We have recently observed, across a variety of clinical settings, an increasing prescribing of psychostimulants to persons with attention-deficit hyperactivity disorder (ADHD) and schizophrenia spectrum disorders (SSD) in both forensic and general mental health consultation settings. This practice appears to arise from greater recognition of ADHD. But it occurs for persons for whom psychostimulants may worsen their psychosis and who are also co-morbid with substance use disorders, increasingly with crystal methamphetamine. ^{Reference Jones, Manetsch, Gerritsen and Simpson1} This is especially concerning given that amphetamines account for a substantial proportion of substance-induced psychosis cases where ongoing amphetamine abuse worsens course and outcome. ^{Reference Ricci, Chiappini, Martinotti and Maina2} This commentary explores the clinical and research uncertainties surrounding psychostimulant prescribing in individuals with SSD.

Historically, stimulant use in individuals with SSD has been approached with caution, grounded in the concern that increasing dopaminergic activity may exacerbate psychotic symptoms. ^{Reference Gough and Morrison3} Childhood ADHD is associated with an increased risk of later developing psychosis. ^{Reference Bamford, Qurashi, Axiaq, Marwaha and Husain4,Reference Corbeil, Brodeur, Courteau, Béchard, Huot-Lavoie and Angelopoulos5} Further, differentiating the symptoms of ADHD from partially treated psychotic symptoms is extremely difficult, especially when patients have residual positive symptoms, negative symptoms, cognitive impairment, disorganisation, affective symptoms, sleep disruption, trauma, substance use, or medication side effects. Many of the symptoms that lead to an ADHD diagnosis (poor concentration, restlessness, impaired task completion, distractibility, low motivation, poor executive function) can be direct manifestations of SSD or secondary phenomena. In that context, ADHD diagnostic and rating scales may mislead unless they are embedded in a careful developmental assessment, which can be difficult or poorly performed.

Published clinical perspectives have emphasised avoidance or, at minimum, careful use of stimulants in persons with SSD. ^{Reference Purkayastha, Patil and Sahu6} Despite this, stimulant medications remain a primary treatment for ADHD in clinical practice, although there are also non-stimulant alternatives that might be preferable. ^{Reference De Pablo, Aymerich, Chart-Pascual, Solmi, Torres-Cortes and Abdelhafez7} This creates a fundamental disconnect; clinicians are treating both ADHD and SSD in the same individuals, but without a clear evidence base to guide whether or how this should be done. ^{Reference Bamford, Qurashi, Axiaq, Marwaha and Husain4} Existing SSD practice guidelines provide little clarity on this issue. Canadian guidelines make no specific mention of stimulant prescribing in schizophrenia, ^{Reference Crockford and Addington8} while American guidelines acknowledge the issue but provide limited practical direction. ^{Reference Keepers, Fochtmann, Anzia, Benjamin, Lyness and Mojtabai9} UK and Australasian guidelines are now somewhat outdated and do not mention psychostimulant prescription at all. ^{Reference Galletly, Castle, Dark, Humberstone, Jablensky and Killackey10,11}

Therefore, the central clinical question on how to treat comorbid ADHD and psychosis remains unresolved. Stimulant medications may increase risk for relapse by exacerbating psychotic symptoms, potentially contributing to instability. ^{Reference Gough and Morrison3} Conversely, stimulant medications may reduce risk by improving impulsivity, attention and behavioural regulation among those with ADHD, ^{Reference Corbeil, Brodeur, Courteau, Béchard, Huot-Lavoie and Angelopoulos5} factors that are themselves associated with poorer outcomes when left untreated. ^{Reference Luykx, Corbeil, Kärkkäinen, Tanskanen, Mittendorfer-Rutz and Tiihonen12} Each of these interpretations is plausible, yet there is very little direct evidence to determine which is more accurate. There is some limited evidence to suggest justification for stimulant prescribing is that it is a form of substitution for illicit methamphetamine use, ^{Reference Carlander, Rydell, Kataoka, Karlén and Bagge13,Reference Ezard, Clifford, Siefried, Ali, Dunlop and McKetin14} but this remains an unevaluated use in persons with SSD.

Some literature suggests that stimulant treatment in individuals with psychotic disorders may not be as harmful as previously assumed and may even be associated with improved outcomes in some cases. ^{Reference Corbeil, Brodeur, Courteau, Béchard, Huot-Lavoie and Angelopoulos5,Reference Luykx, Corbeil, Kärkkäinen, Tanskanen, Mittendorfer-Rutz and Tiihonen12} However, substance use is highly prevalent in both ADHD and schizophrenia populations and is strongly associated with psychosis risk ^{Reference Toba-Oluboka and Dempster15} and poor forensic and correctional outcomes. ^{Reference Jones, Manetsch, Gerritsen and Simpson1,Reference Penney, Marshall and Simpson16} Studies that employ more advanced designs, such as within-individual comparisons or instrumental variable approaches, do not adequately capture time-varying illicit drug use. ^{Reference Corbeil, Brodeur, Courteau, Béchard, Huot-Lavoie and Angelopoulos5,Reference Luykx, Corbeil, Kärkkäinen, Tanskanen, Mittendorfer-Rutz and Tiihonen12,Reference Healy, OHare, Lång, Metsälä, Pulakka and McGrath17} These methods can account for stable individual characteristics but cannot distinguish whether observed changes in outcomes are attributable to prescribed medication or to concurrent substance use. As a result, the literature does not clearly separate the effects of prescribed stimulants from those of illicit stimulant exposure. This limitation is particularly important in populations where substance use is common, as it constrains causal interpretation. ^{Reference De Pablo, Aymerich, Chart-Pascual, Solmi, Torres-Cortes and Abdelhafez7} While findings suggesting that stimulant medications do not increase risk are partially reassuring, they remain difficult to interpret without a clear understanding of underlying substance use patterns. This leaves clinicians in a position where decisions are being made based on incomplete and potentially confounded evidence.

These challenges become even more pronounced in forensic settings where ADHD, psychosis and substance use frequently co-occur and are each independently associated with adverse outcomes, including violence, instability and criminal justice involvement. ^{Reference Cheng, Bryce, Takagi, Pert, Rattray and Fisher18,Reference Fazel, Hayes, Bartellas, Clerici and Trestman19} One pharmaco-epidemiological study of offenders without SSD suggested that prescribing psychostimulants was associated with reduced criminality. ^{Reference Lichtenstein, Halldner, Zetterqvist, Sjölander, Serlachius and Fazel20} However, this finding has proven difficult to replicate in intervention studies. One small study of limited quality suggested that ADHD medications may reduce criminal recidivism, ^{Reference Carlander, Rydell, Kataoka, Karlén and Bagge13} through improvements in impulsivity and behavioural dysregulation, but the study population was small and relied on self-report measures only in the open label follow-up component of the study. Importantly, there remains no evidence about whether these potential benefits extend to individuals with comorbid SSD. If stimulant treatment reduces impulsivity, it may plausibly reduce violence and recidivism in forensic populations. Conversely, if it exacerbates psychosis, particularly in the context of substance use, it may instead increase risk.

From a clinical perspective, this uncertainty supports a cautious approach to the diagnosis and treatment of ADHD in persons with SSD. Diagnostic assessment is particularly challenging because many symptoms suggestive of ADHD overlap with schizophrenia, substance use, mood symptoms, sleep disturbance, dysregulation/impulsivity of cluster B personality traits and medication-seeking effects. At the same time, stimulant prescribing in this population is already occurring and may increase as the trend for adult ADHD diagnosis becomes more common. These challenges may be further compounded where ADHD and SSD are managed by separate clinical services, making coordinated assessment and monitoring more difficult. While definitive prospective studies will take years to complete, there is an immediate need for pragmatic, consensus-based guidance to support safer and more consistent decisions in individuals with SSD, particularly when comorbid substance use is present. Until such guidance is developed, several clinical principles may help with diagnostic confirmation, assessment of psychosis stability and decisions regarding discontinuation.

First, positive symptom remission under established and optimised antipsychotic medication should be considered a prerequisite before stimulant treatment is initiated. A diagnosis of ADHD should be made through a careful developmental history supported by collateral information rather than a screening interview or rating scales. Particularly, differential diagnoses related to other factors including thought disorder and persistent positive symptoms should be carefully considered. Second, in SSD comorbid with ADHD, non-stimulant approaches should be considered first, such as non-stimulant medications, non-pharmacological interventions, sleep optimisation and substance-use treatment. ^{Reference Gough and Morrison3} Finally, where stimulant treatment is initiated, it should begin at a low dose, be titrated gradually, include close monitoring for the emergence or worsening of psychotic symptoms and incorporate a predefined discontinuation plan.

These principles do not substitute for high-quality research but could provide an interim clinical safety framework for a population in which the consequences of misdiagnosis, stimulant exposure, psychotic relapse, or substance-use destabilisation may be substantial. Ultimately, treatment of ADHD in individuals with SSD reflects a broader issue in psychiatric practice: the gap between clinical reality and the available evidence. Comorbidity is common, stimulant prescribing is occurring and yet the data needed to guide these decisions remain limited. Until research more effectively addresses key confounders, particularly substance use, clinicians should adopt a cautious approach confining stimulant use in patients with SSD to a narrow, highly selected indication subject to close and critical monitoring.