The association between cannabinoid use and the development of psychopathology, particularly psychotic symptoms, has been the focus of systematic investigation over recent decades. Also, changes in consumption patterns, sociocultural attitudes toward the substance and the substantial increase in the average potency of available products deserve a higher attention to this problem. Cannabis is currently the most widely used illicit psychoactive substance worldwide, with recent estimates indicating annual prevalence rates exceeding 15% among young adults in several European countries, including Portugal [1-3]. This trend has been accompanied by a marked increase in daily use and consumption of products with high concentrations of delta-9-tetrahydrocannabinol (THC), often containing residual levels of cannabidiol (CBD), representing a significant shift from the chemical profile predominant two to three decades ago [4-6].

Current epidemiological evidence demonstrates a consistent association between regular cannabinoid use (particularly when initiated during adolescence), high frequency of use and high-potency products, increases the risk of developing psychotic symptoms or formal psychotic disorders [7-11]. Multicentre studies such as the European Network of National Schizophrenia Networks Studying Gene-Environment Interactions (EU-GEI) have demonstrated a dose-response relationship between cannabis exposure and risk, estimating that a significant proportion of first-episode psychosis cases in regions with high prevalence of high-potency cannabis use may be attributable to cannabis consumption [10]. Similar findings have been observed in population-based studies in Canada, the United States, Denmark and Israel, particularly following the legalisation or liberalisation of recreational markets [12,13].

Beyond epidemiological observations, controlled studies have demonstrated that THC can induce transient psychotomimetic symptoms in healthy individuals, including thought disorganisation, hallucinations, delusional ideation and perceptual processing disturbances [14-16]. These effects were particularly pronounced in individuals with a family history of psychosis, genetic vulnerability or a prior diagnosis of a psychotic disorder, suggesting clinically relevant gene-environment interactions [14,15].

Understanding of the neurobiological mechanisms underlying the psychotogenic potential of cannabinoids has advanced considerably over the past two decades. THC acts as a partial agonist at cannabinoid receptor type 1 (CB1) receptors, which are densely expressed in structures such as the striatum, prefrontal cortex, hippocampus and amygdala [6,8,14].

Modulation of these receptors interferes with the release of neurotransmitters, including dopamine, glutamate and gamma-aminobutyric acid (GABA). Contemporary neurobiological models suggest that repeated exposure to THC may contribute to striatal dopaminergic dysfunction as a central mechanism in aberrant salience attribution theory and, consequently, in the emergence of positive psychotic symptoms [7,9,14].

The role of CBD is relevant within the pharmacodynamic balance: studies have shown that this non-psychoactive compound may exert anxiolytic, antipsychotic and anti-inflammatory effects, partially modulating the actions of THC. However, most recreational cannabis products currently available contain markedly imbalanced THC:CBD ratios, favouring an increased psychotogenic potential [4,6]. Cannabis-induced psychosis may present with heterogeneous clinical features, including persecutory delusions, auditory or visual perceptual disturbances, formal thought disorder and affective disorders [6,8].

Although persecutory ideation is the most frequently reported, clinical literature documents less common presentations, including somatic, mystical or self-referential delusions [10,11,17]. Among the rare somatic manifestations is delusional infestation (DI), defined by a fixed false belief of being infested with organisms (e.g., insects, parasites, worms), often accompanied by tactile hallucinations, pruritus and behaviours such as body inspection or skin manipulation [18,19]. The syndrome may occur as a primary delusional disorder (also referred to as Ekbom syndrome) or secondary to medical conditions, neurological disease, neurodevelopmental disorders or psychoactive substance use, including cocaine, amphetamines and, more rarely, cannabis.

Differentiating primary psychosis from substance-induced psychosis may be clinically and temporally challenging. Current diagnostic classifications, including the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) and the International Classification of Diseases, Eleventh Revision (ICD-11), state that substance-induced psychosis should be considered when symptoms emerge during or shortly after substance use, are clinically significant, and are not better explained by a primary psychotic disorder. However, it is important to emphasise that prolonged exposure to cannabinoids, particularly high-potency formulations, may trigger transient psychotic episodes but also increase the likelihood of progression to a persistent psychotic disorder, including schizophrenia [9,11,18].

In clinical practice, early recognition of this association has direct implications for prognosis, therapeutic approach and relapse prevention. Evidence indicates that continued cannabis use following a psychotic episode increases the risk of recurrence and symptom severity, whereas sustained abstinence is associated with better functional outcomes and a reduced likelihood of relapse [10-12].

This case report aimed to describe an Ekbom-like somatic presentation within a probable cannabis-induced psychotic disorder and to highlight the practical diagnostic value of structured clinical assessment, targeted investigations and normal neuroimaging findings in excluding secondary causes.