Treatment of the chronic pain patient.

A small percentage of patients with persistent pain are sufficiently angry, demanding, and manipulative to require the negotiation of an explicit treatment and/or management contract. The very few studies in this field suggest that pain is both a function of and a stimulus to abnormal illness behavior, thus requiring special attention to therapeutic "ground rules." Treatment requires an unequivocal assertion by the patient that he wishes to get better and is willing to work at doing so; the specification of clearcut goals and the means of working towards them ("pacing behavior"); and the possible use of electrical neurostimulation and/or weak analgesics for pain control. Explicit understanding of mutual expectations and the patient's and doctor's "rights" is also helpful in fostering goodwill and desirable results.     

Investigate the chronic neurotoxic effects of diquat

Chronic exposure to agricultural chemicals (pesticides/herbicides) has been shown to induce neurotoxic effects or results in accumulation of various toxic metabolic by-products. These substances have the relevant ability to cause or increase the risk for neurodegeneration. Diquat is an herbicide that has been extensively used in the United States of America and other parts of the world. Diquat is constantly released into the environment during its use as a contact herbicide. Diquat structurally resembles 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine (MPTP) and paraquat. Rotenone, paraquat, maneb and MPTP reproduce features of movement disorders in experimental animal models. Based on the structural similarity to other neurotoxins, chronic exposure of diquat can induce behavioral and neurochemical alterations associated with dopaminergic neurotoxicity. However, in the present study, diquat unlike other neurotoxins (rotenone, 6-hydroxydopamine, MPTP, paraquat and maneb) did not induce dopamine depletion in the mouse striatum. Although, notable exacerbation in motor impairment (swimming score, akinesia and open field) were evident that may be due to the decreased dopamine turnover and mild nigrostriatal neurodegeneration. These data indicate that, despite the apparent structural similarity to other dopaminergic neurotoxins, diquat did not exert severe deleterious effects on dopamine neurons in a manner that is unique to rotenone and MPTP.