Stimulant psychosis

Stimulant psychosis
Classification and external resources
ICD-10	F15.5
ICD-9	292.1

Stimulant psychosis is a psychotic disorder that appears in some people who use stimulant drugs. Most commonly, stimulant psychosis occurs in drug abusers who take very large doses but, in rare cases, it can also present in patients taking therapeutic doses under medical supervision. The most common stimulants involved are amphetamines and cocaine, though others have also been reported.

Signs and Symptoms

The symptoms of stimulant psychosis vary slightly between different stimulant drugs, but are shared largely with the symptoms of organic psychosis, including hallucinations, delusions, thought disorder, and, in extreme cases, catatonia.

Physical symptoms of prolonged stimulant abuse or acute overdose tend to accompany these psychotic symptoms in cases of stimulant psychosis (but not organic psychosis). These additional symptoms may include aggression, arrhythmia, dilated pupils, diarrhea, hypertension, hyperthermia, nausea, rapid breathing, restlessness, seizures, sleep deprivation, tremor, and vomiting.

Stimulants Known to Cause Psychosis

Amphetamine

Amphetamine and its derivatives are well known to induce psychosis, typically when abused chronically or in high doses. In an Australian study of 309 active amphetamine users, 18% had experienced a clinical level psychosis in the past year. The generic term "Amphetamines" describes both amphetamine proper, as well as the substituted amphetamines. The amphetamine molecule consists of a phenethylamine core with a methyl group attached to the alpha carbon. The substituted amphetamines consist of the same structure with one or more substitutions; prevalent examples include cathinone, DOM, ephedrine, MDMA, methamphetamine, methcathinone, and methylphenidate, though a large number of such compounds have been synthesized.

The symptoms of acute amphetamine psychosis are very similar to that of the acute phase of schizophrenia. Ampthetamine psychosis may be purely to do with high drug usage or high drug usage may trigger an underlying vulnerability to schizophrenia. There is some evidence that vulnerability to amphetamine psychosis and schizophrenia may be genetically related. Relatives of methamphetamine users with a history of amphetamine psychosis are five times more likely to have been diagnosed with schizophrenia than relatives of methamphetamine users without a history of amphetamine psychosis. The disorders are often distinguished by a rapid resolution of symptoms in amphetamine psychosis, while schizophrenia is more likely to follow a chronic course.

A Japanese study reported a 64% recovery rate within 10 days rising to a 82% recovery rate within 30 days from paranoid amphetamine psychosis after amphetamine cessation. However it has been suggested that about 5-15% of users fail to make a complete recovery from the psychosis in the long term. The psychosis can be quickly reestablished with further use, even of a small dose. Psychosocial stress has been found to be an independent risk factor for relapse, even without further amphetamine use in certain cases.

Cocaine

Cocaine has a similar potential to induce temporary psychosis, with more than half of cocaine abusers reporting some psychotic symptoms at some point. Typical symptoms of sufferers include paranoid delusions that they are being followed and that their drug use is being watched, often with accompanying hallucinations, which supports the delusional beliefs. Delusional parasitosis with formication ("cocaine bugs") is also a fairly common reaction. Cocaine-induced psychosis shows sensitization toward the psychotic effects of the drug, meaning psychosis tends to become more severe with repeated, intermittent use.

Methylphenidate

Methylphenidate is a central nervous system stimulant with a similar mechanism of action as cocaine's, and can also lead to psychosis from chronic abuse. Although the safety profile of short-term methylphenidate therapy has been well-established in clinical trials, the specific effects of long-term use of nearly all psychostimulants, including methylphenidate, is less clear; the long-term effects of using stimulants, even at therapeutic doses, are largely unknown. Short-term clinical trials show a very low incidence (0.01%) of methylphenidate-induced psychosis at therapeutic dose levels. A naturalistic study published in 1999 with an average follow up time of 21 months showed that 6 of 98 children and adolescents prescribed methylphenidate in an outpatient clinic developed psychotic symptoms at therapeutic dosages (the exception being a 17 year old on 80mg daily) , with most improving after drug cessation; however, the lack of a control group makes it impossible to attribute these effects to the medication. The long-term effects on mental health disorders in later life of chronic use of methylphenidate is unknown. Concerns have been raised that long-term therapy might cause drug dependence, paranoia, schizophrenia, and behavioral sensitization in a similar manner as that of other stimulant drugs. Psychotic symptoms from methylphenidate can include, hearing voices, visual hallucinations, urges to harm oneself, severe anxiety, mania, grandiosity, paranoid delusions, confusion, increased aggression, and irritability. Methylphenidate psychosis is unpredictable in whom it will occur, as family history of mental illness does not predict the incidence of stimulant toxicosis in children with ADHD.^{[citation needed]}

Withdrawal symptoms of methylphenidate can include psychosis and depression. Stimulant withdrawal or rebound reactions can occur and should be minimized in intensity, i.e. via a gradual tapering off of medication. A very small study (19 subjects) of abrupt withdrawal from stimulants used at therapeutic doses for ADHD and chronic tic disorder suggests that withdrawal reactions are not typical. Nonetheless, withdrawal reactions may still occur in susceptible individuals.

Caffeine

There is limited evidence that caffeine, in high doses or when chronically abused, may induce psychosis in some individuals.

Caffeine-induced psychosis is infrequently reported in the medical literature and remains controversial due to the lack of supporting information. It is not clear whether it proceeds by a similar mechanism as that of other stimulant psychoses or whether it is an entirely different process. Like other stimulants, caffeine increases dopamine levels, though only indirectly.

Treatment

Treatment consists of palliative care during the acute intoxication phase: maintaining hydration, body temperature, blood pressure, and heart rate at acceptable levels until the drug is sufficiently metabolized to allow vital signs to return to baseline. Typical and atypical antipsychotics have been shown to be helpful in the early stages of treatment. This is followed by abstinence from psychostimulants, supported with counseling or medication designed to assist the individual preventing a relapse and the resumption of a psychotic state.

See also

• Amphetamine
• Delusional parasitosis
• Dopamine hypothesis of psychosis
• Psychosis

Further reading

• Connell, P.H. (1961) Amphetamine Psychosis. Oxford University Press.

External links

• Chronic amphetamine use and abuse - Review published in 2000.