Drug-induced schizophrenia can affect people who take certain drugs or substances that lead to symptoms of this serious mental health condition, including cannabis or amphetamine use. Research finds that more than 25% of people who have a substance-induced psychotic episode will later be diagnosed with schizophrenia. Amphetamine reverses both vesicular monoamine transporter 2 (VMAT2) and the dopamine transporter (DAT) (25) to effectively increase synaptic concentrations of dopamine (DA) in the striatum in the nigrostriatal pathway.

1. In case of severe agitation or anxiety, clinicians may resort to benzodiazepines or antipsychotics as rescue medication (Kasper et al., 2020).
2. No significant difference was found on the Montgomery Ǻsberg Depression Rating Scale (MADRS) scores between the 2 groups.
3. The increase of perfusion in IFG and DLPFC during acute ketamine administration was abolished by inhibition of glutamate release via pretreatment with lamotrigine, which furthermore led to decreased IFG perfusion 24 h later.
4. Spinogenesis is well studied in early development, however these initial spines are not functional and undergo synapse maturation to become functional.
5. Furthermore, a possible interaction with lamotrogine should be considered when patients show a lack of response to ketamine during concomitant lamotrigine use.

Additionally, individuals with pre-existing mental health conditions, such as depression or anxiety, may be more prone to prolonged psychosis. As this article illustrates, studies aimed at addressing ketamine’s mechanism of action built a direct bridge between basic synaptic signaling mechanisms and clinical practice. For decades, neuropsychiatric studies have centered around “slow” neurotransmission predominantly carried out by monoaminergic neurotransmitters [134]. Today, ketamine action and the role of fast glutamatergic neurotransmission in the pathogenesis and treatment of mood disorders present a new set of opportunities and challenges. In order to fully harness the emerging potential of fast neurotransmission in neurotherapies, it will be critical to uncover novel therapeutics to target fast neurotransmission that do not impair its fundamental function in sensory processing as well as learning and memory processes.

Data Availability Statement

Joanna Briggs Institute’s critical appraisal tools for RCTs, quasi-experimental studies, and case reports were used for quality assessment of the included studies (JBI, 2020). This systematic review was written according to the Preferred Reporting Items for Systematic Reviews and Meta-Analysis statement. We therefore conducted a systematic review and meta-analysis of the association of ketamine with positive, negative, and total psychopathological outcomes in healthy volunteers and patients with schizophrenia. This the five rules of recovery specific use of ketamine is the main focus of our review, but we also use the findings to inform understanding of other uses of ketamine. Ajub and Lacerda [22], described the efficacy of esketamine in four patients with psychotic characteristics and severe depression, following the description of these two individuals. Two patients were diagnosed with major depressive disorder with psychotic symptoms, one with bipolar depressive disorder with mixed features, and one with schizoaffective disorder, depressive type.

d-Cycloserine enhances the bidirectional range of NMDAR-dependent hippocampal synaptic plasticity

There is no cure for schizophrenia, although there are effective treatments available that can help manage symptoms and avoid triggers. Stopping drug use does not necessarily mean that symptoms will immediately cease, but it is the first step. Studies show that both the type of substance and the level of use contribute to whether or not a person will develop drug-induced schizophrenia and how it will progress. A https://sober-home.org/ recent review found some evidence that cannabis can have a small effect on causing schizophrenia as well as exacerbating symptoms of existing schizophrenia. However, there was also evidence that the cannabidiol (CBD) component of cannabis may have some therapeutic benefit for existing schizophrenia. This article will discuss the relationship between drug-induced psychosis and schizophrenia and how it’s treated.

Definition and symptoms of ketamine-induced psychosis

Anti-anhedonic effects of subanesthetic dosages of ketamine have been observed without a deleterious impact on the long-term psychotic symptomatology of schizophrenia patients. In a new meta-analysis, the authors synthesize the research on the effects of ketamine for depression in patients with a history of psychosis or current psychotic symptoms, as well as trials evaluating ketamine as a treatment for negative symptoms in schizophrenic patients [7]. Analyzed were nine papers of pilot trials and case reports involving a total of 41 individuals. As side effects were mild and self-limiting, these investigations imply that short-term ketamine treatment for depression and even negative symptoms in patients with a history of psychosis or current psychotic characteristics can be both safe and beneficial. We found no evidence for interactions between lithium and ketamine, nor for the hypothesis that lithium would strengthen the antidepressant effect through inhibition of glycogen synthase kinase 3. Three studies (Anand et al., 2000; Deakin et al., 2008; Doyle et al., 2013) reported attenuating effects of lamotrigine pretreatment on ketamine-induced effects on the BPRS, dissociative symptoms, and BOLD responses.

While other findings in the field suggested that monoamine signaling was relevant to the biology of depression, the mixed findings from the depletion studies suggested that the framework for the biology of depression needed to be broadened to encompass other signaling mechanisms [22]. Interestingly, the cognitive and behavioral effects of PCP and ketamine in animals and humans are strongly similar to the positive and negative symptoms of schizophrenia, suggesting that abnormalities in NMDA receptor function might contribute to the biology of schizophrenia (150, 151). In line with this knowledge, in their randomized, double blind clinical trial, Morgan et al. (36) administered cannabinoids by inhalation to 48 cannabis users; they planned four sessions, THC (8 mg), THC (8 mg) + CBD (16 mg), CBD 16 mg and placebo. They found an increase in psychotomimetic symptoms following administration of THC alone and the combination of THC and CBD, especially negative, perceptual distortions, and cognitive disorganization.

Further research is needed to gain a deeper understanding of this condition and develop more targeted interventions to support those affected. In addition to formal research studies, there have been numerous case studies and reports of individuals who have experienced ketamine-induced psychosis. Some individuals have reported symptoms lasting for several weeks or even months, while others have reported a shorter duration. The findings from these studies suggest that the duration of ketamine-induced psychosis can vary significantly from person to person.