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Bad trip on amphetamines

Amphetamines wake you up and can increase self-esteem - or create fear and panic. The stimulant drug can trigger psychotic episodes with paranoid delusions and hallucinations. The symptoms usually pass after a few days of abstinence, but in some cases residual symptoms can last for months.

Image: © istock.com / Yuri_Arcurs

An 18-year-old had been on amphetamine for a year when he hitchhiked to New York, swallowed about 100 mg of the stimulant, and entered a nightclub. There he got into an argument with a man and left. When he was on the street, he was dominated by the idea that the man might have called friends who want to "get" him. Anyone on the street could be this. He got scared, went to his hotel and barricaded the door with the bed. When he heard a loud radio in the hallway, he assumed it was turned up so that you wouldn't hear his screams when he was murdered. Then suddenly he heard voices saying, "Now we'll get him!" In his panic, he grabbed a knife and ran out of the hotel. Outside, he came across a police officer who arranged for him to be admitted to a mental hospital.

Doctor Burton Angrist published this case to illustrate how amphetamine use can trigger psychosis. For a long time it was assumed that psychoses in amphetamine users were not due to consumption, but to pre-existing diseases. Amphetamine psychoses were only proven beyond doubt in the 1960s and 1970s.

High dose psychosis

In experiments that are ethically questionable from today's point of view, amphetamine was administered to healthy test persons in increasing doses for as long as they could bear it. In a study, a test person had already received 465 mg of amphetamine when he suddenly thought he heard a bunch of gangsters in the hallway. They came to kill him. In his paranoid delusion, he assumed that the experimenter had set a trap for him and that the outcome of the experiment would only amount to killing him. With these and other experiments it was impressively demonstrated that psychoses can be triggered by high doses of amphetamine.

A recent study showed that the risk of psychotic symptoms is also dose-dependent when using methamphetamine. Participants in the 3-year longitudinal study had a 5-fold increased risk of psychosis when they consumed. The more frequently they consumed, the higher the likelihood of psychotic symptoms. If the drug was consumed on more than 15 days per month, the risk of psychosis was even 11 times higher.

Hidden Schizophrenia?

For most of those affected, symptoms usually disappeared after a period of abstinence. However, a minority continued to suffer from psychotic symptoms, which raises the fundamental question of whether long-term psychoses in users are exclusively drug-induced, i.e. due to the substance, or whether in these cases an existing but previously invisible schizophrenia is hidden behind it.

A large study from Finland provides an answer to this. The research team evaluated all clinical data from 1987 to 2003. During this period, over 18,000 patients were in hospital for substance-related psychosis. After developing psychotic symptoms for the first time, 30 percent of people treated for amphetamine use later developed schizophrenia.

In some of the users, the psychotic symptoms were probably only the first signs of a latent schizophrenia. It should be noted, however, that not all of them have developed schizophrenia. Even in the early experiments in which healthy subjects were given increasing doses of amphetamines, not all became psychotic. How can this be explained?

Explanatory model

A Norwegian research team led by study leader Jørgen Bramness suggests in a specialist article the connection between amphetamines and psychosis with the help of the Vulnerability-Stress-Model consider. This model is currently considered to be the best explanation for the development of schizophrenia. Amphetamine psychosis is therefore not the same as the psychotic symptoms of schizophrenia, but both can be related to one another.

The individual susceptibility to psychosis is called vulnerability. Above all, this includes genetic factors. However, it is assumed that genetic susceptibility alone is not enough. This is supported by the fact that, with identical twins, the risk is increased by around 50 percent and not 100 percent if one twin is sick.

This is where the amphetamines come into play. The stimulating drugs can act as a stressor and increase the risk of developing psychosis. Other stressors can be critical life events, traumatic experiences or conflicts in the personal environment. For example, if a person is already at risk of developing psychosis due to a genetically determined vulnerability, even small doses of amphetamine may be enough to cross the threshold to psychosis and reveal the symptoms of latent schizophrenia. In contrast, people with little or no previous exposure only react to very high doses with psychotic symptoms. They then develop an exclusively drug-induced psychosis.

In this model, long-term consumption of amphetamines would increase the vulnerability of the person bit by bit and move them closer to the psychosis threshold, so that, as in the case of the 18-year-old described, at some point only one additional dose is needed to cause the psychosis to break out bring to.

Conclusion

The consumption of amphetamines can trigger psychosis. The symptoms usually disappear after a few days, but in some cases residual symptoms can last for several weeks or even trigger a previously hidden schizophrenia.

In individual cases, however, it is difficult to differentiate whether it is a purely drug-induced psychosis or the first symptoms of schizophrenia. According to Jørgen Bramness and his research team, this has consequences for people who have already experienced psychosis due to amphetamines. They must then be checked carefully to see whether signs of chronic development are emerging - and they are urgently advised against continuing to consume amphetamines or other stimulating drugs.

Swell:

  • Angrist, B. (1994). Amphetamine psychosis: clinical variations of the syndrome. A.K. Cho & D.S. Segal (Eds.), Amphetamine and its Analogs: Neuropharmacology, Toxicology and Abuse (pp. 387-414). New York: Academic Press.
  • Bramness, J. G., Gundersen, Ø. H., Guterstam, J., Rognli, E. B., Konstenius, M., Løberg, E.-M., Medhus, S., Tanum, L. & Franck, J. (2013). Amphetamine-induced psychosis - a separate diagnostic entity or primary psychosis triggered in the vulnerable? BMC Psychiatry, 12, 221.
  • Iversen, L. (2009). Speed, ecstasy, Ritalin. Amphetamines - Theory and Practice. Bern: Huber.
  • McKetin, R., Lubman, D. I., Baker, A., Dawe, S. & Ali, R. L. (2013). Dose-Related Psychotic Symptoms in Chronic Methamphetamine Users. JAMA Psychiatry, 70 (3), 319-324.
  • Niemi-Pynttäri, J. A., Sund, R., Putkonen, H., Vorma, H., Wahlbeck, K. & Pirkola, S. P. (2013). Substance-Induced Psychoses Converting Into Schizophrenia: A Register-Based Study of 18,478 Finnish Inpatient Cases. J Clin Psychiatry, 74 (1), e94-e99.