1. بســم اللَـــه الرحمــن الرحيـــم

2. Prof.Dr.Ragab Shaaban

3. Local Analgesia In Dentistry

24. Pain

25. pain  Definition it is an unpleasant sensory and emotional experience associated with actual or potential tissue damage.

26. Pain perception  It is the term used to describe the integration and appreciation of pain within the CNS which occurs in the cortex and posterior thalamus.  As the mechanism for pain perception works on the “ all or none principle ” it is generally agreed that if a unite stimulus is applied to individuals they should both perceive the same amount of pain. However, experience shows that the response of both individuals is not the same due to the variation in pain reaction and not due to difference in pain perception

27. Type of sensory receptors  Pain free nerve endings  Touch Meissner ’ s corpuscles  Warmth Ruffini ’ s end organs  Cold Krause ’ s end bulbs  Pressure Pacini ’ s corpuscles

28. Pain preceptors (nociceptors)  They are naked nerve endings, mostly unmyelinated fibers in the form of delicate loops or long,naked,hair-like network.

29. stimulus  It is an environmental change in excitable tissue. It may be * electrical in nature * thermal in nature * chemical in nature * mechanical in nature

30. Threshold stimulus  It is the stimulus that is just sufficient to excite free nerve endings by minimal environmental change in tissue.  A subthreshold stimulus will not excite the free nerve endings or create an impulse, regardless of its duration.

31. impulse  It is a wave of excitation that spreads along the nerve fiber. It is self- propagating and of equal intensity regardless the degree of stimulation.

32. Pain threshold  The term is employed when the variable response to pain is being discussed. A patient is said to have a high pain threshold when he exhibits little or no reaction to painful stimulus, while a patient with a low pain threshold is liable to react violently to an identical or even lesser stimulus.  In other word, pain threshold is inversely proportional to pain reaction.

33. Factors affecting pain threshold  Emotional status  Fear and apprehension  Fatigue  Age  Sex  Racial and nationality

34. Pain pathway

35. Nerve conduction It is the process of propagation of the impulse through the nerve. It depends on the electrical potential that exist across the nerve membrane.

36. Nerve conduction (resting potential) At resting potential there is a high concen- tration of Na+ outside the nerve membrane and a high concentration of K+ inside it.

37. Nerve conduction (depolarization) When the nerve is stimulated, Na+ rush into the axon and causes depolarization

38. Nerve conduction (K influx) Localized electrical circuits are established which causes further influx of Na+ and so progression of the impulse. Behind the impulse, K+ begin s to leave the axon.

39. Nerve conduction (repolarization) As the impulse progresses, the influx of K+ causes the nerve membrane to become depolarized behind the impulse.

40. Nerve conduction (sodium pump) After the impulse has passed and the nerve membrane is repolariz- ed Na is once again actively expelled in order to increase the external concentration and allow the passage of another impulse.

41. Pain control As pain is divided into pain perception and pain reaction, therefore any method of pain control will affect either one of the two divisions.

42. Methods of pain control  Removing the cause.  Blocking the pathway of painful impulse  Raising the pain threshold.  Preventing pain reaction by cortical depression.  Using psychosomatic methods.

43. Local analgesia Introduction & maxillary techniques

44. Analgesia Analgesia refers to loss of pain sensation without loss of consciouness. Regional analgesia Regional analgesia refers to loss of pain sensation over a portion of the anatomy without loss of consciouness

45. Regional anesthesia Regional anesthesia would apply not only to loss of pain sensation over a specific area of the anatomy without loss of consciouness, but also to the interruption of all other sensations including temperature, pressure and motor function.

46. Types of regional analgesia  Topical analgesia.  Local infiltration.  Field block  Nerve block

47. Topical Analgesia It is the application of analgesic drug directly to the surface of the area rendering free nerve endings in accessible structure incapable of stimulation.

48. Local infiltration It is the flooding of small terminal nerve endings with anaesthetic solution,rendering them insensible to pain or prevent them from being stimulated and creating an impulse.

49. Field block It is the deposition of anaesthetic drug in proximity to the larger terminal nerve branches, so that the area to be anaethetized is walled off or circumscribed to prevent central passage of afferent impulses.

50. Nerve block It is the deposition of anaesthetic drug within close proximity of a main trunk, thus preventing afferent impulses from travelling centrally.

51. Types of regional analgesia

52. Methods of induction of local analgesia  Submucosal injection.  Paraperiosteal injection.  Intraosseous injection.  Interseptal injection.

53. Submucosal injection It is accomplished by inserting the needle beneath the mucosal layers and depositing the LA so that it diffuses in this particular plane.

54. Paraperiosteal injection The needle is inserted so that it comes into the proximity with or comtact the periostium. LA will diffuses through the periostium and the bone.

55. Interseptal injection It is accomplished by forcing the LA under pressure interseptally.

56. Factors in selection of method of induction  Area to be anesthetized.  Profoundness required.  Duration of anesthesia.  Presence of infection.  Age of the patient.  Condition of the patient  Hemostasis, if needed.

57. Theories of regional analgesia As a result of better understanding of the nature of the nerve impulse, the action of LA may be explained, at least partially, within the framework of the ionic theory of the nervous activity. Several theories have been postulated to explain the exact mechanism of LA. Although good evidence is present to support each theory, none is universally accepted as a complete explanation.

58. Membrane expansion The LA agent produces increased lateral pressure within the nerve membrane resulting in constriction of pores through which Na+ passes during polarization and interrupting Na+ influx and neural excitation.

59. Specific receptors The theory suggested the presence of specific receptors sites to which LA agents may attach to these sites. The attachment of LA to these sites effectivily block the passage-way preventing Na+ transfer and dipolarization.

60. Calcium competition Ca+ exerts a regulatory role in the movement of Na+ across the nerve membrane. The release of Ca ions has been suggested as primary factor responsi- ble for the increase in Na+ permeability of the move membrane.

61. Calcium competition LA agent might compete with Ca+ for same site on the neve membrane resulting in decreased permeability to Na+ and decreased rate of depolarization..

62. Neutralization of transmembrane charge The interaction of the LA agent with the receptor area results in neutralization of the fixed negative charges in cell membrane such that the potential across the membrane would rise although the recorded potential would remain constant.

63. Neutralization of transmembrane charge When the increase in the transmembrane potential is sufficiently great,electronic currents from adjacent un- anesthetized areas would be insufficient to reduce the the membrane potential to its threshold level and blockade would occur.