In this chapter, we have attempted to demonstrate that chronic manganese intoxication, in both animals and man, is a better model of dystonia than of Parkinson's disease. It is proposed that many of the monoamine and endocrine changes in dystonia may be the result of disturbances in manganese metabolism. A search for such modifications in human dystonia victims is presently underway. Preliminary studies indicate that head and pubic hair manganese concentrations are elevated in dystonia patients.