Substance/Medication-Induced Psychotic Disorder refers to the presence of hallucinations or delusions that can be attributed to the effects of a substance, such as a drug of abuse, medication, or toxin exposure. The psychotic symptoms can occur during substance intoxication or withdrawal but are not better explained by another psychotic disorder, such as schizophrenia. These symptoms typically resolve with time and as the substance is metabolized or excreted from the body (American Psychiatric Association, 2013).

Individuals with this disorder may present with hallucinations, which can be auditory, visual, or any other sensory modality. Auditory hallucinations are particularly common, often consisting of voices perceived as distinct from one's thoughts. Visual hallucinations can range from simple visual disturbances to complex scenes. Delusions, or fixed false beliefs, can also be present and may be paranoid, grandiose, or bizarre. The specific presentation of psychotic symptoms often depends on the substance involved. For example, stimulant use (e.g., cocaine or amphetamines) might produce paranoia or auditory hallucinations, while hallucinogenic substances (e.g., LSD or psilocybin) may lead to visual hallucinations. Furthermore, the duration of symptoms may also vary, from transient episodes following acute intoxication to more persistent symptoms in the context of chronic substance use or protracted withdrawal (Moore et al., 2010).

It is worth noting that individuals may also present with other symptoms related to the substance they have consumed, such as anxiety, agitation, or somatic complaints. It can also be challenging to determine whether a sense directly induces psychotic symptoms or manifests as a primary psychotic disorder exacerbated by substance use.

Diagnostic Criteria

The diagnosis of Substance/Medication-Induced Psychotic Disorder is based on specific criteria outlined in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5). Presented in simpler terms:

• Presence of Psychotic Symptoms: The individual experiences hallucinations or delusions. In simpler terms, they might hear, see, or believe things that are not real or true.
• Temporal Relationship with Substance Use: The psychotic symptoms began soon after substance intoxication, withdrawal, or exposure to a medication. This means the hallucinations or delusions occurred after taking a drug or medication or while coming off it.
• Known Substances: The substance or medication taken is known to cause psychotic symptoms. For example, certain drugs like LSD or medications can lead to hallucinations.
• Not Explained by Another Disorder: The psychotic symptoms are not better explained by a psychotic disorder that is not substance-induced. For instance, if someone has a history of schizophrenia with consistent symptoms, it is likely not due to the substance or medication.
• Not Only During Delirium: The symptoms do not occur only during delirium. Delirium is a confused state that can also cause hallucinations, but it has other specific signs and is typically short-lived.
• Causes Significant Distress or Impairment: The hallucinations or delusions cause significant distress to the individual or impair their ability to function in major life areas, such as work, social relationships, or daily activities (American Psychiatric Association, 2013).

Clinicians will rely on clinical interviews, collateral information (information from friends, family, or other healthcare providers), and laboratory tests (like drug screens) to determine whether the presenting symptoms fit these criteria.

Diagnostic Challenges

Distinguishing Substance/Medication-Induced Psychotic Disorder (SMIPD) from primary psychotic disorders or other conditions is complex and can pose diagnostic challenges for clinicians. The symptoms of substance/medication-induced psychotic disorder, such as hallucinations or delusions, can also be seen in primary psychotic disorders like schizophrenia or schizoaffective disorder. The key distinction lies in the temporal relationship with substance use: symptoms in substance-induced cases occur shortly after intoxication or withdrawal. However, in cases of chronic substance use, it can be challenging to ascertain this temporal connection (American Psychiatric Association, 2013).

Some substances can cause prolonged psychotic reactions that outlast the immediate intoxication or withdrawal. For instance, specific individuals might experience psychosis for weeks or months after using a hallucinogen, making it difficult to ascertain whether the symptoms are genuinely substance-induced or if the individual has developed a primary psychotic disorder.

Many individuals with primary psychotic disorders also use substances recreationally or as an attempt at self-medication. This comorbidity can complicate the diagnostic picture. For instance, an individual with schizophrenia who uses methamphetamine may experience an exacerbation of their baseline psychotic symptoms following substance use rather than a distinct episode of substance-induced psychosis (Kavanagh et al., 2004).

The nature and presentation of psychotic symptoms can vary based on the substance or medication involved. For instance, alcohol or benzodiazepine withdrawal might lead to visual or tactile hallucinations, while stimulant intoxication more often leads to paranoid delusions. The variability in symptoms can make it challenging to pinpoint the causative agent (Roncero et al., 2016).

Some medical conditions can present with psychotic symptoms that can be mistaken for substance-induced psychosis. For instance, urinary tract infections in the elderly or metabolic disturbances like hypercalcemia can cause confusion and hallucinations. A thorough medical evaluation is essential to rule out medical causes (American Psychiatric Association, 2013).

Accurate diagnosis often hinges on obtaining a comprehensive substance use history, but patients may be reluctant or unable to provide this. They might withhold information about illicit drug use due to stigma or legal concerns or genuinely not recall specific details because of the substances' effects.

The Impacts

Substance/Medication-Induced Psychotic Disorder can profoundly impact an individual's life, affecting various domains ranging from personal well-being to societal functioning. Here is a look at some of these impacts, supported by relevant literature:

• Cognitive Impairments: Some substances, when used excessively or in combination with others, can lead to cognitive deficits, making it hard for individuals to think, remember things, or make decisions. These cognitive effects can persist beyond the period of intoxication, especially in cases of chronic use (Scott et al., 2007).
• Relationship Strains: Hallucinations, delusions, or erratic behaviors resulting from the disorder can strain personal relationships. Family and friends may find understanding or coping with the individual's symptoms challenging, leading to isolation or conflicts (Gregg et al., 2007).
• Occupational Difficulties: The disorder can impair an individual's ability to work effectively. They may need help concentrating, making rational decisions, or interacting appropriately with colleagues. This can lead to job losses or difficulty maintaining stable employment (Henquet et al., 2010).
• Legal Issues: Individuals with substance-induced psychosis might engage in behaviors that lead to legal problems, including aggressive behaviors, disturbances, or possession of illegal substances (Arseneault et al., 2002).
• Increased Risk of Harm: Individuals under the influence of substances that induce psychosis might put themselves or others at risk due to impaired judgment. This can include accidents, self-harm, or harm towards others (Cantor-Graae & Nordström, 1995).
• Co-morbid Mental Health Issues: Substance use disorders often co-exist with other mental health issues, such as depression, anxiety, or personality disorders. The combination can complicate treatment and prognosis (Conway et al., 2006).
• Health Implications: Chronic substance use can lead to various health issues, including liver damage, cardiovascular diseases, and respiratory problems. These complications can be exacerbated when substance use is combined with psychosis-induced neglect of personal health (Smith & Farrell, 2011).
• Stigma: Individuals with this disorder might face stigma due to substance use and psychotic symptoms. This can result in reduced self-esteem and increased isolation (Livingston et al., 2012).

Differentiating Substance/Medication-Induced Psychotic Disorder and Schizophrenia

Substance/Medication-Induced Psychotic Disorder (SMIPD) and schizophrenia share certain similarities in presentation, given that both can involve psychotic symptoms like hallucinations and delusions. However, they are distinct conditions, and the impacts on individuals' lives can differ significantly.

The origin and duration of Substance/Medication-Induced Psychotic Disorder (SMIPD) and schizophrenia vary significantly. In SMIPD, psychotic symptoms arise primarily from substance or medication use, often diminishing once the substance is metabolized or eliminated. The episodic nature of these symptoms might mean periods of disturbance followed by relative normalcy. In contrast, schizophrenia is chronic, with fluctuating periods of exacerbation and remission. This ongoing nature can lead to prolonged, sometimes permanent, disruptions in many areas of life (Tandon et al., 2009).

Stigma plays a substantial role in both conditions. Individuals with SMIPD might grapple with dual stigmas: one related to substance use and another associated with psychotic symptoms. On the other hand, people with schizophrenia often face societal stigma tied to mental illness, which can profoundly impact self-esteem, relationships, and occupational prospects (Livingston et al., 2012).

Regarding treatment and recovery, the two conditions diverge in their approach. Addressing the substance use issue can lead to a more straightforward recovery in SMIPD, with abstinence or controlled use often preventing further psychotic episodes. Schizophrenia, however, typically demands long-term antipsychotic medications and psychosocial treatments. Achieving symptom remission and functional recovery in schizophrenia can be particularly challenging (McGurk et al., 2007).

Substance use is central to the etiology of SMIPD. For schizophrenia, while many individuals might engage in substance use, it is not a core aspect of the diagnosis. Nevertheless, substance use can complicate the clinical trajectory and exacerbate the disorder's progression (Dixon, 1999).

Both SMIPD and schizophrenia can cause cognitive impairments, but the nature of these deficits can differ. Schizophrenia's cognitive challenges are typically more pervasive, impacting memory, attention, and executive functions consistently, even when other symptoms are in remission (Heinrichs & Zakzanis, 1998). Finally, regarding functional impact, both disorders can impede work, social connections, and daily activities. Still, the chronic nature of schizophrenia often results in a more extended and profound disturbance in these areas (Green et al., 2000).

The Etiology (Origins and Causes)

The etiology of Substance/Medication-Induced Psychotic Disorder (SMIPD) revolves around the consumption of or withdrawal from specific substances or medications that trigger psychotic symptoms. Several factors contribute to the manifestation of these symptoms:

• Type of Substance: The substances most associated with induced psychotic disorders include alcohol, cannabis, cocaine, hallucinogens, stimulants, sedatives, hypnotics, anxiolytics, and even some medications, particularly those that affect neurotransmitter systems in the brain (American Psychiatric Association, 2013).
• Pharmacological Properties: The direct pharmacological effects of the substance on the brain can lead to the manifestation of psychotic symptoms. For example, stimulants such as methamphetamine can induce dopamine release, which might lead to symptoms like hallucinations and delusions (Sulzer et al., 2005).
• Dosage and Duration: The amount of the substance consumed and the duration of use can influence the onset and severity of symptoms. High doses of substances or prolonged use can increase the risk of psychotic episodes (Soyka, 2015).
• Withdrawal: In some cases, psychotic symptoms can emerge during withdrawal from a substance. For example, severe alcohol withdrawal can lead to hallucinations and delusions (Bayard et al., 2004).
• Individual Vulnerability: Personal factors, such as genetics, pre-existing mental health conditions, or previous traumatic experiences, might influence an individual's susceptibility to develop psychotic symptoms after substance use (Arendt et al., 2005).
• Co-occurrence with other Disorders: Individuals with other mental health disorders, like depression or bipolar disorder, may be more susceptible to experiencing psychotic symptoms when using certain substances (Soyka, 2015).

In summary, the etiology of SMIPD is multifaceted, encompassing the pharmacological effects of the substance, the patterns of its use, and individual factors that may increase susceptibility to its effects. It is crucial to understand this etiology to differentiate SMIPD from primary psychotic disorders and to ensure accurate diagnosis and appropriate treatment.

Comorbidities

Substance/Medication-Induced Psychotic Disorder (SMIPD) often does not exist in isolation. Several comorbid conditions frequently co-occur with SMIPD, complicating diagnosis, treatment, and the overall clinical picture.

• Substance Use Disorders (SUDs): Given that SMIPD arises due to the use of substances, it is not surprising that many individuals with this disorder also meet the criteria for a Substance Use Disorder. Whether it is alcohol, cocaine, cannabis, or another substance, problematic use patterns are prevalent (American Psychiatric Association, 2013).
• Mood Disorders: Individuals with SMIPD often experience comorbid mood disorders like Major Depressive Disorder or Bipolar Disorder. Substance use might be a way to self-medicate the symptoms of these disorders, which can lead to the emergence of psychotic symptoms (Khantzian, 1997).
• Anxiety Disorders: Anxiety disorders, including generalized anxiety disorder, panic disorder, and post-traumatic stress disorder (PTSD), may co-occur with SMIPD. Like mood disorders, individuals might use substances to cope with anxiety, which can precipitate psychotic episodes (Turner et al., 2005).
• Personality Disorders: Certain personality disorders, especially borderline and antisocial personality disorders, are comorbid with substance-induced psychotic symptoms. The impulsivity and unstable interpersonal relationships often seen in these disorders can be associated with substance misuse, leading to psychotic symptoms (Trull et al., 2000).
• Cognitive Disorders: In some instances, especially with prolonged and heavy substance use, there might overlap with cognitive disorders or impairments. Substances like alcohol and certain drugs can cause neurocognitive damage, leading to deficits in memory, attention, and executive function (Ersche et al., 2006).

SMIPD often coexists with other psychiatric conditions, making comprehensive assessments vital to delineate the primary issues and any underlying or coexisting disorders. Addressing these comorbidities is essential for holistic treatment and long-term recovery.

Risk Factors

Risk factors influence substance/Medication-Induced Psychotic Disorder (SMIPD). Recognizing these factors is pivotal for prevention, early detection, and appropriate intervention. Here is an overview of the risk factors associated with SMIPD:

• Type and Quantity of Substance: The substance consumed plays a significant role. Stimulants such as cocaine or methamphetamine, hallucinogens like LSD or PCP, and depressants, including alcohol, are frequently implicated in the onset of SMIPD. The higher the dose of the substance consumed, the greater the likelihood of experiencing psychotic symptoms (American Psychiatric Association, 2013).
• Duration of Substance Use: Prolonged and chronic use of psychoactive substances can increase the risk of developing SMIPD, especially when the use is heavy or large (Linszen et al., 1994).
• Age: Adolescents and young adults, whose brains are still developing, are more susceptible to the psychoactive effects of substances and might be at a higher risk for developing psychotic symptoms when using drugs (Bossong & Niesink, 2010).
• Genetic Predisposition: Some individuals may be genetically more susceptible to experiencing psychosis in the context of substance use (Caspi et al., 2005).
• Pre-existing Psychiatric Conditions: Individuals with existing mental health disorders, such as mood or anxiety disorders, might have an elevated risk for SMIPD. Substance use could be a way of self-medicating these conditions, inadvertently increasing the risk of psychosis (Khantzian, 1997).
• Family History: A family history of psychotic disorders or substance use disorders can increase an individual's vulnerability to developing SMIPD (Arendt et al., 2008).
• Traumatic Experiences: Individuals who have experienced trauma, especially during childhood, might be more vulnerable to SMIPD, mainly if they use substances as a coping mechanism (Read et al., 2003).
• Environment and Peer Influence: An environment where substance use is normalized or encouraged can increase the risk of developing SMIPD. Peer pressure, especially during adolescence, can significantly influence substance initiation and misuse (Fergusson et al., 1996).

In summary, the risk factors for SMIPD are multifaceted and encompass individual and environmental elements. Comprehensive assessments considering these risks can help in early detection and intervention strategies.

Case Study

Introduction: Mark is a 38-year-old successful architect known for his precision and innovative designs. He has been happily married for 12 years, has two children, and enjoys an active social life, frequently hosting dinner parties and charity events.

Background: Mark's rise in his profession had been meteoric, from landing high-profile projects to giving keynote addresses at architectural conferences. Amidst the pressures of his profession and the allure of the upscale urban lifestyle, Mark began using cocaine recreationally, especially during late-night brainstorming sessions with colleagues. He believed it gave him an edge, making him more creative and allowing him to work longer hours.

Onset of Issues: After about eight months of occasional use, Mark's consumption of cocaine began to increase. He rationalized it as a necessary tool for maintaining his high performance at work. However, this escalating use started taking a toll. Mark began to experience paranoia, suspecting that his colleagues were conspiring against him or that competitors were stealing his designs. He would often talk about hearing conversations that supposedly took place behind closed doors, suggesting his ideas were being plagiarized.

Crisis Point: One evening, Mark's wife, Lisa, came home to find him frantically tearing apart the living room, claiming he had planted microphones to catch the "thieves" in the act. On another occasion, Mark called the police, convinced someone had broken into their home, though there was no evidence. Mark's family, especially his children, became increasingly distressed by his erratic behavior.

Intervention: Lisa urged Mark to seek help. With the assistance of a psychiatrist, Mark was diagnosed with Substance/Medication-Induced Psychotic Disorder (SMIPD). The psychotic symptoms, including his auditory hallucinations and extreme paranoia, were linked to his cocaine use.

Recovery and Reflection: Mark underwent detoxification and engaged in intensive outpatient therapy. Cognitive Behavioral Therapy was instrumental in helping him recognize the link between his substance use and psychotic symptoms. Group therapy introduced him to others who had experienced similar challenges, helping to alleviate his isolation and stigma.

In time, Mark returned to his profession but made significant lifestyle changes, including avoiding late-night work sessions and seeking healthier coping mechanisms. He also became an advocate, speaking about the dangers of substance abuse in high-pressure professions.

Conclusion: Mark's story highlights the potential dangers of recreational drug use, even for those who appear to "have it all together." The slippery slope from casual use to dependence and severe mental health challenges is a stark reminder of substances' snowball effect on one's life.

Recent Psychology Research Findings

Substance/Medication-Induced Psychotic Disorder (SMIPD) is an area of interest in contemporary psychological research. Given its intricacies and overlaps with primary psychotic disorders, it often presents diagnostic challenges. Here are some of the recent findings:

Recent studies highlight the importance of careful history-taking in differentiating SMIPD from primary psychotic disorders. The temporal relationship between substance use and the onset of psychotic symptoms is crucial. Typically, the onset of symptoms in SMIPD occurs during intoxication or withdrawal and resolves within a month of sobriety (Alderson et al., 2020).

Different substances pose different risks for inducing psychotic symptoms. Research suggests that synthetic cannabinoids ("spice") and methamphetamines have an exceptionally high association with psychotic presentations compared to other drugs (Every-Palmer, 2011; McKetin et al., 2019).

Neuroimaging studies uncover the structural brain changes associated with SMIPD. Alterations in brain regions related to psychosis, such as the prefrontal cortex and limbic system, have been observed in individuals who have used substances linked to psychosis (Rapp et al., 2019).

Research suggests a possible genetic predisposition to developing SMIPD in some individuals. Some gene variations may increase susceptibility to substance-induced psychosis, implying a complex interplay between genetic factors and environmental triggers (Niemi-Pynttäri et al., 2013).

Early intervention, including substance detoxification and behavioral therapies, is essential for SMIPD. Some studies indicate that individuals with SMIPD might also benefit from antipsychotic medications, though the evidence remains inconclusive (Marconi et al., 2016).

While many individuals with SMIPD experience remission after cessation of substance use, a subset may continue to experience persistent psychotic symptoms. Studies suggest this could be due to an underlying vulnerability to psychosis unmasked by substance use (Sara & Lappin, 2017).

In conclusion, recent research underscores the significance of careful diagnostic evaluation when considering SMIPD. The interplay between substances, brain structure, genetics, and environmental factors is intricate and calls for comprehensive, individualized assessments and interventions.

Treatment and Interventions

Substance/Medication-Induced Psychotic Disorder (SMIPD) necessitates an individualized, multifaceted approach to treatment that primarily aims at addressing both the psychotic symptoms and the underlying substance use. Here are some of the mainstays of treatment and intervention:

• Detoxification: The first line of treatment is to discontinue or reduce the causative substance or medication safely. Depending on the substance, medically supervised detoxification might be necessary to manage withdrawal symptoms (American Psychiatric Association, 2013).
• Pharmacotherapy:
• Antipsychotics: In the acute phase, antipsychotic medications can be used to manage psychotic symptoms. Both typical and atypical antipsychotics have been employed, with the latter being preferred due to a more favorable side-effect profile (Zhornitsky & Stip, 2012).
• Mood Stabilizers and Anxiolytics: In cases where mood symptoms or anxiety are prominent, these might be indicated, though caution is needed due to potential interactions or addictive properties (American Psychiatric Association, 2013).
• Substance Use Disorder Treatment: Once the acute psychosis has been managed, it is crucial to address the substance use disorder. This can include:
• Behavioral therapies: Cognitive-behavioral therapy (CBT) can be particularly effective. Motivational Enhancement Therapy (MET) and Contingency Management (CM) have also shown promise for substance use disorders (McHugh et al., 2010).
• Group therapy: Group sessions can offer peer support and shared strategies for avoiding substance use.
• 12-step programs: Programs such as Alcoholics Anonymous (AA) or Narcotics Anonymous (NA) can provide support networks and strategies for sobriety.
• Psychoeducation: Educating the patient (and possibly their family) about the risks associated with substance use, especially psychotic symptoms, can be an essential preventive measure (Tarricone et al., 2014).
• Rehabilitation and Social Support: This encompasses vocational rehabilitation, social skills training, and community reintegration, aimed at restoring the individual's functional capacity and enhancing their quality of life (Bellack, 2006).
• Relapse Prevention: Given the high risk of relapse in substance use disorders, relapse prevention strategies, often embedded within CBT, are paramount. These strategies emphasize recognizing high-risk situations and developing coping responses (Marlatt & Donovan, 2005).
• Family Intervention: Family plays a crucial role in the recovery process. Family-based interventions can be beneficial, including education about the disorder, communication skills training, and crisis intervention (Dixon et al., 2001).

In summary, treating SMIPD requires a comprehensive approach that addresses the psychotic symptoms and substance use at its core. Given the complex interplay between the two, care must be individualized and often requires a multidisciplinary team.

Implications if Untreated

If Substance/Medication-Induced Psychotic Disorder (SMIPD) is left untreated, its repercussions can be layered and deeply concerning.

Chronic substance or medication use has alarming health consequences. The risks span liver damage, cardiovascular disease, complications in the respiratory system, and even the chance of an overdose. The specific substance use greatly influences these health outcomes (World Health Organization, 2014).

An alarming aspect of untreated SMIPD is the potential escalation of psychotic symptoms. Over time, these can manifest as intensified hallucinations, delusions, and an onset of disorganized thinking. Such developments not only become more ingrained but also pose increasing challenges for treatment (American Psychiatric Association, 2013).

As the disorder takes hold, an individual's daily functionality can severely deteriorate. They may struggle with maintaining their job, managing their finances, and even sustaining personal relationships (Lehman et al., 2004). Beyond this, the dual stigma attached to substance use and psychotic symptoms can further isolate them. This often results in broken relationships and diminished community ties, escalating feelings of loneliness, depression, and anxiety (Livingston et al., 2012).

The legal ramifications of substance use, mainly when the substance is illegal, can be significant. This can encompass a range of consequences, from arrests and incarcerations to broader criminal justice system involvement (Chandler et al., 2009). From an economic perspective, the implications of untreated SMIPD extend beyond the direct expenses associated with procuring the substance. The cascading effects can translate to unemployment, escalating medical bills, legal expenses, and, in grave circumstances, even homelessness (Ettner et al., 2006).

The distress and confusion stemming from psychosis substantially heighten the risk of self-harm and suicidal tendencies (Hawton et al., 2005). In some instances, what initiates as substance-induced psychosis might transition to a primary psychotic disorder, such as schizophrenia if not promptly addressed (Alderson et al., 2020). Moreover, continuous use might culminate in a chronic substance use disorder, necessitating more intensive and extended treatment interventions (Sara & Lappin, 2017).

The overarching implication of untreated SMIPD is a drastic degradation in the quality of life. Mounting health challenges mark this decline, pronounced social alienation, and enduring disabilities (Lehman et al., 2004).

Given the profound consequences outlined, it is of utmost importance that individuals exhibiting symptoms of SMIPD receive immediate and effective treatment interventions. Such proactive measures are crucial to counteract these risks and pave the path towards enhanced well-being.

Summary

SMIPD involves the presence of hallucinations or delusions directly attributed to substance intoxication, withdrawal, or exposure to a medication. Key to its diagnosis is that the psychotic symptoms are more pronounced than typically expected from the intoxication or withdrawal syndrome and that another mental disorder does not better explain them.

A crucial step in assessing SMIPD is distinguishing it from other disorders. The symptom onset and resolution timeline, in relation to substance use, offers clues. Unlike primary psychotic disorders, such as schizophrenia, the symptoms in SMIPD arise due to substance use and typically resolve as the substance is metabolized or cleared. This can cause episodic disruptions in life, as opposed to the chronic and persistent nature of disorders like schizophrenia. Moreover, primary psychotic disorders may have a broader range of symptoms, more prolonged course, and do not directly stem from substance use.

Prevention is the first line of defense. Addressing potential triggers and educating communities about the risks associated with substance use can help prevent SMIPD onset. Rehabilitation focuses on both substance use and its psychological ramifications. Effective rehab programs adopt a multifaceted approach, including detoxification, cognitive-behavioral therapy, and family counseling. Addressing the substance use issue, often through abstinence or controlled use, is central to preventing the recurrence of psychotic episodes.

SMIPD is particularly disruptive when it strikes someone previously high-functioning. The sudden onset of the disorder can lead to unexpected challenges, from job losses to strained personal relationships, leaving the individual and their loved ones grappling to adapt.

Recovery is possible, and hope is essential. Leveraging a support system, including family, friends, and professionals, can be invaluable. Psychosocial interventions and therapy can help individuals process their experiences, rebuild their self-confidence, and reintegrate into their personal and professional lives. Early detection and treatment are paramount; the sooner the intervention, the better the prognosis.

While SMIPD presents formidable challenges, understanding its nature, investing in prevention and rehabilitation, and fostering supportive environments are pivotal steps in navigating and overcoming its impacts.

References

Alderson, H. L., Semple, D. M., Blayney, C., & Queirazza, F. (2020). Risk of transition to schizophrenia following first admission with substance-induced psychotic disorder: a population-based longitudinal cohort study. Psychological Medicine, 50(14), 2345-2353.

Alderson, H. L., Semple, D. M., Blayney, C., & Queirazza, F. (2020). Risk of transition to schizophrenia following first admission with substance-induced psychotic disorder: a population-based longitudinal cohort study. Psychological Medicine, 50(14), 2345-2353.

American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Washington, DC: Author.

Arendt, M., Mortensen, P. B., Rosenberg, R., Pedersen, C. B., & Waltoft, B. L. (2008). Familial predisposition for psychiatric disorder: comparison of subjects treated for cannabis-induced psychosis and schizophrenia. Archives of general psychiatry, 65(11), 1269-1274.

Arendt, M., Rosenberg, R., Fjordback, L., Brandholdt, J., Foldager, L., Sher, L., & Munk-Jørgensen, P. (2005). Testing the self-medication hypothesis of depression and aggression in cannabis-dependent subjects. Psychological medicine, 35(7), 935-945.

Arseneault, L., Cannon, M., Poulton, R., Murray, R., Caspi, A., & Moffitt, T. E. (2002). Cannabis use in adolescence and risk for adult psychosis: longitudinal prospective study. Bmj, 325(7374), 1212-1213.

Bayard, M., McIntyre, J., Hill, K. R., & Woodside Jr, J. (2004). Alcohol withdrawal syndrome. American Family Physician, 69(6), 1443-1450.

Bossong, M. G., & Niesink, R. J. (2010). Adolescent brain maturation, the endogenous cannabinoid system and the neurobiology of cannabis-induced schizophrenia. Progress in Neurobiology, 92(3), 370-385.

Cantor-Graae, E., & Nordström, L. G. (1995). Risk factors for substance abuse in schizophrenia. Acta Psychiatrica Scandinavica, 91(5), 316-321.

Caspi, A., Moffitt, T. E., Cannon, M., McClay, J., Murray, R., Harrington, H., ... & Poulton, R. (2005). Moderation of the effect of adolescent-onset cannabis use on adult psychosis by a functional polymorphism in the catechol-O-methyltransferase gene: Longitudinal evidence of a gene X environment interaction. Biological psychiatry, 57(10), 1117-1127.

Chandler, R. K., Fletcher, B. W., & Volkow, N. D. (2009). Treating drug abuse and addiction in the criminal justice system: improving public health and safety. Jama, 301(2), 183-190.

Conway, K. P., Compton, W., Stinson, F. S., & Grant, B. F. (2006). Lifetime comorbidity of DSM-IV mood and anxiety disorders and specific drug use disorders: results from the National Epidemiologic Survey on Alcohol and Related Conditions. Journal of Clinical Psychiatry, 67(2), 247-257.

Dixon, L. (1999). Dual diagnosis of substance abuse in schizophrenia: prevalence and impact on outcomes. Schizophrenia Research, 35(Suppl), S93-S100.

Ersche, K. D., Clark, L., London, M., Robbins, T. W., & Sahakian, B. J. (2006). Profile of executive and memory function associated with amphetamine and opiate dependence. Neuropsychopharmacology, 31(5), 1036-1047.

Ettner, S. L., Huang, D., Evans, E., Ash, D. R., Hardy, M., Jourabchi, M., & Hser, Y. I. (2006). Benefit-cost in the California treatment outcome project: does substance abuse treatment "pay for itself"?. Health Services Research, 41(1), 192-213.

Every-Palmer, S. (2011). Warning: legal synthetic cannabinoid-receptor agonists such as JWH-018 may precipitate psychosis in vulnerable individuals. Addiction, 106(10), 1839-1840.

Fergusson, D. M., Lynskey, M. T., & Horwood, L. J. (1996). The short-term consequences of early onset cannabis use. Journal of Abnormal Child Psychology, 24(4), 499-512.

Green, M. F., Kern, R. S., Braff, D. L., & Mintz, J. (2000). Neurocognitive deficits and functional outcome in schizophrenia: are we measuring the “right stuff”?. Schizophrenia Bulletin, 26(1), 119-136.

Gregg, L., Barrowclough, C., & Haddock, G. (2007). Reasons for increased substance use in psychosis. Clinical Psychology Review, 27(4), 494-510.

Hawton, K., Sutton, L., Haw, C., Sinclair, J., & Deeks, J. J. (2005). Schizophrenia and suicide: Systematic review of risk factors. The British Journal of Psychiatry, 187(1), 9-20.

Heinrichs, R. W., & Zakzanis, K. K. (1998). Neurocognitive deficit in schizophrenia: A quantitative review of the evidence. Neuropsychology, 12(3), 426.

Henquet, C., Krabbendam, L., de Graaf, R., ten Have, M., & van Os, J. (2010). Cannabis use and expression of mania in the general population. Journal of Affective Disorders, 125(1-3), 103-110.

Kavanagh, D. J., Waghorn, G., Jenner, L., Chant, D. C., Carr, V., Evans, M., ... & McGrath, J. J. (2004). Demographic and clinical correlates of comorbid substance use disorders in psychosis: multivariate analyses from an epidemiological sample. Schizophrenia research, 66(2-3), 115-124.

Khantzian, E. J. (1997). The self-medication hypothesis of substance use disorders: A reconsideration and recent applications. Harvard review of psychiatry, 4(5), 231-244.

Lehman, A. F., Lieberman, J. A., Dixon, L. B., McGlashan, T. H., Miller, A. L., Perkins, D. O., & Kreyenbuhl, J. (2004). Practice guidelines for the treatment of patients with schizophrenia. The American Journal of Psychiatry, 161(2_supplement), 1-56.

Linszen, D. H., Dingemans, P. M., & Lenior, M. E. (1994). Cannabis abuse and the course of recent-onset schizophrenic disorders. Archives of general psychiatry, 51(4), 273-279.

Livingston, J. D., Milne, T., Fang, M. L., & Amari, E. (2012). The effectiveness of interventions for reducing stigma related to substance use disorders: a systematic review. Addiction, 107(1), 39-50.

Marconi, A., Di Forti, M., Lewis, C. M., Murray, R. M., & Vassos, E. (2016). Meta-analysis of the association between the level of cannabis use and risk of psychosis. Schizophrenia Bulletin, 42(5), 1262-1269.

McGurk, S. R., Twamley, E. W., Sitzer, D. I., McHugo, G. J., & Mueser, K. T. (2007). A meta-analysis of cognitive remediation in schizophrenia. American Journal of Psychiatry, 164(12), 1791-1802.

McKetin, R., Leung, J., Stockings, E., Huo, Y., Foulds, J., Lappin, J. M., ... & Cumming, C. (2019). Mental health outcomes associated with of the use of amphetamines: a systematic review and meta-analysis. EClinicalMedicine, 16, 81-97.

Moore, T. J., Glenmullen, J., & Furberg, C. D. (2010). Prescription drugs associated with reports of violence towards others. PLoS ONE, 5(12), e15337.

Niemi-Pynttäri, J. A., Sund, R., Putkonen, H., Vorma, H., Wahlbeck, K., & Pirkola, S. P. (2013). Substance-induced psychoses converting into schizophrenia: a register-based study of 18,478 Finnish inpatient cases. Journal of Clinical Psychiatry, 74(1), e94-9.

Rapp, C., Walter, A., Studerus, E., Bugra, H., Tamagni, C., Rothen, D., ... & Borgwardt, S. (2019). Cannabis use and brain structural alterations of the cingulate cortex in early psychosis. Psychiatry Research: Neuroimaging, 290, 53-60.

Read, J., Agar, K., Argyle, N., & Aderhold, V. (2003). Sexual and physical abuse during childhood and adulthood as predictors of hallucinations, delusions and thought disorder. Psychology and Psychotherapy: Theory, Research and Practice, 76(1), 1-22.

Roncero, C., Daigre, C., Gonzalvo, B., Valero, S., Castells, X., Grau-López, L., ... & Casas, M. (2016). Risk factors for cocaine-induced psychosis in cocaine-dependent patients. European Psychiatry, 33, 65-70.

Sara, G. E., & Lappin, J. M. (2017). Childhood trauma: psychiatry's greatest public health challenge?. The Lancet Public Health, 2(7), e300-e301.

Scott, J. C., Woods, S. P., Matt, G. E., Meyer, R. A., Heaton, R. K., Atkinson, J. H., & Grant, I. (2007). Neurocognitive effects of methamphetamine: a critical review and meta-analysis. Neuropsychology Review, 17(3), 275-297.

Smith, M. J., & Farrell, M. (2011). Impaired cognitive performance in drug-free users of recreational ecstasy (MDMA). Journal of Psychopharmacology, 25(5), 669-679.

Soyka, M. (2015). Substance misuse, psychiatric disorder and violent and disturbed behaviour. The British Journal of Psychiatry, 206(4), 276-278.

Sulzer, D., Sonders, M. S., Poulsen, N. W., & Galli, A. (2005). Mechanisms of neurotransmitter release by amphetamines: a review. Progress in neurobiology, 75(6), 406-433.

Tandon, R., Keshavan, M. S., & Nasrallah, H. A. (2009). Schizophrenia, "just the facts" 4. Clinical features and conceptualization. Schizophrenia Research, 110(1-3), 1-23.

Trull, T. J., Sher, K. J., Minks-Brown, C., Durbin, J., & Burr, R. (2000). Borderline personality disorder and substance use disorders: a review and integration. Clinical psychology review, 20(2), 235-253.

Turner, S., Mota, N., Bolton, J., & Sareen, J. (2018). Self-medication with alcohol or drugs for mood and anxiety disorders: A narrative review of the epidemiological literature. Depression and anxiety, 35(9), 851-860.

World Health Organization. (2014). Global status report on alcohol and health-2014. World Health Organization.