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Drug-Induced Psychosis: List Of Causative Agents

Psychosis is a condition that is commonly associated with the mental illness schizophrenia.  It is defined as a detachment from reality and hallmark symptoms include delusions (beliefs that aren’t based in reality) and hallucinations (seeing, hearing, or feeling stimuli that aren’t real).  Those with psychosis are usually admitted to a psychiatric ward and/or hospital and treated with atypical antipsychotics.  These drugs function by inhibiting abnormally high dopamine in certain regions of the brain.

High dopamine and dopaminergic dysfunction is known to contribute to psychotic states.  This is also often the case in drug-induced psychosis in which a person ingests a drug that alters their dopamine system, leading to a temporary psychotic break.  Drug-induced psychosis most often occurs with those that abuse stimulants, which is why there’s a sub-classification known as “stimulant psychosis.”

Although a majority of drug-induced psychosis cases stem from stimulant use (or abuse), there are plenty of other drugs besides stimulants that can cause psychosis.  These drugs include: marijuana, salvia, various hallucinogens, and even some prescription medications (e.g. prednisone, antidepressants, antipsychotics, etc.).

Drug-Induced Psychosis (Toxic Psychosis)

Drug-induced psychosis is characterized by a psychotic break with reality as a result of ingesting or withdrawing from a drug (regardless of whether it’s illicit, pharmaceutical, or unregulated).  Another technical term for this condition is “toxic psychosis” due to the fact that the psychotic break is believed to result from a poisoning effect elicited by the particular drug that was ingested.

Factors influencing drug-induced psychosis

It is important to consider the fact that there are many factors influencing whether someone is susceptible to experiencing drug-induced psychosis as well as the severity of their psychotic break (if they’re experiencing one).

1. The Drug(s)

Firstly, it is important to consider that the drug (or combination of drugs) that you take will have the greatest influence as to whether you experience drug-induced psychosis.  Certain drugs are less associated with psychosis than others.  Those that take stimulant-based substances (e.g. cocaine, methamphetamine, etc.) at high doses are more likely to experience psychosis as a result of abnormally high dopamine concentrations.

Various prescription drugs aren’t associated with as great of a risk of triggering psychosis as stimulants.  Even of the prescription drugs that are stimulants, taking at proper dosing reduces likelihood that a psychotic break will occur.  Experiencing drug-induced psychosis from an antidepressant or corticosteroid is significantly less likely than an illicit street stimulant.

2. Dosage

With any drug or substance, the dosage tends to increase the likelihood that you’ll experience psychosis.  The more you ingest of any particular drug – regardless of its type, the greater the likelihood of side effects.  For this reason it is always recommended to take the minimal effective dose – regardless of the drug that you’re ingesting; this helps reduce side effects while still providing benefit.

Those that take high doses of a particular drug will experience a greater shift within their neurochemistry.  More potent doses are likely to alter various neurotransmitters, brain waves, and regional activation.  Lower doses are associated with less total neurochemical changes than higher ones.  This isn’t to say that some people can’t experience psychosis on a low dose, rather it’s saying that the likelihood is minimized.

3. Short-term vs. Long-term usage

Those that use a drug for a short-term are less likely to experience drug-induced psychosis than those that have used it over a long-term.  This is due to the fact that over a long-term, most people have built up a tolerance and are taking higher doses.  Additionally, long-term usage of certain drugs tends to alter a person’s physiology.  The long-term physiological changes often accumulate, leading to altered functioning (i.e. suboptimal functioning) of the central nervous system.

4. Preexisting mental illness

Those who have a preexisting mental illness are significantly more likely to experience drug-induced psychosis.  Those with mental illness may have abnormal levels of certain neurotransmitters, causing their brain to react more strongly to any psychoactive substance.  It is especially common for those with schizophrenia to experience a psychotic episode as a result of ingesting an illicit drug.

Other mental illnesses such as: bipolar disorder, major depressive disorder, and severe forms of anxiety may also be prone to experience drug-induced psychosis.  This is why many psychiatrists and professionals emphasize to patients that to ensure optimal mental functioning, illicit drugs are to be avoided.

5. Individual factors

There is no “one size fits all” in regards to drug-induced psychosis.  Two people of the same age may ingest the same dosage of a particular drug and one may not experience anything odd, while the other may have a full-blown psychotic break with deluded thinking and auditory hallucinations.  When considering your susceptibility, it is important to take into account: age, sleep deprivation, stress, drug interactions, and genetics.

  • Age: Those that are at a younger age are more likely to experience drug-induced psychosis due to the fact that certain regions of their brain haven’t fully formed.  It is estimated that the brain is fully developed at age 25, but until then, certain regions are likely still forming.  Using or abusing certain drugs can interfere with neural development, and increase susceptibility to drug-induced psychosis.
  • Genetics: It is thought that there are likely some genetic factors that increase a person’s susceptibility to experiencing drug-induced psychosis.  Those with first-degree relatives that have been diagnosed with a mental illness, particularly one like schizophrenia are thought to be at greater risk for drug-induced psychosis.  Certain genes may control both arousal and neurotransmitter levels, potentially making you more likely to experience a drug-based psychosis.
  • Interactions: If you use certain drugs or medications and take another (drug or medication), it is important to consider the potential of interaction effects.  In many cases, taking multiple substances that increase dopamine may have synergistic effects – elevating dopamine to a greater extent than usual.  Even ingesting substances like caffeine, alcohol, or over-the-counter antihistamines can interact with certain medications or drugs to provoke drug-induced psychosis.
  • Sleep deprivation: Another factor to consider in cases of drug-induced psychosis is that of sleep deprivation.  In some cases, severe sleep deprivation can lead to psychotic symptoms.  Therefore you should consider the duration over which you were sleep deprived prior to ingesting the drug and realize that it may have contributed to the psychotic break.
    • It should be noted that certain drugs (e.g. methamphetamine) can cause sleep deprivation (sometimes for days); in these cases the drug’s effect and drug-induced sleep deprivation may act synergistically to trigger psychosis.
  • Stress: If you are highly stressed, you may be more prone than usual to experience psychosis as a result of ingesting a drug.  High stress can elicit a cascade of neurochemical, hormonal, and physiological changes – potentially increasing your susceptibility.  Those who experience less psychological and physical stress are less likely to experience drug-induced psychosis.

6. Previous psychotic episode

Regardless of whether you have a mental illness that triggered a psychotic episode or you used a drug that triggered a psychotic episode, having previously experienced one, your brain may be more likely to experience another.  If you use the same drug that triggered your first episode, you’re setting yourself up for another that is potentially more severe.  Continuous usage of the drug that triggered a psychotic episode (or multiple episodes) may result in permanent neural changes – potentially leading to chronic, lifelong psychosis.

A previous psychotic episode should serve as a warning that your brain is sensitive and you are more susceptible to experiencing another one.  Make an effort to remain drug free if your goal is to avoid another psychotic break.

List of Drugs That Can Induce Psychosis

There are a variety of drugs capable of inducing psychosis.  While most people are familiar with the fact that illicit drugs can cause psychosis, many remain unfamiliar with the fact that legal substances and even pharmaceutical drugs taken at prescribed doses can trigger psychosis in certain individuals.  Below is a list of popular substances that have been documented as triggering psychosis.


It is possible to experience a psychotic break by drinking alcohol.  Those that experience alcohol-induced psychosis tend to abuse alcohol and are battling chronic alcoholism.  Drinking excessive amounts of alcohol impairs brain functioning, and can trigger psychosis in certain individuals.  Drinking is associated with increasing a person’s susceptibility of experiencing psychosis nearly 8x among men, and 3x in women.

Most people can handle a few drinks and won’t experience psychosis.  There are even some lifelong heavy drinkers that never experience a psychotic break.  That said, if you abuse alcohol, you’re putting yourself at greater risk of experiencing drug-induced psychosis.  Your odds of experiencing alcohol-induced psychosis increase if you are a long-term drinker, or have a comorbid psychiatric disorder.

One study documented that most common symptoms associated with alcohol-induced psychosis included: auditory hallucinations, followed by delusions.  In some cases users also experienced visual hallucinations, depression, and speech impairment.  Effective treatment protocols tend to include: anxiolytics and in some cases, antipsychotics.

Fortunately, psychotic breaks as a result of alcohol abuse are generally short-lived assuming the individual stops drinking.  Continuous drinking despite the psychosis may complicate or exacerbate psychotic symptoms.  It should also be mentioned that those undergoing alcohol withdrawal may experience a temporary psychosis – especially if they fail to properly taper their consumption.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/2380692
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/17322182
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/10968157
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/24307180


Both benzodiazepines and barbiturates have been documented as causing psychotic symptoms in the event of overdoses as well as during withdrawal.  Barbiturates are seldom prescribed these days due to safety concerns, and benzodiazepines are preferred for patients with severe anxiety.  In a cases of a 54-year old woman discontinuing butalbital (a barbiturate) was admitted to the hospital with hallucinations and delirium.

Numerous cases of benzodiazepine withdrawal syndrome have resulted in psychotic symptoms, especially among those who conduct too quick of a taper (e.g. quitting “cold turkey”).  Another documented case occurred while a 73-year old woman was taking a standard therapeutic dose of Klonopin (Clonazepam).  She experienced auditory, visual, and tactile hallucinations in addition to paranoid delusions.

This was among the earliest cases of documented benzodiazepine-induced psychosis.  Upon reporting symptoms to the doctor, dose reduction was advised.  As soon as she reduced the dose of Klonopin, her psychotic symptoms abated.  She continued treatment for an additional year and never experienced another episode.  This case demonstrates the fact that dose-sensitive individuals, especially to benzodiazepines may be susceptible to drug-induced psychosis.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/10349206
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/14194223
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/3711371
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/7057171
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/7841856

Cannabis (Marijuana)

There is some evidence that using marijuana increases risk of schizophrenia, especially when used over a long-term.  Those that are dependent on cannabis tend to have increased rates of psychotic symptoms, particularly in young people – regardless of other factors.  It is known that some people experience a psychotic episode while intoxicated with cannabis and others may experience psychosis as a result of cumulative cannabis usage.

The age at which a person starts using cannabis as well as the person’s sex are thought to increase risk of cannabis-induced psychosis.  The younger a person starts using cannabis, the greater their susceptibility to experiencing psychosis.  Additionally males tend to experience cannabis-induced psychosis to a greater extent than females.

Cannabis-induced psychotic disorder (CIPD) isn’t always associated with those who develop schizophrenia.  In fact, research demonstrates that PPI (pre-pulse inhibition) testing differs between those experiencing cannabis-induced psychotic disorder and schizophrenia.  Particularly, those with schizophrenia tend to have significantly worse pre-pulse inhibition when attention is required by comparison.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/25175914
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/17662880
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/12537030
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/16319402


Scientists have studied the effects of hallucinogens with brain imaging and behavioral tracking.  It is thought that hallucinogens may trigger psychotic symptoms as a result of causing hyperactivity in the prefrontal cortex with notable activity changes in other regions of the brain.  Certain hallucinogens are believed to alter functioning of serotonin receptors (5-HT2), which leads to psychosis as a result of “sensory overload.”

  • Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3181663/


There is an array of evidence suggesting that ketamine can provide rapid relief from depressive symptoms.  That said, it is a dissociative and various properties of the drug may induce psychosis in susceptible individuals.  Even among those with no preexisting psychotic episode, ketamine is capable of causing acute psychosis.

There is considerable research suggesting that those who are dependent on ketamine are more likely to have psychotic disorders.  Approximately 30% of all ketamine users had experienced a psychosis stemming from excessive usage of the drug.  Some speculate that there may be some safety concerns regarding long-term usage of ketamine and that risk for psychosis may increase.

Ketamine functions as an NMDA receptor antagonist, and is capable of causing symptoms that resemble schizophrenia in humans.  Furthermore, those that already have schizophrenia or a mental illness tend to experience more severe psychotic episodes after ingesting even subanesthetic doses of ketamine.  It is believed that ketamine impacts both glutamatergic and dopaminergic function to provoke psychosis.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/25761158
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/14603267
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/8526975
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/17591652

LSD (Lysergic acid diethylamide)

There is evidence that those using LSD (Lysergic acid diethylamide) may experience drug-induced psychosis.  It has been reported that episodes of LSD-induced psychosis are subject to significant individual variation.  Some cases seem to be characterized by delirium, while others are more similar to schizophrenia.

Other cases may not resemble delirium or schizophrenia and may contain elements that aren’t commonly associated with organic psychosis.  Some people may experience a more traditional psychosis, while others will report cosmic or mystical psychoses.  There is increasing evidence that using LSD can cause schizophrenia and trigger psychotic episodes among susceptible individuals.

The mechanisms by which LSD causes psychosis may differ based on the individual.  That said, some researchers hypothesize that deficient levels of CNS serotonin (i.e. low serotonin) may be a causative factor.  In one case, a serotonin precursor (L-5-hydroxytrptophan) was administered and successfully treated symptoms of a 23 year old experiencing LSD-psychosis.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/4087079
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/6601463

PCP (Phencyclidine)

PCP also known as “Angel Dust” is a dissociative drug that is capable of inducing psychosis.  PCP functions primarily as an NMDA receptor antagonist, thus inhibiting activity at the NDMA sites.  It is a hallucinatory drug and accounts of PCP-induced psychosis have been reported since the 1980s.

Although psychosis as a result of ingesting PCP isn’t common, those that take high doses and/or use PCP over a long-term may be more likely to become psychotic. Furthermore, the psychosis resulting from PCP usage tends to be long-lasting (e.g. 4 to 6 weeks).  In addition to psychotic symptoms, those ingesting PCP may experience lightheadedness, feel “numb,” or sensations of vertigo.

Cases of prolonged PCP-induced psychosis have been reported among “chronic abusers.”  PCP psychosis can be treated with antipsychotic medications and individuals tend to stabilize quicker than first-onset psychosis as a result of mental illness (e.g. schizophrenia).  Compared to cocaine or stimulant psychosis, PCP psychosis was characterized more by: delusions of physical power, sensory alterations, time distortion, and bizarre experiences (e.g. out-of-body experiences – as opposed to suspiciousness and paranoia.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/6514253
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/17127556
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/9316684
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/710364


It is also important to understand that those using or “huffing” inhalants for the purpose of getting “high” may experience psychotic episodes.  Even excessive huffing of the petrol found in gasoline may be responsible for triggering psychosis in some individuals.  Realize that as long as you aren’t intentionally “huffing” these inhalants, you probably won’t experience psychosis.


In certain countries, butane abuse and dependence is becoming increasingly problematic.  Not only can butane be deadly, but it can cause severe psychotic episodes even among individuals with no previous psychiatric illness.  It is more common among those that abuse butane, especially those that use it regularly over an extended time span.

Butane-induced psychosis could produce symptoms such as: violence, persecutory delusions, and visual hallucinations.  There are few case studies documenting butane-induced psychosis, but most suggest that the psychotic symptoms tend to fade over time with abstinence from inhalants.

  • Source: http://onlinelibrary.wiley.com/doi/10.1046/j.1440-1819.2001.00806.x/full
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/15589716

Gasoline (Petrol)

Reports date back to the 1950s of psychosis resulting from inhalation of petrol fumes.  Initially there was evidence that those frequently handling Petrol (“petrol handlers”) were experiencing abnormal paranoia.  This paranoia was a result of cumulative exposure to petrol gas, and could’ve been mitigated by avoiding petrol.

Those that blatantly inhale gasoline or petrol fumes may exhibit psychotic symptoms such as paranoia, hallucinations, and/or delusions.  It is thought that the longer the span and frequency of exposure influence the severity of the psychosis.  A case was documented in 1965 of a boy who was in charge of mowing his school’s lawn, and found that inhaling the petrol made him less “nervous and edgy.”

He continued inhaling the substance because he liked the relaxation effect.  This eventually lead to dependence and eventually he experienced symptoms like: breathlessness, flushing of the skin, excessive talkativeness, nonsensical speech, and visual hallucinations (in this case of “foxes”).  Another case has been documented in which the sniffer of petrol hallucinated billions of ants.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/14310207
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/14804041
  • Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1845748/


This is an organic solvent that is commonly used in glues, paint thinner, adhesives, varnishes, paints, gasoline, solvents, and even in the production of plastics.  When inhaled in its pure form or from within a product containing Toluene, it is capable of eliciting psychoactive effects.  Those that inhale Toluene for a long-term or become dependent on its effects may experience psychosis.

Furthermore, certain neurological changes as a result of inhaling Toluene may be irreversible, and therefore may make an individual more prone to longer-lasting and more severe future psychotic episodes.  Cases of irreversible schizophreniform psychosis have been reported among an individual who inhaled Toluene chronically for 5 years via his occupation.

Most people that abuse Toluene can recover from psychosis with abstinence.  In a case of a man using 300 ml per day of Toluene, various psychotic symptoms were exhibited.  These included: suspicions that his neighbors were attempting to harm him (delusions of persecution), blurred vision, bizarre behaviors, hearing voices (that commented on his behaviors), and excessive hoarding (particularly of garbage and dead crows).

At the hospital, this man was treated with diazepam (Valium) and it improved his sleep and psychomotor agitation.  During the hospitalization, he remained sober of Toluene and returned to a non-psychotic state within 2 weeks despite the fact that no antipsychotic drugs were administered.

  • Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4211428/
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/1790519
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/23686059
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/4019425
  • Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2802388/


Various opioids have been associated with acute cases of drug-induced psychosis.  Most commonly, opioid psychosis is associated with opioid abuse and/or opioid withdrawal.  In a 2003 study involving 377 individuals that were dependent on opioids, over 10% experienced psychosis.  The psychosis experienced among opioid users is often characterized by delirium and occurs during withdrawal.

Oddly enough, more current research (2014) has suggested that ingestion of opioids at therapeutic doses may actually have antipsychotic properties.  Researchers suggested that opioids warrant further analyses for their potential to treat psychotic symptoms.  In general, opioid-psychosis occurs in cases of abuse and/or during withdrawal.  Common examples include: Methadone withdrawal and Tramadol withdrawal.

Researchers have hypothesized that abuse and/or withdrawal from opioids may alter dopaminergic processing, which contributes to psychotic episodes.  One case study involving a 25-year old woman experienced a psychotic episode (for approximately 30 minutes) after being treated with Nalbphine (an opioid).  Her psychotic symptoms were successfully treated with administration of Naloxone.

Factors that commonly influence opioid psychosis include: abstinence and other medications.  If an opioid abuser is simultaneously abusing alcohol or tranquilizers, this may alter and/or exacerbate psychotic symptoms.  Experiencing acute psychosis from opioid intoxication is considered benign and tends to resolve with abstinence.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/12674698
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/24494084
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/24563427
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/7852256
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/24733134

Over-the-Counter Drugs (OTC)

Various over-the-counter (OTC) medications have been associated with psychotic symptoms when taken at supratherapeutic doses.  In other words, people drinking the whole bottle of cough syrup are more likely to experience psychotic episodes than those taking the recommended doses.  That said, there are still some cases of psychosis resulting from standard dosages.


There are numerous documented cases of individuals that have experienced antihistamine-induced psychosis.  Most cases involve individuals either taking the antihistamines as supratherapeutic levels (e.g. way too much) or taking antihistamines in conjunction with another substance.  Abusing antihistamines for a “high” or taking them at extremely high doses may provoke psychotic symptoms.

  • Diphenhydramine
  • Pheniramine
  • Promethazine

There are a few antihistamines that are abused more than others to achieve a “high.”  These include: Diphenhydramine, Pheniramine, and Promethazine.  Cases have been documented since the 1990s of Diphenhydramine-induced psychosis, even when taken at therapeutic doses.  Symptoms of an antihistamine psychosis often include both auditory and visual hallucinations.

A majority of the severe cases involved individuals taking a large number of antihistamine tablets, particularly with Diphenhydramine, which can be classified as antihistamine poisoning as well. In one case, a patient claimed to have felt insects, spiders, ticks, and beetles crawling on their skin.  Taking large doses of antihistamines results in “anticholinergic syndrome” which leads to the psychosis.

Most cases of antihistamine psychosis can be mitigated with administration of physostigmine salicylate.  This drug rapidly crosses the blood-brain barrier and functions as a reversible acetylcholinesterase inhibitor, thus increasing levels of acetylcholine to decrease psychotic symptoms.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/9270406
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/7497894
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/3338401
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/14709767
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/514934
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/21221288

Cold Medicines

There have been reports of psychosis resulting from non-prescription (over-the-counter) cold and sinus medications.  It is thought that the contents of these medications may affect cholinergic and adrenergic functioning, which triggers psychosis.  When taken at proper doses, most people aren’t going to experience psychotic episodes.

However, when abused or taken in excess, the likelihood of psychosis increases.  In particular, there seems to be a link between the cold medicine Corcidin and psychosis.  The psychosis resulting from Corcidin has been characterized by clouded thinking, paranoia, and various types of delusions.  Most cases of psychosis resulting from cold medicines resolve within a few days – assuming the person has discontinued treatment.

If there’s a history of psychosis, an antipsychotic medication may be administered.  In one  case, a man was able to recover in 2 days upon discontinuation of Corcidin by taking prescribed benzodiazepines.  Corcidin contains both dextromethorphan (DXM) at 30 mg and chlorpheniramine maleate at 4 grams per tablet.  The DXM is considered the causative agent of psychosis from Corcidin.

In other cases, those that ingest Phenylpropanolamine (PPA) from cold medicines may experience psychosis.  There have been reports of acute psychosis stemming from the Phenylpropanolamine, which contains a similar structure to amphetamines.  Documentation of Phenylpropanolamine-induced psychosis can be traced back to the 1980s.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/2386871
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/16076908
  • Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3977765/
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/7995508
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/1912131

Dextromethorphan (DXM)

Those abusing cough syrup (with DXM) may experience psychotic episodes.  Dextromethorphan is a common ingredient in over-the-counter cough suppressants and can be abused.  There are various case studies of individuals experiencing psychosis as a result of DXM intoxication.  Symptoms associated with DXM-induced psychosis include: bizarre feelings, dissociation, and paranoia.

One case of a 35-year old woman demonstrated symptoms of agitation, crying spells, and psychosis.  She experienced auditory hallucinations, was behaving oddly, and became obsessed with her Bible.  She had a college degree, a full-time job, and no history of psychiatric illness.  She was treated with an antipsychotic, an antidepressant, and benzodiazepine and recovered within 7 days.

It is believed that DXM-psychosis occurs as a result of its serotonergic and opioidergic effects.  Other research demonstrates that not only intoxication can produce psychotic symptoms, but withdrawal from dextromethormphan may result in psychosis as well.  Most that end up experiencing DXM psychosis have abused the substance.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/10671422
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/21324299
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/16318953

Plants (Misc.)

There are various plants that when ingested may trigger symptoms of acute psychosis.  These plants include: Belladonna (nightshade), Hawaiian baby woodrose, Jimson weed, Morning glory seeds, and Salvia divinorum.

Belladonna (Nightshade)

Those that ingest the “Nightshade” plant, also known as Atropa Belladonna could experience acute psychosis.  This plant is capable of triggering psychosis as a result of its anticholinergic properties.  There are various case studies of individuals with no preexisting psychiatric illness experiencing psychosis as a result of ingesting Belladonna.

Fortunately cases can be treated relatively easily with administration of the acetylcholinesterase inhibitor Physostigmine. Administration of Physostigmine is typically given intravenously (IV) and works to increase levels of acetylcholine, which helps reverse psychotic symptoms.  The psychosis from Belladonna ingestion is characterized by confusion, hallucinations, and disorientation.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/2330633
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/4830790
  • Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3361210/
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/7267423

Hawaiian Baby Woodrose (Argyreia nervosa)

Those ingesting seeds of Hawaiian Baby Woodrose, especially in large quantities, will be affected by the psychotropic contents of LSA (lysergic acid amine).  It has been documented that the seeds are capable of causing psychosis, but the psychotic states tend to be short-lived.  One study found that individuals recovered from psychosis within 9 hours of experiencing psychotic symptoms.

The psychosis from Hawaiian Baby Woodrose is thought to be similar to LSD due to the fact that it contains lysergic acid.  One would expect the psychosis to be based on the hallucinogenic properties of the seeds.  Symptoms can include: hallucinations, psychomotor agitation, orientation disturbances, and anxiety.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/12768530
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/12886727

Jimson Weed (Datura Stramonium)

This is another plant that when ingested elicits anticholinergic effects, which can lead to psychosis in some individuals.  Several publications have highlighted the possibility that ingesting Jimson Weed could induce psychosis as a result of its atropine-like alkaloids.  The psychosis often involves hallucinations, tachycardia, pupil dilation, and dry mouth.

Those experiencing psychosis can be treated with low dose sedative drugs, but are most commonly given an acetylcholinesterase inhibitor like Physostigmine to offset the anticholinergic effects.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/24895713
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/1750136
  • Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2529415/

Morning Glory Seeds (Ipomoea Tricolor)

Morning glory seeds contain LSA (lysergic acid amine) which produces a psychedelic experience for some users.  There is evidence that these seeds can trigger psychosis similar to LSD.  It is thought that an individual would need to ingest a significant number of morning glory seeds to experience psychosis.

That said, individuals that are prone to psychosis as a result of mental illness and/or people taking other medications may be more prone to morning glory seed psychotic symptoms.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/5591054

Salvia Divinorum

This is a hallucinogen that has become popular in recent years.  It functions as a full kappa opioid receptor agonist and elicits effects of serotonergic agonism and NDMA glutamate agonism.  Most “trips” associated with Salvia tend to be over within 30 minutes of ingestion.  Although cases of prolonged psychosis are rare among Salvia users, they may increase as a result of the drug’s legal status, particularly in the United States.

One case reported a 15-year old male experienced psychosis with symptoms of: paranoia, blunted emotion, thought blocking, and slow speech.  The psychotic episode was documented as occurring over a 3 day span.  Researchers believe that many cases of Salvia-induced psychosis have gone undocumented in the United States.

A second case of a 21-year old male with no psychiatric history developed persistent psychosis after Salvia usage.  Another case documented a girl experienced prolonged hallucinations, dissociative, and self-destructive behaviors after using the drug.  It remains clear that for certain individuals, Salvia usage could lead to psychosis.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/19570943
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/17493110
  • Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3122136/

Prescription Drugs

Many prescription drugs are capable of causing psychotic symptoms and triggering a drug-induced psychosis.  Due to the fact that some drugs used to treat psychosis can actually act as a causative agent, it is important for psychiatrists and doctors to monitor patients for counterintuitive adverse reactions; particularly with antipsychotics.


Anticholinergic agents have a tendency to cause psychotic episodes in certain individuals, particularly when ingested at high dosages.  Two common anticholinergic drugs linked to psychosis include: Atropine and Scopolamine.  Atropine has been documented as psychosis-provoking agent since the 1950s when it was found that eye-drops containing the substance lead to a psychotic episode.

Inhalation of Atropine has been found to trigger psychosis.  Fortunately medical professionals that identify anticholinergic-induced psychosis can successfully treat it by administering Physostigmine, which acts as an acetylcholinesterase inhibitor.  By administering an acetylcholinesterase inhibitor, acetylcholine levels increase, which counteracts the effect of the anticholinergic drugs.

Cases of psychosis as a result of transdermal (skin) administration of Scopolamine have been documented since the 1980s.   Among those that experience psychosis from these drugs, symptoms may include: restlessness, excitement, hallucinations, elevated mood, disorientation, stupor, and possibly coma.  Benztropine mesylate is another anticholinergic that has been linked to an episode of psychosis.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/9697003
  • Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2027628/
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/4178795
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/7449475
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/2901077


Many drugs utilized for the treatment of epilepsy (antiepileptics) elicit psychotropic effects via alterations in GABAergic neurotransmission.  In some individuals, these psychotropic effects trigger psychotic episodes.  That said, psychosis is considered an extremely uncommon reaction among those taking therapeutic doses of antiepileptics.

In a 1999 study, it was discovered that 39% of patients taking an antiepileptic drug experienced psychosis as a result of changes in their antiepileptic drug regimen.  This means that dosing alterations and/or switching to a different antiepileptic may trigger psychotic symptoms in susceptible individuals.  Research published in 2012 discussed various factors that may increase likelihood of psychosis among those taking antiepileptics.

They discovered that those taking phenytoin (PHT) or zonisamide (ZNS) were more likely to experience psychosis than other drugs.  Additionally those that experienced complex partial seizures and had a low level of intelligence were more likely to develop psychosis.  This study suggests that individual factors as well as the specific drug(s) taken may determine whether antiepileptics induce psychosis.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/17159095
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/17105456
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/10406999
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/22406094


It is considered relatively rare for an antipsychotic to cause psychosis, but it has been reported – even among those with no preexisting psychotic episodes. Some individuals experience psychosis when they first start taking an antipsychotic, and others experience psychotic episodes upon discontinuation.  This has lead many people to speculate whether taking antipsychotics could make you psychotic.

Ironically antipsychotics are utilized as a first-line treatment option for many types of drug-induced psychosis, especially if the psychosis is a result of excess dopamine.  Those that experience psychosis from an antipsychotic may need to adjust their dosing, switch medications, discontinue treatment, or taper at a more gradual rate (assuming they are attempting withdrawal).

It is known that long-term administration of an antipsychotic agent results in dopamine supersensitivity.  This means that the drug loses effectiveness over time, and makes the brain more susceptible to psychotic symptoms should a person discontinue the medication.

  • Source: http://www.jneurosci.org/content/27/11/2979.full
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/1677263
  • Source: http://psychrights.org/research/digest/nlps/actadrugwith.pdf


Those utilizing corticosteroids like Prednisone may experience psychotic episodes.  While this is thought to occur in under 5% of users, it is still an adverse reaction that should be noted.  Researchers stated that routes of administration and type of steroid utilized was not predictive of psychotic episodes.  That said, some things that were predictive of psychosis among corticosteroid users were low levels of albumin.

It was also speculated that history of psychiatric illness, low levels of complement proteins, and low creatinine may also be influential factors.  In one case of a 48 year old woman using low doses of prednisone (15 mg/day) for 6 days, acute psychosis became apparent.  She experienced insomnia, euphoria, and visual hallucinations.

Her psychotic symptoms subsided upon discontinuation, followed by re-administration of prednisone at smaller increments of dosing (2.5 mg/day).  Other cases of corticosteroid-induced psychosis involved symptoms such as: agitation, speech changes, anger, and paranoia.  When it comes to steroid-induced psychosis, the biggest influential factor seems to be the dose; the lower the dose, the less likely it is to occur.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/12847167
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/16618985
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/19057637
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/21225577

Decarboxylase Inhibitors

Those that have Parkinson’s disease are commonly prescribed L-Dopa to increase low dopamine levels.  While most people tolerate L-Dopa well, some individuals end up experiencing psychosis as a result of the dopaminergic increase.  Research has demonstrated that levels of both serotonin and norepinephrine tend to increase in certain areas of the brain and may contribute to the psychotic episodes.

Those that experience psychosis from L-Dopa (levodopa), Lodosyn (carbidopa), or dopamine agonists may experience a variety of symptoms including: paranoia, agitation, hallucinations (particularly visual), as well as delusions.  Should an individual experience drug-induced psychosis from a decarboxylation inhibitor, a doctor will typically scale back on dosing and/or administer an antipsychotic medication.

Antipsychotics bind to dopamine receptors and prevent excess circulating dopamine from stimulating the receptors.  Various drugs like Seroquel have been administered at low doses with success for treating levodopa-induced psychosis.  Those that take L-Dopa over a long-term may experience increased levels of dopamine in the prefrontal cortex as well as greater amounts of serum corticosterone – two causative factors for psychosis.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/8555378
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/7766285
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/290736
  • Source: http://www.neurology.org/content/54/7/1538.2


Fluoroquinolones are antibiotics that are associated with causing damage to the CNS and in some cases, irreversible psychotic episodes.  In other words, if a person experiences psychosis as a result of treatment with drugs classified as fluoroquinolones, they may never fully recover and achieve normative mental functioning.  Most people treated with fluoroquinolones do not experience psychosis, but it is important to be aware of adverse reactions and the potential for permanent neurological changes as a result of treatment.

  • Ciprofloxacin
  • Enoxacin
  • Gatifloxacin
  • Levofloxacin
  • Moxifloxacin
  • Ofloxacin
  • Pefloxacin
  • Sparfloxacin

There are several case studies of individuals that have experienced psychosis as a result of Ciprofloxacin treatment.  Ciprofloxacin is a drug commonly administered for urinary tract infections and is considered fairly well-tolerated with minimal side effects.  That said, some people experience psychotic reactions (e.g. acute psychosis).  Many of these psychotic reactions resolve organically upon discontinuation of the medication.

A 2006 paper highlighted the fact that Gatifloxacin caused hallucinations in a 19-year old male.  Evidence shows that Gatifloxacin is capable of producing adverse reactions, but they seldom occur (less than 0.1% of individuals).  The mechanism by which various fluoroquinolones may cause psychosis is thought to be by inhibiting the binding of GABA receptors, which leads to CNS excitement.

Of all the fluoroquinolones, the drug most commonly linked to psychotic episodes is that of Ciprofloxacin.  It is though tot inhibit binding of GABA to the GABA receptors, leaving the nervous system in an excitatory state.  Other medications like Levofloxacin have been found to induce acute psychosis in recent years (2008).  Keep in mind that most cases of psychosis from these medications are rare and can be mitigated via medication discontinuation or taking the minimal effective dose.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/16844899
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/7604468
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/11549784
  • Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2745871/
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/18585545
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/10388331

Isotretinoin (Accutane)

This is a drug that was originally marketed as Accutane for the treatment of severe acne.  Some have also utilized it with the intention of preventing skin cancer, although its efficacy for that purpose is relatively unclear.  It is considered a derivative of vitamin A as a retinoid and trace amounts are already present within the body.

While it is unlikely that you’ll experience drug-induced psychosis as a result of Isotretinoin, a few cases have been documented.  It is thought that psychotic episodes may be experienced by individuals taking the drug that have a preexisting mental illness (e.g. major depression).  Cases of “manic psychosis” marked by elevated mood have been reported specifically as a result of Accutane treatment.

The psychosis experienced from Accutane treatment is generally not considered immediate.  In fact, of 5 psychotic episodes resulting from Accutane, they occurred after an average exposure spanning over 7 months.  In nearly all cases, there was a personal or family history of major mental illness.  Cases of Isotretinoin psychosis are commonly treated via discontinuation and low dose antipsychotics.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/15602115/
  • Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4181187/
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/24167696
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/25316943

Synthetic Drugs

MDMA (Ecstasy)

MDMA differs from hallucinogens in that it elevates mood and increases activity within the prefrontal, limbic, and paralimbic regions.  It also deactivates the amygdala (fear center) and thalamus (sensory processing region).  While experiencing psychosis as a result of MDMA usage isn’t the norm, there are case reports of psychotic episodes among individuals with no preexisting psychiatric conditions.

Some researchers believe that the stimulatory effect of MDMA, especially when taken at high doses, may be the cause of psychosis.  In fact, some have gone as far as to classify MDMA-induced psychosis as a subtype of stimulant psychosis.  MDMA differs from most stimulants though in that it elevates serotonin levels in addition to dopamine and norepinephrine.

It may result in serotonergic toxicity and simultaneous overstimulation of dopamine, which contributes to psychosis.  Additionally, MDMA is known to have some hallucinatory properties, which may also contribute to the symptoms experienced. Case reports of ecstasy psychosis have described symptoms of hearing voices, visual hallucinations, tactile hallucinations, bizarre behavior, poor communication, and stereotypic movements.

In one case, it took a patient over 4 months to improve.  Others may experience flashbacks during their psychotic episodes as a result of MDMA.  While reports of MDMA psychosis are few and far between, it is clear that certain people (with no psychiatric illness) can experience psychosis from this drug.

  • Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2728937/
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/11333007
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/1684523
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/11407274
  • Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1669834/

Mephedrone (“Bath Salts”)

This is a synthetic stimulant that is considered both an amphetamine and cathinone.  It is sometimes referred to as “M-CAT” or “White Magic” and is often the active chemical in the drug “Bath Salts.”  It is considered similar to the aforementioned drug Khat and can also be taken in the form of powder or tablets.  Although the most common side effect of taking mephedrone is teeth grinding, adverse reactions of mephedrone-induced psychosis have been documented.

The stimulatory effects of this drug can lead to psychotic symptoms, particularly in regular users.  It is speculated that the dosing, regularity of usage, and individual susceptibility play a role in determining who will experience psychosis from mephedrone.  Symptoms of psychosis among those that use mephedrone regularly include: delusions of both reference, delusions of persecution, delirium

Psychotic symptoms resolved on their own without antipsychotic medication upon hospital discharge.  Mephedrone-induced psychosis is thought to be a blending of a psychotic state produced from both cocaine and MDMA.  While psychosis isn’t common among mephedrone users, those that experience it can be successfully treated with atypical antipsychotics and possibly benzodiazepines (to combat excess stimulation).

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/22232972
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/22791836
  • Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4207243/
  • Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3661324/

Synthetic Cannabinoids

Most synthetic cannabinoids affect the CB1 receptor to a greater extent than THC (found in the plant forms) compared to the CB2 receptor.  The effect of synthetic cannabinoids may be significantly more potent than those resulting from THC.  The spectrum of positive effects for the treatment of certain conditions may become magnified, but so does the potential for detrimental effects.

The intensity of ingesting synthetic cannabinoids has resulted in many medical emergencies, several of which have been individuals experiencing psychosis.  Additionally, since synthetic cannabinoids haven’t been well-researched, it is unknown as to whether using them may increase your risk of developing chronic psychosis or an extended, more severe psychotic episode.

  • Aroma
  • Dream
  • JWH-018
  • Nice Guy (MNG)
  • K2
  • Kronic
  • Relaxinol
  • Spice

An example would be that of JWH-018 (AM-678) which is an analgesic chemical that functions as a full agonist at both the CB1 and CB2 receptors.  Due to the fact that synthetic cannabinoids like JWH-018 are relatively new, they are finally making their way into scientific research.  A study with 15 subjects reported that both anxiety and “psychotic symptoms” were common after it’s usage.

Researchers have stated that synthetic cannabinoids may cause psychosis as a result of their potency, especially among vulnerable individuals.  Anyone that’s at risk for psychosis may be upping their odds by using synthetic cannabinoids.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/21316162
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/25220897
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/25586398
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/23518784


Below is a list of stimulants (both legal and illicit) that are capable of inducing psychosis.


Those that use cocaine over a long-term or take abnormally high doses are extremely susceptible to experiencing drug-induced psychosis.  When psychosis occurs as a result of ingesting cocaine (or any other stimulatory substance), it is referred to under the sub-classification “stimulant-induced psychosis.”  Of all drugs, stimulants tend to elicit the greatest effect on the dopamine system, which leads to psychosis.

In a study looking at 55 individuals that were diagnosed with cocaine dependence, over half of them reported experiencing psychotic symptoms.  It is very common for cocaine to trigger paranoid thinking, particularly paranoid delusions.  Other symptoms that they experienced as a result of cocaine-induced psychosis included: auditory hallucinations, visual hallucinations, and in some cases, tactile hallucinations.

It appears as though men were more likely than women to develop psychosis as a result of using cocaine.   Another delusion that cocaine users may experience during a psychotic break is that of “delusional parasitosis” – characterized by the cocaine user believing that parasites have burrowed underneath their skin.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/1752853
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/22332864


It is known that amphetamine usage can lead to elevations in the neurotransmitter dopamine.  These elevations are responsible for inducing the psychotic symptoms such as hallucinations and delusions.  At lower doses, the likelihood of experiencing drug-induced psychosis from amphetamines is reduced, it still may occur in an individual that has a preexisting dopamine sensitivity or mental illness.

Higher doses of amphetamines are associated with causing psychosis in that the brain cannot efficiently process the high contents of extracellular dopamine.  This wears out the existing receptors and leads to dysfunction.  It is hypothesized that amphetamine-induced psychosis is similar to psychotic episodes associated with schizophrenia in that dopamine and norepinephrine (stimulatory neurotransmission) levels are altered.

Those that experience amphetamine-induced psychosis are most commonly treated with antipsychotics and/or benzodiazepines.  The antipsychotics help reduce the excess dopamine, while the benzodiazepines reverse the stimulatory effects of the amphetamines (e.g. high heart rate).  Examples of amphetamines that could lead to psychosis include: Adderall, Dexedrine, and Vyvanse.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/7033842
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/11687172


Those that take methamphetamines (e.g. crystal meth) may experience a more potent psychosis than those taking amphetamines. While amphetamines are closely related to methamphetamines, they are engineered to be safer for human consumption.  It has been discovered that there are various genes that may increase susceptibility to experiencing methamphetamine-associated psychosis.

Like amphetamine psychosis, those experiencing psychotic breaks as a result of methamphetamine usage are treated with atypical antipsychotics (to reduce dopaminergic effects) and sometimes benzodiazepines (to reduce stimulatory effects).  Methamphetamine has a more potent effect on a person’s physiology due to the fact that its double-methylated and the way it is processed.

Those experiencing meth-induced psychosis may end up with more severe symptoms and a longer-lasting episode of psychosis than those taking amphetamines.  That said, the ability to recover quickly hinges on various factors like: ability to remain abstinent, medical treatment, and genetics.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/25373627


There have been cases of individuals with ADHD taking Ritalin (methylphenidate) that ended up experiencing psychotic symptoms at therapeutic doses.  Although rare, those medicated for attentional deficits have experienced methylphenidate-induced psychosis at therapeutic doses.  Many people clump methylphenidate with the “amphetamines” but technically it is not an amphetamine.

Those that abuse methylphenidate or take the drug with the intention of getting a stimulatory “high” may be more prone to experiencing psychotic symptoms.  This drug increases dopamine levels based on dosage similarly to the aforementioned stimulants and therefore should be used responsibly.  Methylphenidate-induced psychosis will share many commonalities with other stimulants that cause psychosis.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/20571380


This is a plant that individuals chew for stimulatory effects.  Chewing khat is considered a social custom in countries like Africa.  Khat is capable of producing stimulatory effects greater than caffeine, but slightly less than amphetamines.  It contains cathinone (a monoamine alkaloid) that elicits CNS activation, reduces appetite, and can cause mood boosts.

The World Health Organization (WHO) considers khat to be a drug of abuse that can lead to dependence.  Khat is a controlled substance in many countries and outright illicit in others like the United States.  Cases of khat-induced psychosis have occurred, but are considered relatively uncommon.  Those with preexisting psychiatric conditions may be more prone to psychosis as a result of khat chewing.

Cases of psychosis stemming from khat have generally been considered “brief” and “episodic.”  Those that are heavy khat chewers are thought to be more susceptible to psychotic episodes than those who don’t ingest as much cathinone.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/9577014
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/7993291


Experiencing caffeine-induced psychosis is extremely rare, but can happen when caffeine is consumed at abnormally high doses.  Caffeine may induce psychotic symptoms when an individual becomes more susceptible as a result of: sleep deprivation, stimulant usage, and/or a preexisting psychiatric condition like schizophrenia.

A publication from 2009 acknowledged that caffeine’s mechanism of action as a competitive antagonist of adenosine affects dopamine neurotransmission.  This means that if someone has a preexisting psychiatric illness like schizophrenia, it may provoke and/or worsen psychotic episodes due to the increase in dopamine.  Additionally, there are case reports of chronic caffeine users that have reported both delusions and paranoia.

Caffeine is considered the least potent of the stimulants capable of inducing psychotic symptoms.  That said, one 47 year old experienced a psychotic episode lasting 7 weeks as a result of high caffeine consumption.  His psychosis subsided organically upon reduction of caffeine intake without pharmaceutical intervention (e.g. antipsychotics).

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/19407709
  • Source: http://www.ncbi.nlm.nih.gov/pubmed/1751869

Note: There is a specific code (F17.5) in the DSM-V for tobacco-induced psychosis, but it is extremely rare compared to other stimulants.  In fact, it is so uncommon that a scientific journal search for tobacco-related psychosis fails to produce results.

Drug-Induced Psychosis Symptoms

Those that experience drug-induced psychosis often experience classic psychotic symptoms accompanied by additional symptoms related to the substance they ingested.  For example, someone that took amphetamines may experience delusions and hallucinations, but also drug-related symptoms like increased heart rate, perspiration, and psychomotor agitation.

Classic Symptoms of Psychosis

Below are some classic signs of psychosis including: disorganized thinking, delusions, hallucinations, and  catatonia.

  • Bizarre behavior: A typical sign that a person is experiencing a psychotic break is that they begin to behave oddly, particularly for the environment that they’re in. They may dress inappropriately, yell at people, act violent, or appear confused.  To others that are mentally coherent, their behavior will appear amiss.
  • Catatonia: In rare cases a drug may induce a state of catatonia in which the person remains completely still or appears frozen. They may seem expressionless, and seem to be stuck in a state of stupor.  Although this is very uncommon, it is often treated effectively with benzodiazepines.
  • Delusions: Another classic symptom of psychosis is that of delusions. Delusions are beliefs that aren’t based in reality, but the person experiencing psychosis believes they are fully true.  There are various subtypes of delusions including: persecutory delusions (in which a person thinks people are out to get them), delusions of grandeur (in which the person thinks they are a deity), etc.
  • Disorganized thinking: Those that experience psychosis tend to be highly confused and disorganized in their thinking. They may not be able to formulate clear sentences and if you’re talking to them, nothing may make sense.  It’s as if they are blabbering a bunch of confusing nonsense.  They may not be able to concentrate, remember parts of a conversation, and may talk extremely slow or fast.
  • Hallucinations: It is common for those experiencing drug-induced psychosis to have hallucinations, particularly those that are auditory (i.e. hearing voices). These hallucinations are often related to the delusions that the person is experiencing.  Other types of hallucinations that are less common include: visual hallucinations (seeing things that aren’t real) and tactile hallucinations (feeling things on the skin that aren’t real).

Drug-Based Symptoms

Below are some symptoms that a person may experience specifically related to the drug that was ingested.  Keep in mind that these will be subject to both individual variation and drug variation.  Someone experiencing cannabis-induced psychosis is likely to experience completely different secondary (drug-based) symptoms than someone experiencing methamphetamine-induced psychosis.

  • Aggressive behavior
  • Blood pressure changes
  • Body temperature changes
  • Delirium
  • Diarrhea
  • Heart rate changes
  • Nausea
  • Pupil dilation/contraction
  • Psychomotor agitation
  • Rapid breathing
  • Restlessness
  • Sleep deprivation
  • Tremors
  • Vomiting

Drug-Induced Psychosis Treatment

There are several ways to treat and cope with drug-induced psychosis.  The most effective treatment involves seeking professional (medical) help as well as advising from an experienced psychotherapist.  In some cases, all it may take to decrease the psychosis is an adjustment in your medication dose or a slower taper (if you are withdrawing).  In other cases, a doctor may suggest taking a pharmaceutical to counteract the effects of the drug that induced your psychosis.

Abstinence from the causative agent

To properly treat drug-induced psychosis, the individual needs to discontinue using the drug that caused it.  If the person was smoking cannabis heavily, they’ll need to stop ingesting cannabis.  If the person was using cocaine, they’ll need to stop.  Whatever drug that the person was using, abstinence will be required to make a full recovery.

Should an individual continue using the drug, they may experience more severe psychotic symptoms and/or a longer episode of psychosis.  Additionally, it should be recommended to stop consumption of all other drugs (legal or illegal) unless given medical approval to continue usage.  Even a substance seemingly unrelated like alcohol, caffeine, or nicotine may prolong recovery efforts.

Drugs that treat psychotic symptoms

A psychiatrist or medical professional will treat drug-induced psychosis based on the particular case that’s experienced.  It is impossible to assume that everyone’s psychosis has the same root cause.  In most cases, low doses of atypical antipsychotics are administered to counteract excessive dopamine levels and fix the individual’s neurochemistry.

In other cases, no drug will be given and the person will be monitored and instructed to stay sober for a period of several weeks.  Sobriety is the best option for those that don’t have a preexisting mental illness, but if the psychotic episode is severe, an antipsychotic may be preferred.  In the rare scenario that a person is experiencing psychosis from a therapeutic dose of a prescription drug or from withdrawal, different instructions will be given.

Those experiencing psychosis from a standard medical dose of a drug will usually be instructed to lower the dose and/or discontinue.  There have been cases in which a person taking a therapeutic dose experienced psychosis, lowered the dose and never experienced psychosis again at the lower dose.  Withdrawal-induced psychosis is different in that a person may be instructed to take more of the drug to mitigate psychotic symptoms and eventually taper at a slower rate.

Drugs that counteract the psychotic effect of causative agent

Sometimes a professional will look specifically at the mechanisms of the drug that caused the psychotic episode and prescribe a medication that directly counteracts the effects of that particular drug.  This means if you were taking a drug that inhibited the reuptake of dopamine, a psychiatrist may prescribe a receptor antagonist (e.g. an antipsychotic) to block the effects of the extra dopamine.  Since a majority of drug-induced psychosis cases are related to excess dopamine, antipsychotics are popular treatment options.

Medical Supervision / Therapy

It is highly important that a person experiencing drug-induced psychosis get medical help.  There is a slight chance that they may actually be experiencing life-threatening effects of the drug and end up in a state of excited delirium.  Medical supervision will help the individual stabilize if they are running a fever, exhibit changes in heart rhythms (e.g. arrhythmias), high blood pressure, or dehydration.

In addition to medical professionals for stabilization of the psychotic break, the individual will likely benefit from a skilled psychotherapist.  The psychotherapist will help guide them through their symptoms, can help them with cognitive-behavioral changes, and will be able to get a better idea as to whether the patient is dangerous to society or themselves (e.g. suicidal).

How long does drug-induced psychosis last?

Everyone experiencing drug-induced psychosis and their family probably wants to know a definitive timeline of the psychotic episode.  The truth is that there is no clear-cut universal duration for any type of psychosis, including cases that are drug-induced.  Some people will experience a brief psychotic episode lasting for a few hours and return to normal, while others will deal with psychosis for a period of weeks.

10 Days: Over half of all individuals that experience methamphetamine-induced psychosis will make a full recovery within 10 days.  This recovery generally hinges on whether the individual has fully stopped using methamphetamine and/or other drugs.  For most cases of drug-induced psychosis, it can be estimated that at least 50% of people will recover within 7 to 10 days.  Recovery may be expedited if medical treatments are administered, the person remains sober, and takes care of themselves (e.g. sleep, socialization, diet, etc.).

30 Days: If you don’t recover within 10 days from drug-induced psychosis, there’s a good chance that you’ll recover within a month.  Since not everyone seeks out treatment for their drug-induced psychotic episode, recovery may be prolonged.  Eventually the individual figures out that they need to discontinue the causative drug and function sober for awhile so that they can snap back to reality.  It is estimated that nearly 3/4 people will recover from drug-induced psychosis within a month.

Over 1 Month: For approximately 1/5 individuals, it may take longer than a month to recover from drug-induced psychosis.  Keep in mind that these prolonged recoveries are generally a result of the individual using drugs and/or substances that may impede their recovery.  Additionally those that don’t seek out psychiatric, medical, or therapeutic help may experience delayed recoveries.

Furthermore it should be considered that those taking over 4 weeks to recover from their drug-induced psychosis may have experienced it before and/or be genetically susceptible to a mental illness like schizophrenia.  You should probably be concerned if some symptoms haven’t dissipated, lessened in severity, or improved after a month.

Long-term / Lifetime: It can be scary to think that some people may never recover from a drug-induced psychotic episode and may now have to deal with psychosis for the rest of their lives.  This generally happens in those with a preexisting mental illness or unfavorable genetics.  Additionally those that never recover from a drug-induced psychotic episode tend to be individuals that have experienced drug-induced psychosis before – yet continued using.

Chronic long-term usage can result in an array of physiological, psychological, and chemical changes within the brain and nervous system.  While in certain conditions, it is possible for someone to never recover from drug-induced psychosis after experiencing it just once, this is an exception.  Think of those that never recover as going through a series of “temporary threshold shifts” for the brain.

They experience one episode, come back to reality and are able to function.  Then they use the drug again and experience another, more severe episode.  They return to reality and are able to function once again.  However a couple more psychotic episodes and there’s no coming back – the neural alterations are irreversible and the person has literally jumped off the proverbial cliff.  Now they must treat their psychosis with psychiatric medication for life.

Have you ever experienced drug-induced psychosis?

If you’ve experienced drug-induced psychosis, feel free to share your experience in the comments section below.  Discuss what drug you ingested that caused your psychotic symptoms as well as the dosing (standard vs. high).  You also may want to mention whether you have a preexisting psychiatric condition, were sleep deprived, highly stressed, etc.  To help others get a better understanding of your situation, you may want to tell how long it took to overcome the psychosis and how you mitigated the psychotic symptoms.

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{ 5 comments… add one }
  • Savannah June 14, 2015, 5:48 am

    I have experienced two meth-induced psychoses that were several months apart. The first one completely took me by surprise and snuck up on me, starting in reality but quickly turning into bizarre behavior. My husband was also using and he would often hide drugs around the house. He also lied about his usage. I found myself “searching” for things he may have hidden and within about 2 hours I locked myself in the bathroom with all of our jeans cutting the holes out of all of the pockets thinking he had sewn drugs in them.

    He then tried to confront me but I had the door locked. When he convinced me to open the door, he saw I had all of our clothes out of the closet and they surrounded me along with all of the drawers and cabinets torn apart looking for what he may have hidden. I swore up and down he was deliberately lying to me and I wouldn’t let him near me. The more he said I was crazy and that he didn’t hide anything, the more I was convinced I was right and he was out to get me. Luckily after several minutes he was able to “talk me down” I still had doubts but was calm.

    I have a prescription for Xanax so he gave me two and sat with me until I was able to sleep. He almost hauled me away that night and I really did think he was “the enemy”. I didn’t know how to explain what happened to me and I didn’t realize how severe it was until it happened again at the end of February. I had abstained from stimulants after the first episode because it scared me but I didn’t know just how likely it was to happen again. This next time it happened after only using for two days whereas the first time I had not slept for 3 or so days and had been using consistently for about 4 months.

    This next break took my paranoia and delusions to a whole other level. Slowly but surely I became doubtful of my husband’s honesty and again started searching for hidden drugs. I actually was convinced that he was dealing and hiding large quantities. I thought he hid them in the walls, ceilings and cabinets throughout the house. I also started thinking that people were coming into our apartment and painting the walls after making holes in them in order to hide the drugs. The craziest of my thoughts was that they had lowered the ceilings in the kitchen and were storing things in the plenum of the ceiling.

    Not only did this thought of people renovating my apartment exist inside of our place but I also started thinking that people were painting the outside of the apartments and then lying to me about it. I was much calmer during this episode and it actually felt more “real” than the first one. I took pictures as proof and documented what I saw. Oddly enough, this very specific behavior didn’t extend to anyone else or outside of the apartment. My husband tried to convince me that I might as well be “cutting out the pockets in our jeans” but I didn’t see the correlation.

    I was completely delusional and detached from reality. I eventually went to sleep, again after Xanax but when I woke up, I was still delusional. I was able to work and my husband convinced me not to talk about what I thought was going on to anyone and I stuck to our agreement, except in one instance. I needed to know if the landlord was coming in and painting our apartment while I was at work so I texted him and asked. He is also a doctor! Luckily I did it in such a way that if he said he was not painting, I did not look like a weirdo for asking.

    These delusions lasted severely for about 5 days, they subsided almost completely within 10. However, I must say that the lasting effects are more due to my shock that I could create such a delusion and believe it absolutely when looking back I see how totally irrational it was. What exacerbated these episodes though, is that there was a time when my husband hid things from me, and he did, in fact lie to me about his usage. All of these “reality based” ideas fed into my delusion and gave fuel to the fire.

    It made them all the more believable. I am very grateful not to have touched meth since that second break which occurred end of February into March. March 1 was the last time I did it. Those two experiences combined to scare me straight. I have done extensive reading and research on what happened to me and I know if I ever touch it again, that could be the end of me. Literally my husband almost institutionalized me, twice. We have worked through a lot of the things that contributed to my break and he has since apologized profusely for ever lying to me.

    He has quite meth too. I know I probably still would benefit from seeing a therapist of some kind. It feels good to tell my story as this is something so far out from most people’s experiences that people wouldn’t know what to say. And, with the stigma of meth use, I can’t really think of anyone I could share this with and not be judged in some way or looked at like a freak. I hope this helps someone who is in the throes of an addiction or who has had a drug-induced psychosis.

  • sam December 14, 2015, 12:25 pm

    I am currently on the brink of a psychotic episode, at the point where I know it’s coming and am well aware of the signs, yet am pretty much powerless to stop it, medication only working periodically for me. My use of most substances has left me with lifelong drug-induced psychosis in the form of seeing demons and ghostly figures, unbalanced thoughts, and paranoia. The last paragraph in this article really rang true with me and to be honest I didn’t really believe my therapists when they told me a drug induced psychosis could be life-long.

    If anybody reads this that feels they may be experiencing their first episode brought about through drug use, or just feel different in their thought process after using, give it a break, your mental welfare is most certainly not worth reusing for. Regards, Sam

  • Debs January 12, 2016, 11:22 am

    I am a long term survivor of fluoroquinolone poisoning otherwise known as fluoroquinolone toxicity. I originally developed acute toxic psychosis from Ciprofloxacin. within hours Just to inform you that ALL fluoroquinolone antibiotics & every mode of administration of these including the ear & eye drops is capable of inducing this. Mine was treated with psychotropic drugs which I then had an ADR to as so many do which was then mistaken & misdiagnosed as what is labelled ‘bipolar disorder.’

    I subsequently lost years of my life because of this misdiagnosis I have not to date & will never again touch another psychotropic drug. After being in the world of fluoroquinolone toxicity for a very long time, I would just like to say that the acute toxic psychosis & various other neuropsychiatric symptoms triggered by fluoroquinolone antibiotics is, on the whole, recoverable from.

  • Amber April 8, 2016, 2:46 am

    Monday started taking Vyvanse, was up until Thurs doing that, then added meth to the mix. Still awake Friday night, after a script of 30 70mg Vyvanse and a little over a gram of meth, my friend and I took a couple hits of LSD. An hour later we both were on a new planet in another Galaxy. She was in one room and I in another.

    I became paranoid and mean as hell to people, so I went to my room. A friend cams to check on me and I thought they were some spy who was trying to make me crazy and kill me. This continued for about 9 hrs. I don’t remember much of it. My friend was having close to the same situation in another room. The following day I was still completely delusional, had hidden hundreds of dollars from “them” and don’t remember to this day where I hid it.

    I have memory loss from that night as does my friend. Couldn’t remember my kids names, how to use bathroom..it was scary. Long story short… 5 days no sleep with amphetamine/meth/LSD/and tequila make for a 16-20 hour nightmare!! I’m still paranoid and have visual/auditory hallucinations after a month.

  • Jennifer Von Canon October 1, 2016, 11:59 pm

    Wellbutrin (accidental double dose 10 days psychosis and hospitalization).

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