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. Author manuscript; available in PMC: 2022 Mar 29.
Published in final edited form as: Child Adolesc Psychiatr Clin N Am. 2019 Sep 23;29(1):131–143. doi: 10.1016/j.chc.2019.08.006

Substance-Induced Psychosis in Youth

David Beckmann 1, Kelsey Leigh Lowman 2, Jessica Nargiso 3, James McKowen 4, Lisa Watt 5, Amy M Yule 6
PMCID: PMC8961695  NIHMSID: NIHMS1788978  PMID: 31708042

Introduction

Kevin is a 16-year-old male who recently finished the 11th grade of high school. He has attention deficit hyperactivity disorder (ADHD) which has been effectively treated by his pediatrician since the age of 7. Over the past 3 years he has taken mixed amphetamine salts extended release 25 mg in the morning and an additional 7.5mg of immediate release after school. He has no other psychiatric history; neither his parents nor his pediatrician have ever been concerned about symptoms of a mood, anxiety, psychotic, or substance use disorder. He has no medical problems and does not take other medications.

One evening in July Kevin was brought to the emergency room by his parents for increasing concern about his behavior. Although he spent the first part of the summer with friends, he became increasingly withdrawn and isolated, and his parents believed he may be using cannabis after smelling this a few times. They also found his phone in a plastic bag in the refrigerator, and when they asked him about this, he replied, “It’s just safer that way.” On the night of presentation, his father had broken into Kevin’s room; Kevin had locked himself in and could be heard repeatedly yelling, “Leave me alone!”

In the emergency room, Kevin told staff that he was afraid of “shadow government agents.” He described that they had been observing him through electronic devices for several weeks, and this evening he had seen shadowy figures in his home out of the corner of his eye. He was also able to hear them speaking to one another, and although he could not make out specific words, he felt certain they were conspiring to capture or kill him.

His medical workup was unremarkable except for a urine toxicology screen, which was positive for amphetamines and cannabinoids. He reported he had been smoking cannabis most days over the summer. He also reported that over the summer he was not taking the mixed amphetamine extended release since he often woke up late in the day. Instead he took the immediate release medication and would occasionally take three to four times the prescribed dose when he was tired. He denied other substance use. The emergency room staff recommended voluntary hospitalization which he and his parents declined. He was discharged to home with a plan to follow up in your clinic three days later. He was instructed to not use cannabis and to not take medication for his ADHD until he was evaluated further.

This case is not an uncommon scenario for child and adolescent psychiatrists. The following article will review substance induced psychosis (SIP) including the definition, epidemiology, causes, treatment, and prognosis.

Definitions and epidemiology

Clinicians face a key diagnostic challenge in the differentiation between SIP and a primary psychotic disorder (PPD). SIP is defined in the DSM-5 by the presence of delusions and/or hallucinations that arise and persist in the context of acute intoxication or withdrawal from a substance and are not exclusively attributable to delirium.1 A diagnosis of SIP also requires a lack of insight into one’s symptoms and remission of symptoms within one month of sustained abstinence, although some studies suggest that psychosis can persist long after abstinence. Dawe et al. (2011) interviewed 98 patients with a diagnosis of SIP (n=47; 48%) or PPD (n=51; 52%) within the first two days of admission to an acute psychiatric unit, with intermittent follow-up until discharge or day 51 of admission. Although patients with SIP demonstrated similar positive symptom severity and more severely disturbed behavior at admission compared to patients with PPD, they also exhibited more rapid abatement in both symptom categories.2 However, Mauri et al. (2017) found conflicting results in a follow-up study of 48 patients who initially presented to an inpatient psychiatric unit with SIP (n=23; 48%) versus patients with PPD and concurrent substance misuse (n=25; average of 4.96 years between baseline and follow-up).3 Their results suggested that following cessation of substance misuse, patients initially diagnosed with SIP did not experience more rapid symptom remission compared to patients with a PPD and concomitant substance use. In fact, patients with SIP demonstrated significantly less improvement of hallucinations from baseline to follow-up when compared to patients with PPD.

Although epidemiological research is scarce, one study estimates the incidence of SIP to be approximately 6.5 in 100,000 persons per year, compared to 9.7 with PPD and comorbid substance misuse, and 24.1 with PPD alone.4 Among patients presenting to intervention services for first episode psychosis (FEP), the proportion diagnosed with SIP as opposed to PPD or affective psychosis ranges between 6%5 and 10%.6 However, in studies examining an FEP cohort with past-month substance use, the prevalence of SIP increased dramatically, ranging from 44%7 to 56%.8 Although patients with SIP use substances at higher rates than patients with PPD,6,7 substance use is still pervasive among patients with PPD, with reported rates varying from 35% to 61%.6,8

Substance-specific considerations

Many substances, whether prescribed medically or used recreationally, are known to cause, exacerbate, or increase the likelihood of psychosis. Commonly used substances and substances associated with a high risk for psychosis are summarized below.

Cannabinoids

In 2017, 12.4% of youth ages 12–17 used cannabis at least once that year, and for youth ages 18–25 this number increased to 35%.9 There is a growing body of literature supporting a strong link between the use of cannabis and psychosis.10–12 There also appears to be a strong dose-response effect11 with daily use and the use of high-potency delta-9-tetrahydrocannabinol (THC) carrying the largest risk of psychosis.10,11 THC potency in marijuana plants has increased dramatically over past 20–30 years. Specifically, the average potency of seized marijuana plants by the drug enforcement agency was 4% in 1995 and increased to 12% in 2014.13 In addition to the potency of marijuana plants continuing to rise, other products with even higher potency that are made by various processes of chemical extraction are now available. Examples of products with high levels of THC, often referred to as “concentrates,” include hash oil, wax, and edibles. In the state of Washington where cannabis is legal, high potency products including marijuana plants with at least 20% THC content and concentrates with at least 60% THC content make up the largest share of the cannabis market.14 In one large study, individuals using high-potency cannabis (THC >10%) daily had a more than 4-fold risk of being diagnosed with a psychotic disorder compared to persons who do not use cannabis. Switching to cannabis with a lower THC content decreased this risk in half, even for people who continued to use cannabis daily.10 This study provided the first direct evidence that cannabis use increased the incidence of psychotic disorders, suggesting that high potency cannabis is responsible for the onset of first episode psychosis in a portion of individuals.10

Stimulants

Psychostimulants (often simply called stimulants) are commonly prescribed to treat ADHD, and are commonly misused by youth (i.e. taken at higher doses than prescribed, using stimulants that were prescribed to someone else, or crushing and insufflating these medications). In 2017, 1.8% of youth aged 12–17 misused prescription stimulants, as did 7.5% of youth aged 18–25.9 Each type of stimulant (a class which also includes cocaine and methamphetamines) has a unique profile with regards to the risk of psychosis, and in general, there is a dose-response with symptoms of psychosis.

Amphetamines -

Use of amphetamines can result in acute psychosis. Otherwise healthy individuals in lab settings begin to experience symptoms of psychosis in doses between 100 – 300 mgs.15 SIP has been described in youth with ADHD being prescribed amphetamines, although this is rare when taken at prescribed doses.16 Studies have found that between 8% and 46% of persons who regularly misuse amphetamines experience SIP, and binge pattern of use may increase the likelihood of psychosis. The clinical presentation of amphetamine-induced psychosis is similar to schizophrenia spectrum illnesses, and can include disorganized thoughts, impaired concentration, delusional beliefs (often persecutory in nature), hallucinations, and hyperactivity.15

Methylphenidates –

Rare cases of psychosis from the use of methylphenidates have been described,17 with higher doses (>120mg) likely carrying a higher risk. However, when the risk for SIP-associated prescription stimulant use was examined using a dataset derived from two U.S. commercial insurance claims, methylphenidates were associated with a lower risk for SIP compared with amphetamines, although a causal relationship cannot be concluded.18 Nevertheless, given their equal efficacy on average for the treatment of ADHD, there may be benefit in using methylphenidate products as first-line agents in treating youth with this condition.

Cocaine -

Transitory paranoia resulting from acute effects of cocaine use are one of the most common effects of use, occurring in about 90% of cases.19 Common clinical characteristics of paranoia resulting from cocaine use including suspiciousness, distrust, compulsive behaviors, dysphoria, as well as aggressiveness and agitation. The majority of psychotic symptoms related to cocaine use remit within 24–28 hours.

Methamphetamines –

Transient psychosis is one of the best documented effects of heavy methamphetamine use. According to one study, methamphetamine-associated psychosis is experienced in about 23% of individuals who use methamphetamines.20 Common clinical characteristics of methamphetamine-associated psychosis include persecutory delusions, auditory and visual hallucinations, hostility, anxiety, depression, cognitive disorganization, and hyperactivity.21 There is inconsistent evidence whether negative symptoms of psychosis are associated with this phenomenon.21 As with other substances, the risk of psychosis appears higher with increased drug potency and frequency of use.

Hallucinogens

Hallucinogens describes a diverse group of both naturally occurring substances (such as psilocybin and mescaline) as well as synthetic lysergic acid diethylamide (LSD) and LSD-like substances. As hallucinations are the intended toxidrome, these substances cause some psychosis by definition, but symptoms might persist beyond the initial period of intoxication.

Hallucinogen Persisting Perception Disorder is characterized by spontaneous reoccurrence of perceptual disturbances, most commonly visual, that are similar to the individual’s experience during acute intoxication. For people who use hallucinogens the reported prevalence of flashbacks (re-experiencing of perceptual disturbances) ranges from 5% to 50% with a smaller subset meeting criteria hallucinogen persisting perception disorder.22 Two different clinical syndromes for this disorder have been identified: Type 1 usually reflects a short-term, reversible, benign course where the individual experiences one or more perceptual symptoms, usually spontaneous visual images. Individuals experiencing Type 1 generally do not experience significant impairment or distress from these experiences (and may even find the experience pleasurable), so psychiatric care is rarely sought. Hallucinogen persisting perception disorder Type 2 typically reflects a more chronic, severe syndrome.23 Individuals with Type 2 re-experience one or more perceptual symptoms causing significant distress or functional impairment.

Symptoms related to hallucinogen persisting perception disorder usually include afterimages, halos, trails, or visual snows, without affecting other modalities (e.g., auditory hallucinations). Prodromal symptoms are more often reported in cases of Type 2. Type 1 episodes tend to occur less frequently, with shorter duration or intensity, following onset. In Type 2, the frequency, duration, and intensity can increase over time,23 and it has been suggested that this may convert into persistent psychotic illness. The majority of individuals experiencing hallucinogen persisting perception disorder do not report delusional beliefs related to perceptual disturbances, suggesting involvement of the primary visual cortex, and potentially distinguishing it from a schizophrenia spectrum disorder. A systematic review found very few well-designed studies examining hallucinogen persisting perception disorder,22 making it difficult to summarize effective approaches for managing this condition.

Nicotine

Individuals who use cigarettes during adolescence have an increased risk for subsequent psychotic experiences. Daily tobacco use has been associated with an increased risk of psychosis and an earlier age at onset of psychotic illness.24 Patients with FEP tend to have smoked for years prior to the onset of psychosis, have high prevalence of tobacco use at the time of treatment, and are more likely to smoke than age-matched controls.25 Genetics may influence this association, as genes associated with psychosis have been shown to overlap with those for cigarette smoking.26

Research Chemicals and “Club Drugs”

Research chemicals, also known as New Psychoactive Substances, include synthetic cannabinoids (Spice, K2), synthetic cathinones (bath salts, flakka, methylone), psychedelics such as tryptamines (DMT, 5-MeO-DMT) and phenethylamines (MDMA, Ecstasy, Molly). Research on New Psychoactive Substances is limited. The prevalence and even exact composition of these substances are rapidly changing as suppliers work to create new chemical variations to circumvent laws implemented to prevent their use. One case series describing psychosis associated with acute recreational drug toxicity found synthetic cannabinoids and tryptamines to be the most frequently involved substance.27 Reviews on psychosis and synthetic cannabinoids suggested that these have stronger physiological and psychological effects than THC and may either exacerbate previously stable psychotic symptoms or trigger new-onset psychosis.28 Prolonged psychosis and the potential for violence have been reported with synthetic cathinones.29 A case-control study also supported an association between ecstasy use, psychosis, aggression, and violent behaviors.30

Kratom

Kratom is a psychoactive plant preparation used medicinally for its stimulant effects, and as an opioid substitute.31 Case reports have associated kratom exposure with psychosis, seizures, and death.32 A study involving calls to U.S. poison centers for kratom exposure over a five-year period found close to 50% of callers reported moderate to severe adverse outcomes. Forty percent of callers described non-life-threatening outcomes but required treatment, and another 7% had life-threatening outcomes with some residual disability.33 Adverse effects from chronic use of kratom include sleep and eating disorders, psychosis, and addiction;31 the risk of psychosis appears to be much greater than in other opioids. While the FDA has labeled kratom an opioid since it has activity at the opioid receptor and warned of its risk, kratom is currently not regulated at the federal level. The absence of federal regulation has raised concerns that exposure to kratom may increase amidst the current opioid crisis.

Commonly prescribed medications

Steroids are commonly prescribed to reduce inflammation and immune activation in various diseases. This class of medications is known to have major systemic side effects including fractures, infections, gastrointestinal bleeds, and cataracts.34 Sometimes less appreciated are the neuropsychiatric side effects which include affective, behavioral, and cognitive changes. These changes are often characterized as “steroid psychosis,” regardless of whether the patient truly experiences psychosis.35 Symptoms tend to be mild and reversible and may include emotional lability, hypomania, mania, depression, psychosis, delirium, and confusion. Specifically, psychotic symptoms of hallucinations, delusions, and paranoid ideation have been documented.35

Antibiotics such as fluoroquinolones can also be associated with a variety of psychiatric and neurological problems including psychosis, as highlighted in a recent black box warning from the FDA. Specifically, psychotic symptoms of auditory and visual hallucinations as well as delusions have been documented.36

Differentiating SIP from PPD

Recent studies have strengthened the argument that at least some forms of SIP in adolescents and young adults, such as psychosis due to daily use of high-potency cannabis, can convert to a PPD that otherwise would not have developed.10 Nevertheless, the relationship between substance use and psychosis is complex, and how much of the correlation is causal remains controversial. Individuals predisposed to developing PPD might also have a predisposition to using substances and/or substance use may accelerate the course of an underlying psychotic disorder.

There is no single feature that differentiates SIP from PPD in a young patient using substances, and it is often only the presence or absence of psychotic symptoms during prolonged periods of abstinence—if this can be achieved—that will definitively determine the need for ongoing treatment of psychosis. That said, there are some clinical features that may point to one etiology over another. SIP often features a later age of onset,6,7 increased insight into symptoms of psychosis,7 fewer or less severe negative symptoms,2,7 and a weaker family history of psychosis compared to patients with a PPD.8 Other characteristics of psychosis that have been examined to help differentiate SIP from PDD have demonstrated inconsistent findings. For example, the majority of evidence suggests that patients with SIP experience more positive symptoms,4,7,37 but others have demonstrated that positive symptom severity is similar between SIP and PPD.2,6

Assessing for Substance Use Disorders

As outlined above, the prevalence of heavy substance use is high in adolescents with psychosis, whether the psychosis is primary or substance-induced. Although the focus of this chapter is on the psychosis, it is important to evaluate and treat any comorbid substance use disorder (SUD).

The description and classification of SUD changed substantially with the publication of the DSM-5. In place of the prior discrete categories of “abuse” and “dependence, SUD is now classified by severity. Each SUD (alcohol use disorder, cannabis use disorder, etc.) has eleven criteria, which differ little between different types of substances. If a patient meets 2 or 3 criteria the SUD is classified as “mild,” 4 or 5 is classified as “moderate,” and the presence of 6 or more criteria is classified as “severe.” The eleven criteria are useful both in initially determining, and then following, the severity of illness in patients.

Despite the recognized importance of screening for and evaluating youth for SUD, there are few standards for how to do so in psychiatric settings. The most widely validated screening tool for adolescent SUD is the CRAFFT,38 and although most of this evidence comes from primary care settings, the tool has been shown to have validity for screening in psychiatric patient populations.39 There are several newer screeners that have promise as easier-to-use alternatives and are available for free from the National Institute on Drug Abuse. In particular, Screening to Brief Intervention (S2BI); Brief Screener for Tobacco, Alcohol, and Other Drugs (BSTAD) for adolescents; and the Tobacco, Alcohol, Prescription medication, and other Substance use (TAPS) tool for young adults.

Patients who screen positive for at-risk substance use should be further evaluated for a SUD—which assesses how the substance is affecting the patient’s functioning—for each substance they are using since polysubstance use is common in youth. Insight into SUD severity is often low, so collateral information from family and toxicology screening can be useful.

After his initial presentation to the emergency room, Kevin stopped smoking cannabis because he was worried about his symptoms and concerned that cannabis may be playing a role. His parents safely secured his medication for ADHD and stopped giving it to him. By the time you see him three days later, he is feeling a bit better. He seems to have improved insight into some of his symptoms, and no longer believes that there are intruders in his home. He has continued to largely isolate in his room, however, and while he has been using his phone and computer, he acknowledges avoiding certain sites because he “can’t shake the feeling” that he, specifically, is being monitored in a nefarious way. His parents are very concerned about his prognosis, and you explain the ambiguity. Cannabis almost certainly contributed and abstinence from cannabis use will be important. His misuse of stimulants may have also played a role. You recommend treatment with a non-stimulant medication, atomoxetine, and start that medication now, since it takes a longer time to take effect and the new school year is a month away. You explain that these changes may be enough for all of his symptoms to resolve—or they may not.

You also assess his substance use further and determine Kevin meets criteria for cannabis use disorder, moderate. You refer him to a colleague for SUD therapy and find a local resource that provides both group therapy and parent guidance for guardians of youth with SUD. Kevin declines to engage in these services, as he feels sufficiently motivated to stop using cannabis.

You continue to meet with him at short intervals for the rest of the summer to assess his symptoms of psychosis and his response to atomoxetine. Kevin appears to be doing well and by the beginning of his senior year he is feeling healthy and confident. He denies symptoms of psychosis as well as cannabis use, which is corroborated by urine toxicology screens that are negative for THC.

Management

Pharmacotherapy

If a young person is prescribed a medication that may have contributed to SIP then this medication should be stopped. If continued pharmacotherapy is needed to treat an ongoing psychiatric or medical condition an alternative medication should be prescribed if possible. If a young person with SIP has a co-occurring SUD, medication to treat the SUD should be discussed with the patient and family. There are several FDA -approved medications for adults with alcohol, nicotine, and opioid use disorders. Although there is limited research on the use of these medications in adolescents, there have been randomized controlled trials with positive findings for nicotine use disorder, as well as adolescents ages 16 years and older with an opioid use disorder.40

Antipsychotic medication is indicated for individuals with symptoms of psychosis that persist when they are not acutely intoxicated or withdrawing from substances, or individuals who are not able to establish periods of abstinence. To our knowledge, no clinical trials have been conducted in individuals with SIP, and the literature is limited on medication treatment for individuals with schizophrenia and a co-occurring SUD. Some small studies have suggested treatment with atypical antipsychotic medications, including clozapine, is associated with decreased substance use.41 When prescribing antipsychotic medications to individuals with SIP who also smoke tobacco regularly clinicians should remember that smoking tobacco increases CYP1A2 enzyme activity which leads to increased metabolism and lower levels of clozapine, olanzapine, haloperidol, and fluphenazine.42 CYP1A2 activity is impacted by the products of tobacco smoke and not nicotine; therefore, if an individual begins nicotine replacement therapy and/or begins exclusively using an electronic cigarette, the dose of their medication will need to be decreased accordingly.

Psychosocial interventions

Different approaches have been developed for the treatment of patients with a SUD and a psychotic disorder. One approach is referred to as “parallel treatment,” and involves simultaneous treatment for both disorders, but by different agencies or providers with expertise in their specific area. An alternative approach is “sequential treatment,” where a patient receives either psychosis or substance-use focused treatment first, in isolation, based on the idea that resolving one problem allows the other to be more effectively treated. Kavanagh and Mauser (2011) highlight concerns about two approaches given the risk of poor communication between providers, additional burden on the patient to see two clinicians or extend the time in care, and most significantly, may ignore the nuances of how substance use impacts psychosis and visa-versa.43 Integrated care in which both disorders are addressed simultaneously by the same clinician has thus been identified as the gold standard for the treatment of SUD and comorbid psychiatric illness.

Regarding psychosis in the presence substance use specifically, most studies on integrated psychosocial treatment have been conducted with (older) adults with schizophrenia and co-morbid SUD.44,45 Few studies have examined individuals identified as having SIP, and most studies with PPD and co-morbid SUD do not distinguish between substances of use. Nevertheless, integrated motivational interviewing and cognitive behavioral therapy (MI-CBT), which combines MI techniques for addressing substance misuse and CBT for SUD and psychosis, is one intervention that has been associated with a reduction in substance use in persons with a co-occurring psychotic disorder and SUD when compared to treatment as usual.46 MI fosters a non-confrontational, patient-centered, approach inherently necessary when working with those with SUD. Exploring ambivalence about substance use, the pros and cons of a substance, how use impacts an individual’s life goals (job, college, relationships), and potential long-term risks of use is key to exploring drivers of behavior. CBT for psychosis provides a theoretical model accessible for patients explaining distal and proximal triggers to their psychotic thinking patterns (e.g. how to understand the links between thoughts-feelings-behaviors as they underpin, and potentially perpetuate, hallucinations and delusions. CBT for psychosis and SUD aims to teach skills in managing stress, unhelpful and unrealistic thinking patterns and behaviors, and challenge cognitions that may support ongoing substance use, such as, “Marijuana is the only thing that calms my thoughts.”

Other evidence-based treatments in addressing youth substance use such as the Adolescent Community Reinforcement Approach47 can complement MI-CBT by enhancing motivation to engage in competing activities that do not involve substance use, improve communication and problem-solving, and increase parental bonds. Indeed, involvement of parents is critical in working with youth both for keeping youth engaged in care, but also to enhance treatment gains by providing families with psychoeducation about addiction, psychosis, medication management, and recovery. Emerging data indicates that family-based treatments show promise for improving substance use in persons experiencing psychosis. Mueser et al. (2009) developed a Family Intervention for Dual Diagnosis which included family psychoeducation, communication and problem-solving skills training, and stress management with improvements in both substance use and psychosis.48

Effective integrated treatment programs for adults with schizophrenia and SUD highlight the importance of social support.45 Leveraging pro-social connections may also be of benefit for youth with SIP and SUD. Identifying a relationship with an adult trusted by the adolescent such as a teacher, coach, or work supervisor might be helpful in monitoring the youth’s symptoms, substance use, and functioning. Sometimes having multiple community members identified as “part of the team” can be helpful, but alliance with the youth is likely best preserved if he or she feels involved in the selection of a limited number of adults.

Prognosis

SIP is associated with the development of severe mental illness. Larger registry studies have found 24% to 32% of patients with a diagnosis of SIP subsequently developed a schizophrenia spectrum disorder or bipolar disorder.12

Overall prognosis may be affected by the specific substance causing psychosis. Amphetamine- and other stimulant-induced psychosis tends to resolve within days, although some research suggests psychotic symptoms may persist for years.15 Starzer et al. (2017) found that 32.3% of individuals diagnosed with SIP related to amphetamine use were later diagnosed with either schizophrenia or bipolar disorder. The conversion rate for individuals’ experiencing SIP related to hallucinogen use to PPD was lower, at 24%.12 Cannabis-induced psychosis is associated with the highest risk for severe mental illness with about 46% of patients subsequently developing schizophrenia.12

Several registry studies have found patients converted from SIP to a serious mental illness within two to three years. Of relevance to clinicians working with young people, patients ages 16 to 25 years have been found to be at highest risk of converting from SIP to schizophrenia.12

Kevin returns to your office in the early fall and is very upset to have failed the first quiz of the year. You assess further and learn that he missed some classes because he believes that a government organization has infiltrated his school in an to attempt to monitor and target him. When comparing this to his recent period without these beliefs, he reluctantly admits that he never stopped worrying about being monitored by the agency but did not want to admit this to you. He is also hesitant to provide a urine sample for toxicology testing, and when he does, acknowledges, “It’s going to show weed. Wouldn’t you smoke, too, if they were after you?” He does not appear depressed but demoralized from his situation.

In discussions with Kevin and his parents, everyone agrees to a trial of an antipsychotic medication to reduce his symptoms and optimize his functioning. His parents wonder if this means he has schizophrenia, or if he will have to be on medications for the rest of his life. You explain that it remains too early to know. It is unclear how much cannabis may still be contributing to his symptoms. Depending on his response to treatment and the amount of cannabis he continues to use, it is reasonable to try without medication in the future.

In the meantime, you offer to continue to see Kevin regularly to try to minimize symptoms of psychosis and continue to address his substance use using MI. His parents agree to engage in parent guidance at the nearby adolescent SUD clinic to learn more about SUD and psychosis, as well as ways they can support Kevin’s engagement in treatment. After a few more meetings with you and encouragement from his parents, Kevin agrees to attend individual and group sessions at the adolescent SUD clinic, as well.

Summary and conclusions

Cases like Kevin’s are not uncommon when working with youth. This complex presentation illustrates several of the ambiguities of these symptoms that cross diagnostic categories. Psychosis may be substance-induced, or substance use may co-occur with PPD. Looking for patterns in symptoms, and how they do or do not track with substance use, might be helpful, as may looking at clues such as family history, age of onset, and prominence of negative symptoms—although none of these variables, alone or together, can conclusively differentiate the etiology of psychosis. Removing agents that are likely to contribute to psychosis, such as cannabis, stimulants, and hallucinogens is important, but this can be clinically difficult, and in some cases symptoms might persist for months.

A comprehensive approach is the best management for SIP, ideally including 1) medication management, 2) psychosocial treatment (individual and/or group therapy), and 3) engagement of family (and possibly other important social connections). This combination of highly specific treatment can be difficult to find even in relatively resource-rich locations. Except in cases where all symptoms of psychosis clearly resolve in the absence of the offending agent, treating psychosis and SUD simultaneously is more effective than trying to address these challenges sequentially.

Finally, these suggestions for clinical management are based on limited evidence, and further study of both pharmacologic and psychological interventions is needed to better understand how to provide the best care to vulnerable youth experiencing both symptoms of psychosis and substance use.

Synopsis.

Youth experiencing psychosis also frequently misuse substances, making it clinically challenging to differentiate substance-induced psychosis (SIP) from a primary psychotic disorder (PPD), which has important implications for management and prognosis. This paper presents practical considerations related to differentiating SIP from PPD including information on substances associated with symptoms of psychosis. Recommendations for management of SIP will also be reviewed, including screening for and treating comorbid substance use disorder(s) and using evidence-based medication and psychosocial interventions.

Key Points.

  • Substance-induced psychosis (SIP) is typically defined as hallucinations and/or delusions caused by intoxication or withdrawal from a substance and occurs in approximately 6.5 in 100,000 persons per year.

  • Because primary psychotic disorders (PPD) and substance use disorders (SUD) are so frequently comorbid, SIP can be difficult to differentiate from PPD, although there can be some differences in the clinical presentation.

  • Substances that are of particular clinical interest due to their risk of inducing psychosis are reviewed individually, including hallucinogens, cannabis, stimulants (particularly methamphetamine and cocaine), nicotine, “research chemicals,” and some commonly prescribed medications.

  • Treatment for SIP ideally involves a comprehensive approach including psychosocial and pharmacological treatment that simultaneously address psychosis and substance use. The most effective psychosocial interventions also involve parents or other supports of the youth experiencing psychosis.

Financial disclosures:

Dr. Yule has served as a consultant (clinical services) for Phoenix House (2015–2017) and Gavin House (2018-present). She currently receives research funding from 5K12DA000357-17.

Contributor Information

David Beckmann, Addiction Recovery Management Service and First Episode and Early Psychosis Program, Massachusetts General Hospital, Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, 55 Fruit Street WACC 812, Boston, MA 02114

Kelsey Leigh Lowman, Department of Psychiatry, Massachusetts General Hospital, 101 Merrimac Street, Suite 320, Boston MA 02114

Jessica Nargiso, Addiction Recovery Management Service, Massachusetts General Hospital, Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, 55 Fruit Street WACC 812, Boston, MA 02114

James McKowen, Addiction Recovery Management Service, Massachusetts General Hospital, Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, 55 Fruit Street WACC 812, Boston, MA 02114

Lisa Watt, Addiction Recovery Management Service, Massachusetts General Hospital, Department of Psychiatry, Massachusetts General Hospital, 15 Parkman Street YAW 6A, Boston, MA 02114

Amy M. Yule, Addiction Recovery Management Service, Massachusetts General Hospital, Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, 15 Parkman Street YAW 6A, Boston, MA 02114

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