Table 2.

Summary of major mechanism of action, nature of evidence and prevalence of psychotic symptoms for each substance.

Substance	Major mechanism of action	Nature of evidence	Prevalence of psychotic symptoms
Cannabinoids	Partial agonist activity on CB1	Partial agonist activity on CB1	0.8–10% (14)
Synthetic cannabinoids	Agonist activity on CB1	Case reports	NA
Synthetic catinones	Increase of dopamine release and inhibition of the reuptake of monoamines (15–19).	Cross-sectional studies	NA
Cocaine	SERT, DAT, and NET block (20), antagonism of the 5-HT3 receptor (21), and block of sodium channels (22)	Cross-sectional studies	Across the lifespan: 60.0–86.5% (23, 24)
Methamphetamines	Increase DA concentration by reversing VMAT2 and DAT (25)	Cross-sectional studies	17–37.1% (26, 27)
Hallucinogens	Increase 5-HT concentration, through agonist or partial agonist activity on 5HT receptors (28)	Case reports	NA
Entactogens	Increase 5-HT concentration through the inhibition of SERT and by reversing SERT, NA concentration, through the inhibition of NET and by reversing NET and DA concentration through the inhibition of DAT (28, 29).	Cross-sectional studies	NA
Phencyclidine and ketamine-induced psychosis	Antagonist activity on NMDA receptors Agonist activity on D2	Cross-sectional studies, randomized placebo-controlled clinical trial	NA

5-HT, 5-hydroxytryptamine receptors; CB1, cannabinoids receptor 1; D2, dopamine deceptor 2; DA, dopamine; NMDA, N-methyl-D-aspartate; NA, evidence lacking in current literature.