Psychotic reactions in people taking amphetamines werefirst reported many years ago and the question was posedwhether it was due to the amphetamines or to co-existingand exacerbated paranoid schizophrenia. In one study,most of the psychotic symptoms remitted before theexcretion of amines had fallen to its normal basal value（SED-9, 8）. The psychotic syndrome was indistinguish-able from paranoid schizophrenia, with short periods ofdisorientation, and could occur after a single dose （manyhad taken the equivalent of some 500 flag of amfetamineor metamfetamine orally） with or without simultaneousalcohol, and was most pronounced in addi&s （SED-9, 9）.Amfetamine psychosis was also seen in 14 people inAustralia （1）; the predominant hallucinations were visual,which is unusual for schizophrenia （SED-8, 11）. Similarly, in contrast to schizophrenia, vision was the primary sen-sory mode in thinking disorders and body schema distor-tions in 25 amfetamine addicts （50）. In other studies, volunteers previously dependent onamphetamines were dosed to a level at which amfetaminepsychosis was produced, in order to examine the mechan-ism of action and pharmacokinetics of amfetamine and itspossible relation to schizophrenia （51,52）. Psychosis wasinduced by moderately high doses of amfetamine and thepsychotic symptoms were often a replication of thechronic amfetamine psychosis, raising the question ofwhether the establishment of chronic stimulant psychosisleaves residual vulnerability to psychosis precipitated bystimulants. The mechanism might be similar to that whichoperates in the reverse tolerance that has been seen inexperimental animals （53）. In some cases an underlyingpsychosis can be precipitated; an increase in schizo-phrenic symptoms （SED-8, 12） was observed in 17actively ill schizophrenic patients after a single injectionof amfetamine.