Psychosis

Psychosis is a cluster of symptoms in which a person loses reliable contact with shared reality. The two most recognisable features are hallucinations — perceiving things that are not present — and delusions — holding fixed false beliefs that resist correction. Disorganised thinking and speech are also common.

Psychosis is not a diagnosis in itself but a symptom state that can arise from several causes: primary psychiatric conditions such as schizophrenia or bipolar disorder, medical causes, and direct effects of certain substances. When a substance triggers it, the episode is described as substance-induced psychosis — and it may resolve after the drug clears, or persist well beyond it.

How it works · its role

The leading neurobiological explanation centres on dopamine. Excess dopaminergic signalling in the mesolimbic pathway — the brain's reward and salience circuit — is thought to drive the core positive symptoms: hallucinations and delusions. Antipsychotic medications work largely by blocking dopamine D₂ receptors, which supports this framing.

A second, complementary model focuses on glutamate. Blocking NMDA receptors — a subtype of glutamate receptor — reliably produces psychosis-like states in healthy volunteers, pointing to glutamatergic disruption as another pathway. In practice the two systems interact: loss of NMDA-mediated inhibition can cause downstream dopamine dysregulation.

Serotonin, particularly at the 5-HT₂A receptor, is also involved. This partly explains why some substances that act on serotonin produce perceptual disturbances resembling psychosis, even though their primary mechanism differs from the dopamine model.

Relevance to substances & effects

Several substance classes can precipitate psychosis, each through a somewhat different route.

High-dose stimulants — amphetamines, cocaine, and related compounds — flood the synapse with dopamine, and prolonged heavy use can produce a stimulant psychosis that closely resembles acute schizophrenia, including paranoid delusions and auditory hallucinations. It typically resolves after abstinence, though recovery can take days to weeks.

Cannabis, particularly high-THC preparations, carries a well-established association with psychotic episodes. The risk is not uniform: it is concentrated in people with a personal or family history of psychosis, those who begin use in adolescence, and those using very frequently or at high potency. The relationship is thought to be bidirectional — cannabis can trigger episodes, and early psychosis may increase cannabis use.

NMDA receptor antagonists such as ketamine and phencyclidine (PCP) produce a dissociative psychosis-like state even at recreational doses. Because the glutamate model of psychosis was partly built on observations of these drugs, they are sometimes described as having a psychotomimetic profile — meaning they chemically mimic aspects of psychosis.

Classic psychedelics (LSD, psilocybin, mescaline) can produce acute perceptual disturbances that resemble psychotic features. In most people these are time-limited and resolve as the drug clears. However, in individuals with existing vulnerability to psychotic disorders, a psychedelic experience may precipitate or accelerate a first episode.

Clinical · risk note

Substance-induced psychosis is a medical situation that warrants evaluation, not a state to wait out at home. In a meaningful proportion of cases — particularly with cannabis and stimulants — what begins as a substance-induced episode does not fully remit and transitions into a persisting psychotic disorder.

Risk is not evenly distributed. The most consistently identified vulnerability factors are a personal history of psychotic episodes, a first-degree relative with a psychotic disorder, and early age of first use. For cannabis, potency and frequency of use matter as well.

Anyone experiencing a first psychotic episode — whether substance-linked or not — should be assessed by a clinician. Early intervention is associated with better outcomes.