title: Neuropathic orofacial pain part 1--prevalence and pathophysiology.
abstract: Neuropathic pain is defined as "pain initiated or caused by a primary lesion or dysfunction in the nervous system". Neuropathic orofacial pain has previously been known as "atypical odontalgia" (AO) and "phantom tooth pain". The patient afflicted with neuropathic oral/orofacial pain may present to the dentist with a persistent, severe pain, yet there are no clearly identifiable clinical or radiographic abnormalities. Accordingly, multiple endodontic procedures may be instigated to remove the likely anatomical source of the pain, yet the pain persists. There have been few studies and limited patient numbers investigating the condition. Two retrospective studies revealed the incidence of persistent pain following endodontic treatment to be 3-6% and 5% of patients; one author with wide experience in assessing the condition estimated its prevalence at 125,000 individuals in the USA alone. In one study, 50% of neuropathic orofacial pain patients reported persistent pain specifically following endodontic treatment. Patients predisposed to the condition may include those suffering from recurrent cluster or migraine headaches. Neuropathic pain states include postherpetic neuralgia (shingles) and phantom limb/stump pain. The aberrant developmental neurobiology leading to this pain state is complex. Neuropathic pain serves no protective function, in contrast to physiological pain that warns of noxious stimuli likely to result in tissue damage. The relevant clinical features of neuropathic pain include: (i) precipitating factors such as trauma or disease (infection), and often a delay in onset after initial injury (days-months), (ii) typical complaints such as dysaesthesias (abnormal unpleasant sensations), pain that may include burning, and paroxysmal, lancinating or sharp qualities, and pain in an area of sensory deficit, (iii) on physical examination there may be hyperalgesia, allodynia and sympathetic hyperfunction, and (iv) the pathophysiology includes deafferentation, nerve sprouting, neuroma formation and sympathetic efferent activity.
authors.affiliation: Department of Anaesthesia and Pain Management, University of Sydney, Royal North Shore Hospital. rvickers@med.usyd.edu.au
authors.forename: E R
authors.initials: ER
authors.lastname: Vickers
authors.forename: M J
authors.initials: MJ
authors.lastname: Cousins
mesh_terms: D003027:Cluster Headache / Q000503:physiopathology; D004198:Disease Susceptibility; D005157:Facial Pain / Q000145:classification / Q000503:physiopathology*; D006562:Herpes Zoster / Q000503:physiopathology; D006801:Humans; D006930:Hyperalgesia / Q000503:physiopathology; D015994:Incidence; D008881:Migraine Disorders / Q000503:physiopathology; D009437:Neuralgia / Q000145:classification / Q000503:physiopathology*; D009463:Neuroma / Q000503:physiopathology; D009473:Neuronal Plasticity / Q000502:physiology; D009475:Neurons, Afferent / Q000502:physiology; D009476:Neurons, Efferent / Q000502:physiology; D010591:Phantom Limb / Q000503:physiopathology; D015995:Prevalence; D012189:Retrospective Studies; D012390:Root Canal Therapy / Q000009:adverse effects; D012678:Sensation Disorders / Q000503:physiopathology; D013564:Sympathetic Nervous System / Q000503:physiopathology; D014098:Toothache / Q000503:physiopathology