Aghabeigi, Behnam; (1994) Pathophysiological aspects of chronic idiopathic orofacial pain. Doctoral thesis (Ph.D), UCL (University College London).

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Abstract

This study addresses some of the questions related to the pathophysiology of chronic idiopathic orofacial pain. 1. Chapter II describes the psychological characteristics of the patients assessed by a structured interview (SCID) according to DSM-III-R criteria. Patients had a higher lifetime prevalence of major depression than the general population. However, this did not seem to be causally related to the pain in any way. The study also revealed a significant number of patients suffering from a post-traumatic stress disorder, the onset of which coincided with the onset of the pain. The implications of this finding in diagnosis and management is discussed. 2. Chapter III aims to test the hypothesis that chronic pain and depression share a common biological pathogenesis. Tyramine conjugation deficit, an established trait marker of endogenous depression was shown to be present in pain patients independent of a coexisting history of depression. This therefore confirmed a common metabolic abnormality predisposing to both idiopathic pain and depression even if both do not occur in the same individual. However, platelet monoamine-oxidase activity level was not significantly different between patients and controls. 3. Chapter IV is concerned with the systemic role of oxygen free radicals(OFR) in chronic pain. It also investigates the influence of experimental stress on free radical metabolism. Two biochemical assays were chosen for this purpose: The measurement of 2,3,-dihydroxybenzoic acid was found to be flawed by a number of methodological problems and was therefore abandoned. An alternative method was standardized for future investigations. Furthermore the thiobarbituric acid test did not show a significant difference between the patients and controls. Also, acute experimental stress did not affect the level of thiobarbituric acid reactive substances in the blood in either patient or control group. 4. Chapter V consists of 3 separate studies on TMJ synovial fluid. The first part deals with the measurement of hyperalgesic eicosanoids in the joint. We could not find support for the published reports of the presence of PGE₂ and LTB₄ in the joint. However, considerable levels of hyperalgesic products of 15-lipoxygenase such as 15-HETE were demonstrated. The second part, describes a method for estimation, of the volume of synovial fluid of TMJ. This is based on simultaneous measurement of salicylate in plasma and saline aspirates. The third part, studies the role of OPR in the local damage in the joint. The findings imply that the local release of OPR may play a role in the pathogenesis of TMJ disorders. However, the lack of positive objective clinical or arthroscopic finding in some painful joints and the well recognized effect of predisposing life events on a vulnerable personality, emphasizes the role of central modulating factors in the pain experience.

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