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Central Mechanisms of TMJ Pain
Symposia event of an emergency. Legal standards mandate having a team that can resuscitate a patient just as if they were from an ICU unit at a hospital or were EMTs. This course will show you how to create that team, through organization and effective staff training. You will learn how to organize your “Crash Cart” and train the members of your staff to be knowledgeable, effective team members in the management of emergencies. We will review how to store and organize your emergency medications, intravenous drip supplies, etc. in your crash cart for instant retrieval. Plans for virtually “fool proof” labeling and organization will be discussed. Tips will be
provided on how to effectively use your office computer to help provide first-rate teaching materials for your entire office staff. These will assure that the appropriate medications will be procured, prepared and administered rapidly and efficiently in the event of an emergency. References Office Anesthesia Evaluation Manual, The American Association of Oral and Maxillofacial Surgeons. 7th Edition, 2006 Medical Emergencies in the Dental Office, Stanley F. Malamed’s, 5th Edition, Mosby 2000 Advanced Cardiovascular Life Support, American Heart Association, 2006
SYMPOSIUM: MECHANISM OF TMJ PAIN Thursday, September 18, 2008, 7:30 am–9:30 am
Peripheral Mechanisms of TMJ Pain Ken Hargreaves, DDS, PhD, San Antonio, TX No abstract provided.
Central Mechanisms of TMJ Pain Barry Sessle, BDS, MDS, BSc, PhD, Toronto, ON, Canada This presentation will focus on the neural changes that are induced by injury or inflammation of TMJ and related craniofacial tissues and that are reflected in an increased excitability of the trigeminal nociceptive pathways in the brain, and their clinical implications. The nociceptive afferent nerve fibres that innervate the TMJ and other craniofacial tissues project to the brainstem and can activate nociceptive neurones in the pain pathways. Some nociceptive neurones in the brainstem, as well as higher brain centres, respond exclusively to cutaneous sensory inputs and have features suggesting they are critical brainstem elements involved in our ability to localize and sense an acute superficial craniofacial pain, but many receive convergent inputs also from afferents supplying deep craniofacial tissues (e.g. TMJ) as well as skin, and are involved in the sensing of deep pain and in pain referral. Such convergence also contributes to the neural substrate underlying neuroplastic changes in neuronal properties that may occur following tissue injury or inflammation, e.g. increased responsiveness to noxious stimulation, decreased activation threshold and receptive field expansion in nociceptive neurons, and increased masticatory muscle reflex activity. The neuroplastic changes reflect a central sensitisation which may last hours or days depending on the type of injury or inflammatory state. Central sensitisation contributes to the increased sensitivity (e.g. hyperalgesia, allodynia) that characterizes a peripheral in2
jury or inflammation site, and to the development of a chronic pain state. It involves a number of neurochemical mechanisms, including purinergic, neurokinin, and NMDA receptor mechanisms, and may also be influenced by other factors (e.g. genetic, environmental, hormonal) as well as non-neural (e.g. glial) cells. Central sensitisation normally appears to be reversible, and a major research focus, and challenge, in the pain field is to determine the factors and processes that lead to its maintenance. There are several important clinical implications of these findings, including that the central substrates for TMJ pain do not represent immutable processes and “hard-wired” connections but rather that they are plastic and can be influenced by peripheral events and changes in intrinsic modulatory systems. Moreover, some of the central neurochemical mechanisms may be involved in the changes in psychological state (e.g. related to anxiety, stress, depression, etc) that may enhance the expression of pain, whereas others may contribute to the efficacy of a number of centrally acting drugs and other analgesic approaches used for pain relief. Also, since nearly all centrally acting pain-relieving drugs have been developed to target neural processes, the recent findings that non-neural (glial) cells and genetic and environmental factors may influence some of the central nociceptive mechanisms provide new targets for novel approaches to control pain, including that from the TMJ. References Sessle BJ. Acute and chronic craniofacial pain: brainstem mechanisms of nociceptive transmission and neuroplasticity, and their clinical correlates. Crit Rev Oral Biol Med 11:57-91, 2000 Lund JP, Lavigne GJ, Dubner R, Sessle BJ, eds. Orofacial Pain: From Basic Science to Clinical Management. Chicago, IL: Quintessence, 300 pp, 2001 Sessle BJ. Sensory and motor neurophysiology related to temporomandibular joint function. In: Temporomandibular Disorders. An Evidence-Based Approach to Diagnosis and Treatment, eds. D. Laskin, C.G. Greene and W. Hylander, Quintessence, Chicago, pp 69-88, 2006
AAOMS • 2008
provided on how to effectively use your office computer to help provide first-rate teaching materials for your entire office staff. These will assure that the appropriate medications will be procured, prepared and administered rapidly and efficiently in the event of an emergency. References Office Anesthesia Evaluation Manual, The American Association of Oral and Maxillofacial Surgeons. 7th Edition, 2006 Medical Emergencies in the Dental Office, Stanley F. Malamed’s, 5th Edition, Mosby 2000 Advanced Cardiovascular Life Support, American Heart Association, 2006
SYMPOSIUM: MECHANISM OF TMJ PAIN Thursday, September 18, 2008, 7:30 am–9:30 am
Peripheral Mechanisms of TMJ Pain Ken Hargreaves, DDS, PhD, San Antonio, TX No abstract provided.
Central Mechanisms of TMJ Pain Barry Sessle, BDS, MDS, BSc, PhD, Toronto, ON, Canada This presentation will focus on the neural changes that are induced by injury or inflammation of TMJ and related craniofacial tissues and that are reflected in an increased excitability of the trigeminal nociceptive pathways in the brain, and their clinical implications. The nociceptive afferent nerve fibres that innervate the TMJ and other craniofacial tissues project to the brainstem and can activate nociceptive neurones in the pain pathways. Some nociceptive neurones in the brainstem, as well as higher brain centres, respond exclusively to cutaneous sensory inputs and have features suggesting they are critical brainstem elements involved in our ability to localize and sense an acute superficial craniofacial pain, but many receive convergent inputs also from afferents supplying deep craniofacial tissues (e.g. TMJ) as well as skin, and are involved in the sensing of deep pain and in pain referral. Such convergence also contributes to the neural substrate underlying neuroplastic changes in neuronal properties that may occur following tissue injury or inflammation, e.g. increased responsiveness to noxious stimulation, decreased activation threshold and receptive field expansion in nociceptive neurons, and increased masticatory muscle reflex activity. The neuroplastic changes reflect a central sensitisation which may last hours or days depending on the type of injury or inflammatory state. Central sensitisation contributes to the increased sensitivity (e.g. hyperalgesia, allodynia) that characterizes a peripheral in2
jury or inflammation site, and to the development of a chronic pain state. It involves a number of neurochemical mechanisms, including purinergic, neurokinin, and NMDA receptor mechanisms, and may also be influenced by other factors (e.g. genetic, environmental, hormonal) as well as non-neural (e.g. glial) cells. Central sensitisation normally appears to be reversible, and a major research focus, and challenge, in the pain field is to determine the factors and processes that lead to its maintenance. There are several important clinical implications of these findings, including that the central substrates for TMJ pain do not represent immutable processes and “hard-wired” connections but rather that they are plastic and can be influenced by peripheral events and changes in intrinsic modulatory systems. Moreover, some of the central neurochemical mechanisms may be involved in the changes in psychological state (e.g. related to anxiety, stress, depression, etc) that may enhance the expression of pain, whereas others may contribute to the efficacy of a number of centrally acting drugs and other analgesic approaches used for pain relief. Also, since nearly all centrally acting pain-relieving drugs have been developed to target neural processes, the recent findings that non-neural (glial) cells and genetic and environmental factors may influence some of the central nociceptive mechanisms provide new targets for novel approaches to control pain, including that from the TMJ. References Sessle BJ. Acute and chronic craniofacial pain: brainstem mechanisms of nociceptive transmission and neuroplasticity, and their clinical correlates. Crit Rev Oral Biol Med 11:57-91, 2000 Lund JP, Lavigne GJ, Dubner R, Sessle BJ, eds. Orofacial Pain: From Basic Science to Clinical Management. Chicago, IL: Quintessence, 300 pp, 2001 Sessle BJ. Sensory and motor neurophysiology related to temporomandibular joint function. In: Temporomandibular Disorders. An Evidence-Based Approach to Diagnosis and Treatment, eds. D. Laskin, C.G. Greene and W. Hylander, Quintessence, Chicago, pp 69-88, 2006
AAOMS • 2008