Diese Präsentation wurde erfolgreich gemeldet.
Wir verwenden Ihre LinkedIn Profilangaben und Informationen zu Ihren Aktivitäten, um Anzeigen zu personalisieren und Ihnen relevantere Inhalte anzuzeigen. Sie können Ihre Anzeigeneinstellungen jederzeit ändern.

Pain and pain pathways

277 Aufrufe

Veröffentlicht am

This presentation provides an overview of pain and its related aspects in dentistry.

Veröffentlicht in: Bildung
  • Als Erste(r) kommentieren

Pain and pain pathways

  1. 1. PAIN AND PAIN PATHWAYS B. MRUDULA DEVI I MDS
  2. 2. CONTENTS 1. INTRODUCTION 2. DEFINITION 3. HISTORY 4. THEORIES OF PAIN 5. PAIN RECEPTORS 6. NEUROTRANSMITTERS 7. NERVE CONDUCTION 8. PAIN PATHWAYS 9. TYPES OF PAIN 10. ASSESSMENT OF PAIN 11. MANAGEMENT OF PAIN 12. CONCLUSION 13. REFERENCES
  3. 3. INTRODUCTION • Pain is one of the most commonly experienced symptoms in Dentistry. • It is an intensely subjective experience, and is therefore difficult to describe. • Often spoken of as a protective mechanism. • Produced by real or potential injury to the body.
  4. 4. DEFINITION “An unpleasant emotional experience associated with actual or potential tissue damage or describe in terms of such damage.” (International Association for the Study of Pain) “An unpleasant emotional experience usually initiated by noxious stimulus and transmitted over a specialized neural network to the Central Nervous System where it is interpreted as such.” (Monheim)
  5. 5. HISTORY • Derived from Greek word, “Poin” meaning penalty. • In Latin “Poena” means punishment from God. • Aristotle – “Passion of the soul”. • Plato – Pain is an emotional experience more than a localized body disturbance. • John Bonica – Father of Pain
  6. 6. Warning signal Reflex withdrawl Minimizes the activities Urges to take treatment BENEFITS OF PAIN SENSATION
  7. 7. THEORIES OF PAIN • INTENSITY THEORY • SPECIFICITY THEORY • PATTERN THEORY • GATE CONTROL THEORY
  8. 8. Descartes (1644) : Straight through channel from skin to brain. Muller : Information transmission by sensory nerves Von Frey : Pain receptors – Free nerve endings ; Pain centre - Brain SPECIFICITY THEORY INTENSITY THEORY (Mumford & Newton) “Pain Is A Non Specific Sensation And Depends On High Intensity Stimulation”
  9. 9. PATTERN THEORY (Goldscheider, 1894) Critical determinants of pain : Stimulus intensity and central summation Summation of sensory input Nerve impulses Source : Massieh Moayedi and Karen;Theories of pain: from specificity to gate control, J Neurophysiol 109: 5–12, 2013.
  10. 10. GATE CONTROL THEORY (Melzack and Wall, 1965) Postulates : ‣ Information is transmitted to CNS by small peripheral nerves. ‣ Cells in the spinal cord are also facilitated or inhibited by large peripheral nerves. ‣ Descending control systems modulate the excitability of cells that transmit information.
  11. 11. Source : Massieh Moayedi and Karen;Theories of pain: from specificity to gate control, J Neurophysiol 109: 5–12, 2013.
  12. 12. Threshold and Intensity Adaptation Localization Rate of tissue damage CHARACTERISTICS OF PAIN
  13. 13. PAIN RECEPTORS Sensory receptors can be classified into : • Exteroceptors 1. Cutaneous receptors 2. Chemoreceptors 3. Telereceptors • Interoceptors 1. Visceroceptors 2. Proprioceptors
  14. 14. • ALL PAIN RECEPTORS ARE FREE NERVE ENDINGS (NOCICEPTORS) ‣ They are not enclosed in a capsule. ‣ A nerve ending that responds to noxious stimuli can actually or potentially produce tissue damage. • Three types of stimuli excite Pain Receptors 1. Mechanical 2. Thermal 3. Chemical
  15. 15. COMPONENTS OF PAIN • Sensory discriminative component ‣ Processes sensory inputs in the cortex ‣ Assess intensity and duration of pain • Motivational Affective component ‣ Attention and arousal ‣ Somatic and Autonomic reflexes ‣ Emotional changes associated with pain
  16. 16. NEUROTRANSMITTERS Neurotransmitter is a chemical substance that acts as a mediator for the transmission of nerve impulse from one neuron to another neuron through a synapse. • Excitatory neurotransmitters Responsible for the conduction of impulse from the presynaptic neuron to the postsynaptic neuron. Acetylcholine Nitric oxide Histamine Glutamate Aspartate.
  17. 17. • Inhibitory Neurotransmitters Inhibit the conduction of impulse from the presynaptic neuron to the post synaptic neuron. GABA Glycine Dopamine Serotonin. • Excitatory and Inhibitory Noradrenaline Adrenaline
  18. 18. NEUROANATOMY
  19. 19. NERVE FIBERS Based on diameter and rate of conduction of impulses (Eerlanger and Gasser) : 1. Type A fibres – Aα fibers Aβ fibers Aγ fibers A∂ fibers 2. Type B fibers 3. Type C fibers
  20. 20. NERVE CONDUCTION 1. RESTING STATE 2. DEPOLARIZATION 3. REPOLARIZATION
  21. 21. PAIN PATHWAYS Neural Pain Pathways (Field) : • Transduction: Noxious stimuli leads to electrical activity in the appropriate sensory nerve ending. • Transmission: Neural event that carry the nociceptive input into the central nervous system for proper processing. • Modulation: Neural impulses (nociceptive) are changed or altered before reaching the higher centers (Cortex). • Perception: Interaction of the (cortex, thalamus, and limbic system) higher centers.
  22. 22. SENSORY NEURONS First Order Neurons Second Order Neurons Third Order Neurons
  23. 23. First Order Neuron ‣ Carries impulses to the Central nervous System. ‣ Synapses with the second order neuron. Second Order Neuron ‣ Transfers impulses to higher centers (Transmission Neuron). Third Order Neuron ‣ Relay thermal sensory information to the somesthetic cortex.
  24. 24. COMPONENTS OF PAIN PATHWAY
  25. 25. Dual Pain Pathways : The pain signals take two pathways to brain via 1. The Neospinothalamic Tract 2. The Paleospinothalamic Tract
  26. 26. Neospinothalamic tract for fast pain • Neurotransmitter - Glutamate • A∂ fibres transmit mechanical and thermal pain. • Termination in the spinal cord : Lamina I (Lamina Marginalis) of the dorsal horn. • Excite second-order neurons
  27. 27. Termination of neospinothalamic tract Few fibers terminate in the reticular areas. Most fibers passes to thalamus and terminate in the ventrobasal complex. Few fibers terminate in the posterior nuclear group of thalamus. Basal areas of brain and somatosensory cortex.
  28. 28. Paleospinothalamic Pathway for slow pain • Type C fibres • Neurotransmitter – Glutamate and Substance P • Termination in spinal cord : Lamina II and Lamina III (Substantia Gelatinosa)
  29. 29. Reticular nuclei of medulla, pons and mesencephalon Tectal area of the mecencephalon deep to the superior and inferior colliculi Periductal gray region surrounding the Aqueduct of Sylvius Intralaminar and ventrolateral nuclei of the thalamus and certain portions of hypothalamus Termination of Paleospinothalamic tract
  30. 30. DUAL NATURE OF PAIN • Pain perception Stimulus Impulse Transmission • Pain reaction Inversely proportional to pain threshold
  31. 31. TYPES OF PAIN SOMATIC : Pain arising from skin and deep structures like muscles , bone , joint and ligament . ‣ Well defined and is generally caused by inflammatory reactions in the tissues. i. SUPERFICIAL OR CUTANEOUS ‣ Pain arising from the skin and superficial mucous membrane ‣ Often felt as pricking type.
  32. 32. ii. DEEP PAIN ‣ It has a dull character and is poorly localized. VISCERAL PAIN : ‣ It is diffuse in nature and is often referred. ‣ Dull aching in character and is accompanied by sweating, nausea and fall in B.P. REFERRED PAIN ‣ It is deep pain , whether visceral or somatic which may be felt in some parts of the body other than the site of stimulation. Eg. cardiac pain referred to the left arm and diaphragmatic pain to shoulder.
  33. 33. PSYCHOGENIC OR FUNCTIONAL PAIN ‣ No obvious cause is found for the pain. ‣ Vague in nature and does not follow any anatomical distribution . NEUROPATHIC PAIN: ‣ Persistent pain that arises from functional changes occurring in CNS secondary to peripheral nerve injury. ‣ Damaged nerve elicits sustained activation of nociceptors, causing neuropathic pain.
  34. 34. PERIODONTAL PAIN PULPAL PAIN Somatic Visceral More localized Less localized Related to masticatory function Does not respond to masticatory function Not a threshold type Threshold type
  35. 35. Emotional States Fatigue Age Racial and Nationality Characteristics Gender Fear and apprehension FACTORS AFFECTING PAIN
  36. 36. ASSESMENT OF PAIN Problem Identification • Self report of pain • Direct observation of pain-related behaviours Pain assessment tools Uni-dimensional measurement tools : ‣ Visual Analogue Scale ‣ Verbal Rating Scale ‣ Numerical Rating Scales
  37. 37. Multi-dimensional Pain Measurement Tools ‣ McGill pain questionnaire ‣ Brief pain inventory ‣ Behavioural pain scales ‣ Pain cognition questionnaire ‣ Pain Disability Index
  38. 38. MOLECULAR MARKER FOR PAIN Gene c-fos ‣ Proto-oncogene It can promote vast intracellular changes. ‣ It is almost certainly involved in the long-term neurological consequences of noxious stimulation.
  39. 39. Removing the cause Blocking the pathway of painful impulses Raising the pain threshold Preventing pain reaction by cortical depression Using psychosomatic methods MANAGEMENT OF PAIN
  40. 40. Elimination of tissue change No excitation of free nerve endings No initiation of impulses REMOVING THE CAUSE BLOCKING THE PATHWAY OF PAINFUL IMPULSES • Prevents Depolarization of nerve fibres • Prevents conduction of impulses Use of Local Anesthetic agent
  41. 41. Pharmacological action of drugs possessing analgesic properties. Cause of the original stimulus may not be eliminated. Pain perception is unaffected, reaction threshold is raised. RAISING THE PAIN THRESHOLD
  42. 42. ANALGESIC AGENTS 1. NONOPIODS ‣ Action : Peripheral nerve endings ‣ Inhibit Prostaglandin synthesis ‣ Mild to Moderate pain 2. OPIODS ‣ Action : CNS ‣ Depress the central nervous system ‣ Moderate to Severe pain
  43. 43. Anticonvulsants: • Act by blocking sodium channels and suppressing neuronal discharge Eg. Carbamazepeine and phenytoin sodium Antidepressents: • They act by inhibiting the reuptake and storage of neurogenic amines Eg.Serotonin, Norepinephrine, Aminotripyline Antihistamines: • They may have analgesic activity by virtue of inflammation Eg.Diphenhydramine, Hydroxyzine, Pyrilamine
  44. 44. INHIBITION OF PAIN (ANALGESIA) Two mechanisms : 1. Stimulation produced Analgesia ‣ Segmental inhibition ‣ Supraspinal inhibition 2. Release of endogenous opioid peptide
  45. 45. Stimulation produced Analgesia Electrical stimulation of specific areas of CNS Pain reduction by inhibiting pain pathways. Segmental inhibition : ‣ Activation of group A afferent nerve fibres. ‣ Stimulation of dorsal column of spinal cord.
  46. 46. Clinical application : ‣ Touching or shaking an injured area decreases the pain. ‣ Acupuncture Needles are introduced into specific parts of the body to stimulate afferent fibres.
  47. 47. Transcutaneous Electrical Nerve Stimulation (TENS) : ‣ Electrodes placed on the surface of skin stimulate the pain site.
  48. 48. Supraspinal inhibition : Mesencephalic pain inhibitory system ‣ Arises from midbrain ; Descends to dorsal horn cells. ‣ Contains opiate receptors. ‣ Stimulation of this system causes inhibition of second order neurons.
  49. 49. Release of endogenous opioid peptides : ‣ Substance P ‣ Opiate receptors ‣ Enkephalins and Endorphins (opioid peptides)
  50. 50. Surgical management Peripheral neurectomy Electrosurgery Cryosurgery
  51. 51. CONCLUSION ‣ Determining the source and cause of pain is more important than mere locating the site. ‣ Eliminating the cause of pain is more important than mere treating the symptom.
  52. 52. REFERENCES 1. Arthur C Guyton, John E Hall. Text book of medical physiology. 10th ed. WB Saunders. 2. K Shambhulingam, Prema Shambhulingam. Essentials of medical physiology. 5th ed; 2010. 3. C Richard Bennett. Monheim’s local anesthesia and pain control in dental practice. 10th ed 4. A.K.Jain. Textbook of Human Physiology.3rd ed;2006.
  53. 53. 5. Massieh Moayedi and Karen;Theories of pain: from specificity to gate control, J Neurophysiol 109: 5–12, 2013. 6. Woolf CJ et al. Pain : Moving from symptom control toward mechanism specific pharmacologic management. Ann Intern Med. 2004 Mar 16;140(6);441-51.

×