| 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.[1] The most common stimulants involved are amphetamines and cocaine, though others have also been reported.
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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.[2]
Amphetamine and its derivatives are well known to induce psychosis, typically when abused chronically or in high doses. 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.
A 2007 article examined the limited amount of documentation and research currently available on methamphetamine-induced psychotic syndromes. In nearly every case, the symptoms of methamphetamine-induced psychosis (as well as stimulant psychosis in general) ceased within 7-10 days after discontinuation of the drug. However, in some cases, discontinuation symptoms were reported to last for months.
A small percentage of long-term or high-dose users may continue to experience intermittent psychotic episodes on an ongoing basis within the first year of abstinence.[3] Though uncommon, these experiences offer some anecdotal evidence regarding the neurotoxic effects of long-term amphetamine use, and the improvements that users tend to experience when these neurotoxic conditions are partially or fully reversed.
Spontaneous and long-term recurrences (similar to "flashbacks") are hypothesized to be triggered or exacerbated by high stress and sleep deprivation. In extremely rare cases, this condition is documented to persist beyond one year.
A key distinction between persistent stimulant psychosis and organic psychotic disorders like schizophrenia is that the symptoms of a amphetamine-induced psychotic disorder are not considered to be permanent and will eventually subside with a sufficient duration of abstinence.
Cocaine has a similar potential to induce temporary psychosis, with more than half of cocaine abusers reporting some psychotic symptoms at some point.[4] 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.[5][6]
Methylphenidate is a central nervous system stimulant with a similar mechanism of action as cocaine's,[7][8] 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.[9] Short-term clinical trials show a very low incidence (0.01%) of methylphenidate-induced psychosis at therapeutic dose levels.[10] A naturalistic study published in 1999 showed that 6 of 98 children prescribed methylphenidate in an outpatient clinic developed psychotic symptoms; however, the lack of a control group makes it impossible to attribute these effects to the medication.[11] The long-term effects on mental health disorders in later life of chronic use of methylphenidate is unknown.[12] 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.[13] 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.
Withdrawal symptoms of methylphenidate can include psychosis and depression.[14] Stimulant withdrawal or rebound reactions can occur and should be minimized in intensity, i.e. via a gradual tapering off of medication.[15][16][17] A very small study of abrupt withdrawal from stimulants suggests that withdrawal reactions are not typical. Nonetheless, withdrawal reactions may still occur in susceptible individuals.[18]
There is limited evidence that caffeine, in high doses or when chronically abused, may induce psychosis in some individuals.[19][20][21]
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.[22][23]
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.[24] 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.
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