Hypotheses for Etiology and Treatment

A comprehensive review discusses the therapeutic management of RA (Turesson and Matteson, 2004). Epidemiological studies link extra-articular rheumatoid arthritis manifestations with premature mortality and support aggressive anti rheumatoid therapies for those patients. Cyclophosphamide is favored in patients with systemic rheumatoid vasculitis and methotrexate in those cases with other manifestations of extra-articular rheumatoid arthritis (Turesson and Matteson, 2004). Cyclophosphamide and TNFa inhibitors such as infliximab have some positive success in treatment resistant vasculitis associated with RA (Unger et al., 2003). However, TNFa inhibitors have also been associated with the opposite effect, an induction of extra articular rheumatoid arthritis so their use should be used only in specific cases when close monitoring is in place. 

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Overall, neither neurotoxin nor genetic models account for the majority of apparently spontaneous or sporadic cases of PD (48). Nevertheless, the discovery that a specific pyridine, MPTP, can produce a severe, acute parkinson syndrome in humans and some laboratory species stimulated unprecedented interest in both neurotoxic hypotheses concerning the etiology of PD and in developing a very useful experimental model for the disorder that has supported a great deal of recent research aimed at developing innovative treatments for the disease. This compelling model of a neurotoxin-induced form of the parkinsonism syndrome is described next. 

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