taraxein and hallucinations

   The name taraxein comes from the Greek verb tarassein, which means to confuse, to disturb. It was introduced in or shortly before 1957 by the American psychiatrist and neurologist Robert Galbraith Heath (1915-1999) and his team at Tulane University, New Orleans, to denote a serum protein fraction of the blood of individuals with a clinical diagnosis of * schizophrenia. It was speculated at the time that this serum protein fraction constitutes a potent endogenous toxin, capable of evoking * psychotic symptoms in nonpsychotic individuals when injected intravenously. Its alleged effects were initially established in animal studies with monkeys (who reportedly displayed motor behaviour reminiscent of catatonia, and changes on the electroencephalogram (EEG) indicative of limbic pathology), and spiders of the species Zilla-X-notata (which, upon having been fed taraxein stuffed inside the dried abdomen of a fly, reportedly built webs with a rudimentary structure designated as 'catatonic' in nature). Over the years taraxein was administered to numerous species ofanimals, including the tadpole, the larvae of Xenopus levis, the larvae of Rana temporaria, and the isolated frog's heart, where it was reported to cause toxic effects of varying nature. When tested in a group of prisoner volunteers and four physicians, the group of Heath noted that "all human subjects in this series who received active taraxein displayed symptoms indicating disturbances in the boundaries of the self. All exhibited fundamental symptoms of schizophrenia, as described by Bleuler, and within the group a wide variety of accessory symptoms were manifest. In reviewing this series, we note that 5 of the 35 subjects described overt hallucinatory experiences. All had auditory hallucinations which in no way differed in character from those seen in patients diagnosed as undeniably schizophrenic. No visual hallucinations resulted from the administration of taraxein." Because of the effects reported by the group of Heath and others, it was speculated that tarax-ein might be the famous 'toxin X' or 'neurotoxin' postulated by authorities such as Emil Kraepelin (1856-1926) and Carl Gustav Jung (1875-1961) as the biochemical cause of dementia praecox or schizophrenia. Comparisons were made between taraxein and * hallucinogens such as mescaline and LSD, and expectations as to its potential to help unravel the etiology of the major psychotic disorders were running high. However, the success rate of the taraxein studies declined over time, and ultimately the validity of the taraxein phenomenon was called into question.

   References

   Bercel, N.A. (1960). A study of the influence of schizophrenic serum on the behavior of the spider: Zilla-x-notata.In: The etiology of schizophrenia. Edited by Jackson, D.D. New York, NY: Basic Books.

   Heath, R.G., Martens, S., Leach, B.E., Cohen, M., Angel, C. (1957). Effect on behavior in humans with the administration of taraxein. American Journal of Psychiatry, 114, 14-24. Heath, R.G., Leach, B.E., deBalbian Verster, F. (1962). Mechanisms related to the hallucinogenic effects of taraxein. In: Hallucinations. Edited by West, L.J. New York, NY: Grune & Stratton.

   Kety, S.K. (1960). Recent biochemical theories of schizophrenia. In: The etiology ofschizophrenia. Edited by Jackson, D.D. New York, NY: Basic Books.

   Malis, G.Yu. (1959). Research on the etiology of schizophrenia. Translated by Haigh, B. Edited by Wortis, J. New York, NY: Consultants Bureau.