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Neural Mechanisms and Pathways in Craniofacial Pain

Published online by Cambridge University Press:  02 December 2014

Barry J. Sessle*
Affiliation:
Faculty of Dentistry, and Department of Physiology, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada
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Abstract

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Many free nerve endings of small-diameter afferents (A-delta or C nerve fibres) respond to craniofacial noxious stimuli and a number of neurochemicals are involved in their activation or sensitization. The small-diameter nociceptive afferents project to the trigeminal (V) brainstem complex where they can excite nociceptive neurones that have been categorized as either nociceptive-specific (NS) or wide dynamic range (WDR). These neurones project to other brainstem regions or to the contralateral thalamus. The lateral and medial thalamus contain NS and WDR neurones which have properties and connections with the overlying cerebral cortex or other thalamic regions indicative of a role for most of them in the sensory-discriminative, affective or other dimensions of pain. Some of the V brainstem NS and WDR neurones respond exclusively to cutaneous sensory inputs and have features indicating their involvement in acute superficial craniofacial pain. Many of the neurones, however, receive convergent inputs from afferents supplying other craniofacial tissues (e.g. cerebrovascular, muscle) as well as skin, and are likely involved in deep pain, as well as spread and referral that is typically seen in headache and several craniofacial pain conditions involving deep tissues. Convergence may also be an important factor underlying the neuroplastic changes in V neuronal properties that may occur with peripheral injury or inflammation. These changes include a prolonged enhancement of the cutaneous as well as deep afferent inputs to most NS and WDR neurones and expansion of their cutaneous or deep mechanoreceptive field and increased EMG activity in the jaw musculature. They involve NMDA, non-NMDA and opioid neurochemical mechanisms within peripheral tissues as well as within the CNS. Such modulatory effects on brainstem neuronal properties reflect the functional plasticity of the central V system, and may be involved in the development of headache and other conditions that manifest craniofacial pain.

Résumé

RÉSUMÉ

Plusieurs terminaisons nerveuses libres des afférents de petit diamètre (fibres nerveuses A-delta ou C) répondent à des stimuli crâniofaciaux douloureux. Plusieurs substances neurochimiques sont impliquées dans leur activation ou leur sensibilisation. Les afférents nociceptifs de petit diamètre ont des projections au complexe du trijumeau (V) dans le tronc cérébral où ils peuvent exciter les neurones nociceptifs qui ont été classés comme nociceptifs-spécifiques (NS) ou comme ayant un spectre dynamique étendu (WDR). Ces neurones projettent à d’autres régions du tronc cérébral ou au thalamus contralatéral. Le thalamus latéral et médian contient des neurones NS et WDR qui ont des propriétés et des connections avec le cortex cérébral sus-jacent ou avec d’autres régions thalamiques, ce qui indique que la plupart ont un rôle dans les aspects sensitifs-discriminatifs, affectifs ou autres de la douleur. Certains des neurones NS et WDR du complexe V du tronc cérébral répondent exclusivement aux influx sensitifs cutanés et ont des caractéristiques indiquant leur implication dans la douleur crâniofaciale superficielle aiguë. Cependant, plusieurs des neurones reçoivent des influx convergents d’afférents innervant d’autres tissus crâniofaciaux (i.e. tissus cérébrovasculaires, musculaires) ainsi que la peau et sont probablement impliqués dans la douleur profonde, incluant la douleur étendue et référée qui est observée typiquement dans la céphalée et dans plusieurs autres pathologies crâniofaciales douloureuses impliquant les tissus profonds. La convergence pourrait également être un facteur important, sous-jacent aux changements neuroplastiques dans les propriétés nerveuses du complexe V qui pourraient survenir lors d’un traumatisme périphérique ou de l’inflammation. Ces changements incluent un rehaussement prolongé des influx des afférents cutanés et profonds à la plupart des neurones NS et WDR, une expansion de leur champ mécanoréceptif cutané ou profond et une augmentation de l’activité ÉMG de la musculature de la mâchoire. Ils impliquent des mécanismes neurochimiques NMDA, non-NMDA et opioïdes dans les tissus périphériques ainsi que dans le SNC. De tels effets modulateurs sur les propriétés des neurones du tronc cérébral reflètent la plasticité fonctionnelle du système V central et peuvent être impliqués dans le développement de la céphalée et d’autres conditions qui se manifestent par de la douleur crâniofaciale.

Type
Research Article
Copyright
Copyright © The Canadian Journal of Neurological 1999

References

1. Dubner, R, Storey, AT, Sessle, BJ. The Neural Basis of Oral and Facial Function. New York: Plenum Press, 1978.Google Scholar
2. Hargreaves, KM, Roszkowski, MT,Jackson, DL, et al. Neuroendocrine and immune response to injury, degeneration, and repair. In: Sessle, BJ, Bryant, PS, Dionne, RA, eds. Temporomandibular Disorders and Related Pain Conditions. Progress in Pain Research and Management, Vol 4. Seattle: IASP Press, 1995: 273292.Google Scholar
3. Lund, JP, Sessle, BJ. Neurophysiological mechanisms related to chronic pain disorders of the temporomandibular joint and masticatory muscles. In: Zarb, GE, Carlsson, G, Sessle, BJ, Mohl, ND, eds. Temporomandibular Joint and Masticatory Muscle Disorders. Copenhagen: Munksgaard, 1994: 188207.Google Scholar
4. Dubner, R. Recent advances in our understanding of pain. In:m Klineberg, I, Sessle, B, eds. Oro-Facial Pain and Neuromuscular Dysfunction: Mechanisms and Clinical Correlates. Oxford: Pergamon Press, 1985: 319.Google Scholar
5. Sessle, BJ. The neurobiology of facial and dental pain: present knowledge, future directions. J Dent Res 1987; 66: 962981.Google Scholar
6. Sessle, BJ. Mechanisms of trigeminal and occipital pain. Pain Reviews 1996; 3: 91116.Google Scholar
7. Sessle, BJ. Acute and chronic craniofacial pain: brainstem mechanisms of nociceptive transmission and neuroplasticity, and their clinical correlates. Crit Rev Oral Biol & Med, in press, 1999.Google Scholar
8. Hathaway, CB, Hu, JW, Bereiter, DA. Distribution of fos-like immunoreactivity in the caudal brainstem of the rat following noxious chemical stimulation of the temporomandibular joint. J Comp Neurol 1995; 356: 444456.Google Scholar
9. Hoskin, KL, Kaube, H, Goadsby, PJ. Sumatriptan can inhibit trigeminal afferents by an exclusively neural mechanism. Brain 1996; 119: 14191428.Google Scholar
10. Nozaki, K, Moskowitz, MA, Boccalini, P. CP–93,129, sumatriptan, dihydroergotamine block c-fos expression within rat trigeminal nucleus caudalis caused by chemical stimulation of the meninges. Br J Pharmacol 1992; 106: 409415.Google Scholar
11. Shepheard, SL, Williamson, DJ, Williams, J, Hill, RG, Hargreaves, RJ. Comparison of the effects of sumatriptan and the NK1 antagonist CP–99,994 on plasma extravasation in dura mater and c-fos mRNA expression in trigeminal nucleus caudalis of rats. Neuropharmacology 1995; 34: 255261.Google Scholar
12. Burstein, R, Yamamura, H, Malick, A, Strassman, AM. Chemical stimulation of the intracranial dura induces enhanced responses to facial stimulation in brain stem trigeminal neurons. J Neurophysiol 1998; 79: 964982.CrossRefGoogle ScholarPubMed
13. Dostrovsky, JO, Davis, KD, Kawakita, K. Central mechanisms of vascular headaches. Can J Physiol Pharmacol 1991; 69: 652658.Google Scholar
14. Sessle, BJ, Hu, JW, Yu, X-M. Brainstem mechanisms of referred pain and hyperalgesia in the orofacial and temporomandibular region. In: Vecchiet, L, Albe-Fessard, D, Lindblom, U, eds. New Trends in Referred Pain and Hyperalgesia. Pain Research and Clinical Management, Vol 7. Amsterdam: Elsevier, 1993: 5971.Google Scholar
15. Iwata, K, Tsuboi, Y, Tashiro, A, Sakamoto, M, Sumino, R. Integration of tooth-pulp pain at the level of cerebral cortex. In: Nakamura, Y, Sessle, BJ, eds. Neurobiology of Mastication – from Molecular to Systems Approach. Amsterdam: Elsevier, 1999, in press.Google Scholar
16. Casey, KL, Minoshima, S. Can pain be imaged? In: Jensen, TS, Turner, JA, Wiesenfeld-Hallin, Z, eds. Proceedings of the 8th World Congress on Pain. Progress in Pain Research and Management, Vol 8. Seattle: IASP Press, 1997: 855866.Google Scholar
17. Fields, HL, Basbaum, AI. Central nervous system mechanisms of pain modulation. In: Wall, PD, Melzack, R, eds. Textbook of Pain, 3rd ed. London: Churchill Livingstone. 1994: 243257.Google Scholar
18. Chiang, CY, Park, SJ, Kwan, CL, Hu, JW, Sessle, BJ. NMDA receptor mechanisms contribute to neuroplasticity induced in caudalis nociceptive neurons by tooth pulp stimulation. J Neurophysiol 1998; 80: 26212631.Google Scholar
19. Hu, JW, Sessle, BJ, Raboisson, P, Dallel, R, Woda, A. Stimulation of craniofacial muscle afferents induces prolonged facilitatory effects in trigeminal nociceptive brainstem neurones. Pain 1992; 48:5360.CrossRefGoogle Scholar
20. Hu, JW, Tsai, C-M, Bakke, M, et al. Deep craniofacial pain: involvement of trigeminal subnucleus caudalis and its modulation. In: Jensen, TS, Turner, JA, Wiesenfeld-Hallin, Z, eds. Proceedings of the 8th World Congress on Pain. Progress in Pain Research and Management, Vol 8. Seattle: IASP Press, 1997: 497506.Google Scholar
21. Yu, X-M, Sessle, BJ, Haas, DA, et al. Involvement of NMDA receptor mechanisms in jaw electromyographic activity and plasma extravasation induced by inflammatory irritant application to temporomandibular joint region of rats. Pain 1996; 68: 169178.CrossRefGoogle ScholarPubMed
22. Coderre, TJ, Katz, J. Peripheral and central hyperexcitability: differential signs and symptoms in persistent pain. Behav Brain Sci 1997; 20: 404419.Google Scholar
23. Dubner, R. Spinal cord neuronal plasticity: mechanisms of persistent pain following tissue damage and nerve injury. In: Vecchiet, L, Albe-Fessard, D, Lindblom, U, eds. New Trends in Referred Pain and Hyperalgesia. Pain Research and Clinical Management, Vol 7. Amsterdam: Elsevier, 1993: 109 117.Google Scholar
24. Bakke, M, Hu, JW, Sessle, BJ. Morphine application to peripheral tissues modulates nociceptive jaw reflex. NeuroReport 1998; 9: 33153319.Google Scholar
25. Cairns, BE, Sessle, BJ, Hu, JW. Evidence that excitatory amino acid receptors within the temporomandibular joint region are involved in the reflex activation of the jaw muscles. J Neurosci 1998; 18: 80568064.Google Scholar