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Physiology of pain2003
This document provides an overview of the physiology of pain. It begins with a brief history of pain theories, then defines pain and discusses its classification. The document outlines the mechanism of pain perception, including the roles of sensory receptors, neurons, and ascending and descending pain pathways in the spinal cord and brain. It also addresses factors that affect pain perception as well as electrophysiology concepts like action potentials. The document concludes by discussing pain in unborn children and referencing additional resources.
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Physiology of pain2003
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- 3. “PAIN A PERCEPTION, NOT REALLYA SENSATION” PRESENTED BY KHUSHBOO BARJATYA PG STUDENT DEPT OF PEDODONTICS
- 4. CONTENTS • Introduction. • History. •Definition. • Classification. • Mechanism of pain perception. • Pain control theory. • Factors affecting pain. • Electrophysiology of pain. • Pain of unborn • Conclusion. • References.
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- 6. PAIN A PROTECTIVE MECHANISMOF BODY
- 7. HISTORICALLY • Arrow shotby god •Magic, Evils, Demons. •The Greeks and Romans first who gave theory of sensation and idea that brain responsible for perception of pain.
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- 9. The Latin word"poena" meaning a fine, a penalty. • First given as early as 1968 by Margo McCaffery: • “Pain is whatever the experiencing person says it is, existing whenever he says it does” • WHO has defined pain as “An unpleasant sensory or emotional experience associated with actual or potential tissue damage, or described in terms of such damage”. The International Association for the Study of Pain • The American Academy of Pain Medicine defines pain as – “An unpleasant sensation and emotional response to that sensation
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- 11. ALLODYNIA 1. Certain typesof noxious stimulus (e.g. sunburn, injury, post-surgical wounds) may result in the individual perceiving pain in response to stimuli that are not normally painful, such as a light stroking of the skin 2. Certain noxious stimuli (e.g. severe bruising) can result in the individual perceiving abnormally high levels of pain in response to normal noxious stimuli such as a small scratch; in such cases, patients often perceive spontaneous pain HYPERALGESIA
- 12. • PARESTHESIA: • Itis abnormal sensation which is described as “pins and needles”. It can occur either spontaneously or evoked by certain stimuli. • DYSESTHESIA: • An unpleasant abnormal sensation, whether spontaneous or evoke. • Note: difference being paresthesia is not unpleasant while dysthesia is! • .
- 13. • HYPERPATHIA: • Itis painful syndrome resulting from abnormally painful reaction to stimulus. The stimulus is repetitive with an increased pain threshold. • PAIN THRESHOLD: • Amount of pain required before individual feel the pain. the higher the threshold, the more pain one can endure. • PAIN TOLERANCE LEVEL • The greatest level of pain which a subject can tolerate.
- 14. Complex Regional PainSyndrome I:
- 15. Complex Regional PainSyndrome II Causalgia, Damaged nerve
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- 20. SENSORY RECEPTORS Free nerveendings,are referred to as nociceptors. • C-fiber mechano/heat-sensitive nociceptors (CMH) • A-fiber mechano/heat –sensitive nociceptors (AMH). • A-delta fibers are thinly myelinated fibers which conduct in the range of 2 m/s to 20 m/s. are termed high threshold mechanoreceptors.(first pain) • C-fibers are non-myelinated fibers that conduct in the range of 0.5 m/s to 2 m/s and transmit noxious information from a variety of modalities including mechanical, thermal, and chemical so, they are termed C-polymodal nociceptors.(second pain) DETECTION
- 21. Classification of nervefibres Fibre type Function Axon diameter mm Conduction / Myelin + - velocity, m per s Aα (I) motor a - fibres 9-18/+ 70-120 spindle afferents (Ia) tendon organs (Ib) Aβ(II) touch and pressure 5-12/+ 30-75 Aγ (II) motor to muscle spindles 3-6/+ 18-36 Aδ(III) pain, pressure, temperature 1-5/- 4-30 B (III) Preganglionic ANS 3/- 3-12 C (IV) pain, sympathetic 1/- 1-2
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- 29. QUESTIONS ? • WhyAnginal pain felt in left arm? • Is pain from one Tooth transferred to another? • Why pain in Neck leads to Headache?
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- 33. INFLAMED DENTAL PULP •Normally nociceptors remain quiescent, but activated by modest temperature change or stimuli leads to pain. • Process involve complex neuro-immune interactions. • Both pheripheral and central projections are important.
- 34. Peripheral Nerve Sensitivity •Tissue damage results in a drop in pH and release of chemicals, e.g. histamines and bradykinin, to which small non-myelinated C fibers are sensitive. • Substance P may also be released peripherally with resultant increase in peripheral vasodilation and further sensitization of the C fibre's peripheral ending.
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- 36. Allodynia in IrreversiblePulpitis
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- 42. Tract Lateral-STT Lateral-STT Spinoreticulartract (SRT) Origin Lamina I & IV, V Lamina I, IV,V, (and VII, VIII) Somatotopic organisation Yes No Body representation Contralateral Bilateral Synapse in reticular formation No Yes Sub-cortical targets None Hypothalamus Limbic system Autonomic centres Thalamic nucleus Ventral posterolateral (VPL) Intra-laminar nuclei Other midline nuclei Cortical location Parietal lobe (SI cortex) Cingulate gyrus Role Discriminative pain (quality intensity, location) Affective-arousal components of pain Other functions Temperature Simple touch
- 43. Temporal summation. Ifa stimulus arrives at the synapse in the dorsal horn more frequently than once every 3 seconds, the post-synaptic electrical discharge becomes more prolonged, with consequent increase in the severity of the pain. This temporal summation is termed "windup"
- 44. IS THERE A “CORTICALPAIN” CENTER?
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- 46. Dennis Turk's claimthat "the reign of pain is mainly in the brain". But there is no one centre "in control".
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- 48. SPECIFICITY THEORY • Painand touch sensors on the skin are wired to a pain centre in the brain. • This theory does not account for pain when there is no organic basis for the pain. BY DESCARTE IN 1644
- 49. SENSORY DECISION THEORY Thistheory relies heavily on the psychological perception of a painful stimulus. Painful stimuli is perceived according to the individuals cognitive processesPATTERN THEORIES By Goldscheider in 1894 Pain conducting nerves are shared with other sensory nerves- pattern of activity from the nerve cells dictates how the pattern is interpreted.
- 50. GATE CONTROL THEORY •The idea that the perception of pain is not a direct result of activation of nociceptors, but instead is modulated by interaction between different neurons, both pain-transmitting and non-pain-transmitting. The theory asserts that activation of nerves that do not transmit pain signals can interfere with signals from pain fibers and inhibit an individual's perception of pain. Ronald Melzack (a Canadian psychologist) and Patrick David Wall (a British physician) in 1962,
- 51. Inhibition is inblue, excitation in yellow
- 52. Inhibition is inblue, excitation in yellow
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- 54. AGE • Children andelderly are of concern. Children, more sensitive than adults. • As- • Show more inflammatory response to pain. •The pain signals reach brain in full intensity without getting modified by the dorsal horn of spinal cord. •Their descending pain inhibiting pathways are less developed than in adults.
- 55. Sex Women are moreprone, than males, due to difference in hormonal levels Emotional status People in general suffering from depression and anxiety pain Smoking • nicotine reduces body stores of vitamin C, adversely affects the pain processing mechanisms of the brain and interacts with opioid pain medications. • Trauma • People who have experienced childhood injuries and trauma show more pain sensitivity.
- 56. FACTORS :- • Weather •People experience arthritic pain more during winter season. • Sleep • Sleep deprivation increases pain perception.
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- 58. Step 1 •Nerve possessresting potential of – 70 mV that exists across the nerve membrane, produced by ions on either side of the membrane. Sodium Potassium pump keeps the potential by pump in K+ in and Na+ out.
- 59. Step 2 INITIAL PHASEOF SLOW DEPOLARIZATION. The electrical potential within the nerve becomes slightly less negative. • Rapid phase of depolarization This phase results in a reversal of the electrical potential across the nerve membrane. Nerve becomes positive in relation to the outside. An electrical potential of +40 mV exists inside of the nerve . Termed as threshold potential or firing threshold.
- 60. Step 3 • PHASEOF REPOLARIZATION . • The electrical potential gradually becomes more negative inside – 70 m V is again achieved. • Time required 1 millisecond (msec) depolarization takes 0.3 msec; repolarization takes 0.7 msec
- 61. PAIN OF UNBORN •An unborn child at 20 weeks gestation “is fully capable of experiencing pain. ( EEG Shows) ”
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- 63. REFRENCES • INGLE ENDODONTICS6TH EDITION • PRINCIPLES OF ANATOMY AND PHYSIOLOGY,TORTORA,8TH EDITION • SEMULINGUM PHYSIOLOGY. • MONHEIMS LOCAL ANESTHETICS AND PAIN CONTROL IN DENTAL PRACTICE.
- 64. REFRENCES • P.D. Wall,R. Melzack, "On nature of cutaneous sensory mechanisms," Brain, 85:331, 1962. • R. Melzack, P.D. Wall, "Pain mechanisms: A new theory," Science, 150:171-9, 1965. • Kandel, Eric R.; James H. Schwartz, Thomas M. Jessell (2000). Principles of Neural Science, 4th edition, New York: McGraw-Hill, 482–486
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Editor's Notes
- #15 Complex Regional Pain syndrome I also called as Reflex Sympathetic Dystrophy is a continuous pain in the form of either allodynia or hyperalgesia in the extremities resulting from trauma which is associated with sympathetic hyperactivity. The pain does not correspond to the distribution of a single nerve and it is worsened by movement. The person affected usually complains of cool, clammy skin which later becomes pale, cold, stiff and atrophied Schematic diagram summarizing the sensory, autonomic and somatomotor changes in complex regional pain syndrome I (CRPS I) patients. The figure symbolizes the CNS (forebrain, brain stem and spinal cord). Changes occur in the central representations of the somatosensory, the motor and the sympathetic nervous system (which include the spinal circuits) and are reflected in the changes of the sensory painful and non-painful perceptions, of cutaneous blood flow and sweating, of peripheral tissues (edema, inflammation, trophic) and of motor performances. They are triggered and possibly maintained by the nociceptive afferent input from the somatic and visceral body domains. It is unclear whether these central changes are reversible in chronic CRPS I patients. The central changes may include changes of the endogenous control system of nociceptive impulse transmission. Coupling between the sympathetic neurons and the afferent neurons in the periphery (see red arrow) is one component of the pain in CRPS I patients with sympathetically-maintained pain (SMP). However, it seems to be unimportant in CRPS I patients without SMP. From Jänig and Baron (2002, 2003)
- #16 Complex Regional Pain Syndrome II also called as Causalgia is a burning type of pain along the distribution a partially damaged peripheral nerve. The pain extends beyond the distribution of the nerve. This results from abnormal connections between various nerves. The skin of the person affected is classically cold, moist and swollen, becoming atrophic later
- #17 Phantom limb pain is the pain that is felt in the amputated part of the body. The brain misinterprets the nerve signals as coming from the amputated limb. The phantom limb pain is described as squeezing, burning, or crushing sensations, but it often differs from any sensation previously experienced
- #35 This is referred to as peripheral sensitization in contrast to central sensitization which occurs at the dorsal horn. Both occur in chronic pain.
- #49 Problem (Melzack and Wall, 1988). Even though the senses can be in contact with pain, we do not feel it; and Vice versa - gentle touch can trigger a painful reaction (Neuralgia and Causalgia).
- #50 Painful stimuli is perceived according to the individuals cognitive processes eg * perceptual habits * beliefs * expectations * costs and rewards * memory of previous pain experiences
- #52 The projection neuron determines pain. The inhibitory interneuron decreases the chances that the projection neuron will fire. Firing of C fibers inhibits the inhibitory interneuron (indirectly), increasing the chances that the projection neuron
- #53 the Aβ fibers activates the inhibitory interneuron, reducing the chances, projection neuron will fire, even in the presence of a firing nociceptive fiber
- #59 The interior of the nerve is negative in relation to the exterior semi permeable membrane which is impermeable to Sodium