. Psychologic factors affecting a medical condition
- 15. Brain and spinal cord (CNS)
- 16. STRUCTURE OF A NEURON
- 18. STRUCTURE OF SPINAL CORD
- 20. Components of pain FIBRE TYPE FUNCTION CONDUCTIO N VELOCITY (mts. / sec) SPIKE DURATIO N (milisec) Myeli nated Fibre s Aα Proprioception, somatic motor 30-120 0.4-0.5 Aβ Touch, pressure and motor function 30-120 Aγ Motor to muscle spindles 15-35 Aδ Pain, temperature, touch 5-25 Myelinat ed fibres B Preganglionic autonomic fibres 3-15 1.2 Unm yelina ted Fibre s C Pain, temperature, touch and conducts impulses generated by cutaneous receptors 0.7-1.3 2
- 21. FAST PAIN Felt within 0.1 sec Sharp, pricking, acute, electric pain When needle is struck into the skin/electric shock/cuts Not felt in most deeper tissues of body. Transmitted through A pain fibres SLOW PAIN Felt after a second or more/maybe minutes. Burning, aching, throbbing, chronic pain. Associated with tissue destruction. Can occur in skin and in any deep tissue or organ. Results from primitive type C fibres.
- 23. PAIN RECEPTORS Sensory Receptors : At the distal terminals are the afferent (sensory) nerves, specialized sensory receptors that respond to physical or chemical stimuli Once these receptors are adequately stimulated, an impulse is generated in the primary afferent neuron that is carried centrally into the CNS. Classified in 3 main groups: 1. Exteroreceptors 2. Proprioceptors 3. Interoreceptors
- 25. EXTEROCEPTORS Stimulated by immediate external environment. Provide information from the skin and mucosa. Examples: 1. Merkel’s corpuscles ( tactile receptors in the submucosa of tongue) 2. Meissner’s corpuscles: tactile receptors in skin 3. Free nerve endings: perceive superficial pain and touch
- 26. PROPRIOCEPTORS Provide information from the musculoskeletal structures concerning the position and movement of the body. Automatic functioning Examples: 1. Muscle spindles: mechanoreceptors found between skeletal muscle fibres. 2. Golgi tendon organs: mechanoreceptors in the tendons of muscles signal muscle tension 3. Periodontal mechanoreceptors respond to biomechanical stimuli
- 27. Proprioception, which refers tooth position and movement of the limbs (kinaesthesia), is determined by mechanoreceptors located in skin, joint capsules and muscle spindles. The CNS integrates information received from these receptors, while keeping track of previous motor responses that initiated limb movement – a process known as efferent copy or corollary discharge (reviewed by Matthews, 1982).
- 28. INTEROCEPTORS Located in and transmit impulses from viscera of the body. Examples: 1. Pacinian corpuscles: concerned with perception of pressure. 2. Free nerve endings: perceive visceral pain and other sensations.
- 29. Development of Nociceptors Develop from neural crest stem cells. Neural crest cells are responsible mainly for development of the peripheral nervous system. Cells split off from the neural tube as it closes, and nociceptors grow from the dorsal part of this neural crest tissue. Forms late during neurogenesis.
- 30. Nociceptor Sensory input from various stimuli (either external or internal) is received by specific peripheral receptors, called as nociceptors. Nociception – responds as transducers and transmit impulses. Perception of pain. Found in all areas of body.
- 31. External nociceptors – skin, cornea and mucosa. Internal nociceptors – muscle, joint, bladder, gut and continuing along the digestive tract. Cell bodies of these neurons are located in either the dorsal root ganglia or the trigeminal ganglia. Trigeminal ganglia are specialized nerves for the face, whereas the dorsal root ganglia associate with the rest of the body.
- 32. Sensory neurons FIRST ORDER NEURONS (POSTERIOR NERVE ROOT GANGLIA) SECOND ORDER NEURONS (SUBSTANTIA GELATINOSA THIRD ORDER NEURONS (THALAMIC NUCLEUS, RETICULAR FORMATION, TECTUM, GREY MATTER) SOMATOSENSORY CORTEX
- 33. First Order Neuron Each sensory receptor is attached to a first order primary afferent neuron that carries the impulses to the CNS. The axons of these first-order neurons are found to have varying thickness. It has long been known that a relationship exists between the diameter of nerve fibers and their conduction velocities. The larger fibers conduct impulses more rapidly than smaller fibers. A general classification of neurons divides the larger fibers from the smaller ones.
- 34. Type A fibers Alpha fibers: size - 13 to 20 µm, velocity - 70 to 120 m/ s. Beta fibers: size – 6 to 13 µm, velocity – 40 to 70 m/s. Gamma fibers: size – 3 to 8 µm, velocity – 15 to 40 m/s. Delta fibers: size – 1 to 5 µm, velocity – 5 to 15 m/s. Type C fibers Size – 0.5 to 1 µm, velocity – 0.5 to 2 m/s.
- 35. Second Order Neuron The primary afferent neuron carries impulse into the CNS and synapses with the second-order neuron. This second-order neuron is sometimes called a transmission neuron since it transfers the impulse on to the higher centers. The synapse of the primary afferent and the second-order neuron occurs in the dorsal horn of the spinal cord.
- 36. Third Order Neuron Cell bodies of third order neurons of the nociception-relaying pathway are housed in: the ventro posterio lateral, the ventro posterioinferior, and the intralaminar thalamic nuclei Third order neuron fibers from the thalamus relay thermal sensory information to the somesthetic cortex.
- 39. Transduction Activation of nociceptor. 1. Intense thermal and mechanical stimuli, noxious chemicals, noxious cold 2. Stimulation of inflammatory mediators Damaged tissue release bradykinin, potassium, histamine, serotonin and arachidonic acid. Arachidonic acid produce prostaglandins and leukotrienes.
- 40. Bradykinin + Leukotriene + Prostaglandin Plasma extravasation Edema •PG stimulate nociceptors directly.
- 41. LK stimulates nociceptors indirectly by PMNs Release chemical mediators Stimulates nociceptor BK causes sympathetic nerve terminal to release PG thus stimulates nociceptor.
- 42. Sympathetic nerve terminal release another PG in response to its own neurotransmitter (norepinephrine). Such ongoing inflammatory state causes physiologic sensitization of nociceptors thus generating a response even to a non-painful stimuli and exaggerated response to noxious stimuli.
- 43. Transmission Process by which peripheral nociceptive information is relayed to CNS. First order neuron synapses with the secondary order neuron from where impulse is carried to higher structures of brain. Repeated or intense C fibre activation brings specific changes on N-methyl-D-aspartate receptors resulting in central sensitization, thus, response of second order neurons increases as well as size of the receptive field also increases.
- 44. Perception It is the subjective experience of pain. It is the sum of complex activities in CNS that may shape the character and intensity of pain perceived and ascribe meaning to pain.
- 45. Modulation • It is the mechanism by which transmission of impulse to the brain is reduced. • Nociceptive transmission is influenced by : a) Descending inhibitory systems that originate supraspinally b) Periaqueductal gray c) Nucleus raphe magnus d) Nucleus tractus solitarius e) Locus ceruleus/subceruleus f) Endogenous opioid peptides
- 46. Endogenous opioid peptides are naturally occurring pain- dampening neurotransmitters and neuromodulators employed in suppression and modulation of pain because they are present in large quantities in areas of brain associated with these activities.
- 47. Neurogenesis NEW NEURONS GENERATED FROM NEURAL STEM CELLS AND PROGENITOR CELLS.
- 48. Location of neurogenesis: 1) Subgranular Zone: (SGZ) Found between the hilus and granule cell layer and Dentate gyrus in hippocampus. Contains: SGZ astrocytes Precursor cells Granule neurons 2) Subventricular Zone: (SVG) Found along the wall of lateral ventricle as layer of dividing cells. Contains: Neuroblast SVZ astrocytes Immature precursors
- 49. Process of Neurogenesis (Cell proliferation) Cell proliferation is the generation of new cells. These new cells are produced within the ventricular zone.
- 50. Process of Neurogenesis (Cell Migration) Cell migration is the movement of newly generated cells to their final destination. Many daughter cells (called neuroblasts) migrate by slithering along thin fibers (radial glial cells) that radiate from the ventricular zone toward the pia
- 51. Process of Neurogenesis (Cell Differentiation) This is the stage when a newly generated cell begins to take on the appearance and characteristics of a neuron. Neuronal differentiation occurs first, followed by astrocyte differentiation and then oligodendrocyte differentiation.
- 52. 2nd Part (Pain pathway) Contents: Pain pathways Theories of pain Visceral pain Referred pain tooth pulp pain Pain assessment visual analogue scale Applied physiology Conclusion References
- 53. PAIN IMPULSE PATHWAYPAIN IMPULSE PATHWAY
- 54. Fibers from lateral spinothalamic tract Fibers from lateral spinothalamic tract Ventral posterolateral nucleus of thalamus, reticular formation & midbrain. Ventral posterolateral nucleus of thalamus, reticular formation & midbrain. Sensory cortexSensory cortex Receptor First order neuron Second order neuron Third order neuron center
- 55. Theories of pain: 1) Convergence Theory: 2) Facilitation Theory 3) Gate Control Theory
- 56. Convergence theory both somatic & visceral afferent fibers converge upon 2nd order neuron Somatic fibers conduct impulses more frequent. Visceral pain is felt as somatic pain because brain is familiar with somatic regions.
- 57. Facilitation theory Visceral & somatic fiber join at adjoining spinothalamic neurons( 2nd order neurons) Activation of spinothalamic neurons occurs due to strong impulses resulting in impulses passing through spinothalamic pathway This results in misinterpretation in location of pain.
- 58. Gate Control Theory Proposed by Ronald Melzack(Psychologist) & Pat-rick Wall (Anatomoist) The pain stimuli transmitted by afferent fibers are blocked by Gate mechanism located in posterior gray horn of spinal cord. If gate is OPENED, pain is felt. If gate is CLOSED, pain is suppressed.
- 59. Mechanism of Gate Control at Spinal cord: 1) When pain stimulus is applied on any part of body, besides pain receptors, then the receptor of other sensation such as touch sensation are also stimulated. 2) When all these impulses reach the spinal cord through posterior nerve root, then the fibers of touch sensation sends collaterals to the neurons of pain pathway 3) Impulses of touch sensation to passing to these collaterals inhibit the release of glutamate and substance-P from the pain fiber. 4) This closes the gate and pain sensation gets blocked.
- 61. Significance of Gate Control: Due to this, relief of pain through rubbing, massage technique, application of ice pack, acupuncture and electrical analgesia .
- 62. Visceral pain They are dull & diffuse, poorly localized, and associated with symptoms like nausea & referred to other areas Stimuli for visceral pain ischemia, obstruction, spasm, chemical stimuli.
- 63. Referred pain Pain felt in a part of the body other than its actual source Pain at diaphragm is felt over tip of shoulder Pain at maxillary sinus felt at nearby teeth. A tooth abscess can cause jaw bone pain.
- 64. Tooth pulp pain 1)Exposure of dentinal tubules causes toothache & other non noxious sensation. 2)Both Aδ & C fibers respond to stimuli in dentine 3)Transmission of stimuli across dentin, mediated by movement of fluid in dentinal tubules.
- 65. 4) Fibers terminate at medullary dorsal horn & synapse and also at trigeminal sensory nucleus 5) From trigeminal nucleus send to thalamus & sensory cortex 6) Pulpal innervation are capable of regenerating & reinnervating
- 66. Determinants of painful experience during dental treatment Pain occurs due to invasive procedures like extractions & surgeries or non invasive procedures. With regard to children, studies have shown that dentists do not believe in pain referred by children & tend not to use available methods to control pain. Conclusion: anxiety is determinant for pain during dental care & pain is related to local anesthetic procedures. There are evidences that dentists attitude are determinants for pain.
- 67. Pain assessment visual analogue scalePain assessment visual analogue scale
- 69. The sensory functions are affected by lesions in sensory pathways or other nervous disorders. 1)Anesthesia – loss of sensation 2)Hyperesthesia- increase sensitivity to sensory stimuli 3)Hypoesthesia- decrease sensitivity to sensory stimuli 4)Hemiesthesia – loss of sensation to one part of body 5)Paresthesia- abnormal sensation
- 70. 6) Dissociated anesthesia- loss of some sensation with loss of consciousness produced by anesthetic agents 7) General anesthesia- loss of all sensation with loss of conciousness produced by anesthetic agents 8) Local anesthesia- loss of sensation restricted area of body 9) Tactile anesthesia- loss of tactile sensation
- 71. 10) Hyperaglasia-increase in sensitivity to pain 11) Paraglesia- abnormal pain sensation 12) Thermic anesthesia- loss of thermal sensation 13) Analgesia- loss of pain sensation
- 72. Herpes zoster: Viral infection affecting dorsal root ganglion. Results in severe pain which facilitates the pain towards the ganglion.
- 73. Symptoms: The earliest symptoms of herpes-Headache, Fever 1) Burning pain 2) Itching 3) Hyperesthesia 4) Paresthesia Pain can be mild to extreme in the affected dermatome, with sensations that are often described as stinging, tingling, aching, numbing or throbbing.
- 74. Treatment: Analgesics Mild to Moderate - Topical lotions containing calamine Severe pain - Opioid medication such as morphine. Once the lesions have crusted over, capsaicin cream can be used. Topical lidocaine and nerve blocks may also reduce pain. Administering gabapentin along with antivirals may offer relief of post herpetic neuralgia
- 75. Antiviral: Antiviral drugs may reduce the severity and duration but they do not prevent post herpetic neuralgia. Acyclovir has been the standard treatment, but the new drugs Valaciclovir and Famciclovir having superior efficacy and good safety and tolerability.
- 76. Brown-Sequard syndrome All sensations are blocked at one side due to Damage to one half of the spinal cord. Sensations like pain, heat & cold, vibrations are Blocked. Causes 1) Spinal cord tumour, 2) Trauma -such as a gunshot wound 3) Ischemia Due to obstruction of a blood vessel 3) Infectious 4) Inflammatory diseases such as tuberculosis
- 77. Trigeminal neuralgia: Trigeminal neuralgia is a chronic pain disorder that affects the trigeminal nerve. Types: 1)Typical 2)Atypical
- 78. Treatment: Medical t/t: The anticonvulsant carbamazepine is the first line treatment; second line medications include baclofen, lamotrigine, oxcarbazepine, phenytoin, gabapentin and pregabalin. Uncontrolled trials have suggested that clonazepam and lidocaine may be effective. Antidepressant medications, such as amitriptyline have shown good efficacy in treating trigeminal neuralgia, especially if combined with pregabalin.
- 79. Non destructive Surgery: Microvascular decompression - this involves a small incision behind the ear and some bone removal from the area. And incision through the meninges to expose the nerve. Any vascular compressions of the nerve are carefully moved and a sponge-like pad is placed between the compression and nerve. Surgical t/t:
- 80. Destructive Surgery: •Glycerol injection- deposition of a corrosive liquid called glycerol at this point causes damage to the nerve to hinder pain signals. •Radiofrequency (thermocoagulation rhizotomy) - application of a heated needle to damage the nerve at this point. •Stereotactic radiosurgery (gamma knife surgery)- is a form of radiation therapy that focuses high-power energy on a small area of the body
- 81. Conclusion Pain can induce physiological & anatomical changes within the nervous system. The complexity of pain transmission means there are many pharmological targets & multimodel therapy is required to optimize pain control.
- 82. THANK YOU
- 83. References Essential of oral physiology- Robert M Bradley Textbook of medical physiology- Guyton & Hall Essential of medical physiology- K.Sembulingam & Prema Sembulingam Textbook of human physiology- S Chand Articles •Determinants of painful experience during dental treatment- Ruth Suzanne et al Rev.Dor 2012;13(4) •Case report study on Brown sequard syndrome- Ponachi et al Neurology Asia 2007;12;65-67 •Anatomy, physiology & pharmacology of pain- Ryan Moffat, Colin P.Rae anesthesia & intensive care medicine; 2010;12(1)