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Review

Substance-Induced Psychosis: Diagnostic Challenges and Phenomenological Insights

by
Valerio Ricci
1,*,
Giovanni Martinotti
2 and
Giuseppe Maina
3
1
San Luigi Gonzaga Hospital, University of Turin, 10043 Orbassano, Italy
2
Department of Neurosciences, Imaging and Clinical Sciences, Università degli Studi G. D’Annunzio Chieti-Pescara, 66100 Chieti, Italy
3
Department of Neurosciences “Rita Levi Montalcini”, University of Turin, Via Verdi 8, 10124 Torino, Italy
*
Author to whom correspondence should be addressed.
Psychiatry Int. 2024, 5(4), 759-772; https://doi.org/10.3390/psychiatryint5040052
Submission received: 3 September 2024 / Revised: 10 October 2024 / Accepted: 12 October 2024 / Published: 15 October 2024
Versions Notes

Abstract

:
Substance-induced psychosis (SIP) is an increasingly prevalent and complex condition that presents significant diagnostic and therapeutic challenges. With the rising use of novel psychoactive substances (NPSs) and potent traditional compounds like cannabis and cocaine, particularly among adolescents and young adults, understanding the mechanisms and clinical manifestations of SIP has become more critical. This review examines the psychopathological characteristics of SIP, focusing on the differentiation between substance-induced and primary psychotic disorders. Two key concepts are explored: Gaëtan de Clérambault’s “mental automatism”, which describes involuntary thoughts and sensations experienced as alien to the self, and the “twilight state” of consciousness, characterized by an altered perception of space, time, and social interaction. These phenomena are essential in understanding how substance use triggers psychotic processes and how SIP differs from endogenous psychosis. This review also highlights the clinical and phenomenological distinctions between acute and chronic psychotic episodes, emphasizing the potential transition from SIP to persistent psychosis, especially in cases of frequent and potent substance use. It discusses the diagnostic and therapeutic importance of recognizing specific psychopathological markers such as alterations in temporality, spatiality, and intersubjectivity. Understanding these features enhances the clinician’s ability to accurately differentiate SIP from primary psychotic disorders, which is often complicated by the widespread use of substances that may not be easily detectable in standard tests. This review concludes by advocating for a clinical–phenomenological approach to empathically engage with patients and provide a solid diagnostic framework for improved treatment strategies, particularly for those at risk of transitioning to chronic psychosis.

1. Introduction

The psychopathological manifestations associated with substance use, including induced psychotic experiences, are increasingly relevant but not well-understood within the medical community. Novel psychoactive substances (NPSs) [1,2] and potentiated traditional compounds like cannabis and cocaine have emerged as global concerns, particularly among adolescents and young adults.
Substance-induced psychosis is a complex and multifaceted condition that poses significant diagnostic and therapeutic challenges. The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) [3], characterizes substance-induced psychotic disorder as a mental condition marked by delusions and/or hallucinations occurring during or shortly after substance intoxication or withdrawal. Additionally, the symptoms of psychotic disorders that are not related to substance use remain insufficiently understood. The increasing prevalence of substance use disorders and the concomitant rise in psychotic episodes necessitate a deeper understanding of the underlying mechanisms and risk factors. The global increase in the use of NPSs and the potentiation of traditional substances such as cannabis and cocaine have led to a surge in psychotic episodes that are directly linked to substance abuse. This trend is particularly alarming among adolescents and young adults, who are more likely to experiment with these substances and are at a critical stage of brain development [2]. One of the key concerns in the field of psychopharmacology is the transition from acute, substance-induced psychotic episodes to chronic, persistent psychosis. Research indicates that this transition is particularly significant in cases of cannabis-induced psychosis. Studies have shown that the likelihood of developing chronic psychosis increases with the frequency and potency of cannabis use [4,5,6]. This is of particular concern given the increasing potency of cannabis (K2, Spice) available in the market today, which can have profound effects on brain chemistry and increase the risk of prolonged psychotic episodes [7,8]. In addition, patients with substance-induced psychosis (SIP) tend to have shorter durations of untreated psychosis (DUP), are predominantly male, exhibit more pronounced positive symptoms at the initial assessment, and have lower academic performance during early adolescence [9,10].
The differentiation between substance-induced psychosis and primary psychotic disorders such as schizophrenia is crucial for accurate diagnosis and effective treatment. Substance-induced psychosis can present with symptoms that are remarkably similar to those of primary psychotic disorders, including hallucinations, delusions, and cognitive impairments. However, the etiology of these symptoms differs significantly. In substance-induced psychosis, the symptoms are directly linked to the acute or chronic effects of the substance on the brain, whereas in primary psychotic disorders, the symptoms arise from endogenous factors such as genetic predisposition and neurodevelopmental abnormalities. It is also possible that an initial schizophrenia-like psychosis (SIP) may progress to a primary form with predominantly endogenous symptoms, especially in chronic phases, where typical schizophrenic symptoms prevail [11].
The clinical presentation of SIP is often marked by a rapid onset of psychotic symptoms following substance use. These symptoms can include severe agitation, paranoia, hallucinations, and delusions. The intensity and duration of these symptoms can vary depending on the substance used, the amount consumed, and the individual’s biological and psychological predispositions. For instance, psychostimulants like cocaine and methamphetamine are known to induce intense psychotic episodes that can include violent behavior and severe paranoia [12]. In contrast, hallucinogens like LSD and psilocybin can lead to profound alterations in perception and thought processes, often accompanied by visual and auditory hallucinations [13]. In addition to the immediate effects of substance-induced psychosis, there is growing evidence that prolonged substance use can lead to lasting changes in brain function and structure [14,15,16]. Neuroimaging studies have shown that chronic use of substances such as cannabis, cocaine, and methamphetamine can result in structural abnormalities in brain regions associated with cognition, emotion regulation, and reward processing [17]. These changes can underlie the persistent cognitive and emotional disturbances observed in individuals with a history of substance-induced psychosis [18].
Furthermore, the socio-cultural context in which substance use occurs plays a significant role in the development and progression of substance-induced psychosis. Factors such as social stress, peer pressure, and socio-economic status can influence an individual’s likelihood of engaging in substance use and their subsequent risk of developing psychotic symptoms. For example, individuals from socio-economically disadvantaged backgrounds may have higher rates of substance use due to stress and lack of access to mental health resources, increasing their risk of SIP [19].

Objectives

This study aims to identify the key characteristics of substance-induced psychoses from both clinical and psychopathological perspectives, with a focus on differentiating them from primary psychotic disorders. Section 1 of the text will outline the clinical differences between substance-induced psychoses and endogenous psychoses. Subsequently, the analysis will focus on two fundamental concepts in the development of substance-related psychoses: mental automatism, as defined by De Clérambault, and the twilight state of consciousness. In Section 2, we will explore in greater detail how these two factors interact: the twilight state as a foundational alteration of consciousness in substance users, particularly affecting spatial, temporal, and intersubjective dimensions, and mental automatism as a necessary psychopathological structure for the emergence of psychotic symptoms. Furthermore, through these concepts, we attempt to define the transition from acute psychosis to a persistent form. In conclusion, we provide insights for clinicians on the complexities of managing patients with substance addiction and highlight the benefits of the phenomenological approach.
Our approach will utilize a clinical–phenomenological method, which seeks to illuminate mental states and psychological phenomena as they appear to the clinician. This method emphasizes direct patient experience and encourages reflection on the substance user’s condition without preconceived theories or assumptions. It fosters an empathetic understanding of the patient’s suffering while also encouraging the exploration of the psychopathological foundations that contribute to symptom development. This exploration is particularly relevant in light of the increasing prevalence of new psychoactive substances and the corresponding rise of atypical psychoses, which often present significant clinical challenges and leave many questions unanswered.

2. Relevant Section

2.1. Background

The etiology of SIP is directly linked to the acute or chronic effects of psychoactive substances on the brain. Substances such as cannabis, cocaine, methamphetamine, and hallucinogens like LSD can induce psychotic symptoms by altering neurotransmitter systems, particularly dopamine and serotonin pathways. These alterations can lead to significant disruptions in perception, cognition, and behavior. In contrast, primary psychotic disorders like schizophrenia are thought to arise from a complex interplay of genetic, neurodevelopmental, and environmental factors. Genetic predisposition plays a significant role, with numerous studies identifying specific genetic markers associated with increased risk of schizophrenia [20].
Neurobiological studies have shown that individuals with primary psychotic disorders often exhibit structural and functional abnormalities in brain regions involved in cognition, emotion regulation, and sensory processing. For instance, reductions in gray matter volume in the prefrontal cortex and hippocampus and alterations in white matter integrity are commonly observed in schizophrenia [21,22,23]. These neurobiological changes contribute to the core symptoms of schizophrenia, including hallucinations, delusions, disorganized thinking, and cognitive deficits [10,11,12,13,14,15,16,17,18,19,20,21,22,23,24,25]. In contrast, the neurobiological effects of SIP are more transient and directly related to the substance used. For example, acute cannabis use can increase dopamine release in the striatum, leading to heightened sensory perceptions and paranoia [26] Chronic use, however, can result in downregulation of dopamine receptors, contributing to the persistence of psychotic symptoms even after cessation of use [27,28]. Similarly, methamphetamine use can cause neurotoxic damage to dopaminergic neurons, resulting in long-lasting cognitive and emotional disturbances [13,14,15,16,17,18,19].
The clinical presentation of SIP and primary psychotic disorders can overlap significantly, but certain features may help differentiate them. SIP typically presents with a rapid onset of psychotic symptoms following substance use. These symptoms can include severe agitation, paranoia, hallucinations, and delusions. The intensity and duration of these symptoms can vary depending on the substance used, the amount consumed, and the individual’s biological and psychological predispositions. Psychostimulants like cocaine and methamphetamine are known to induce intense psychotic episodes characterized by violent behavior and severe paranoia, whereas hallucinogens like LSD can lead to profound alterations in perception and thought [29,30]
Primary psychotic disorders, on the other hand, usually have a more insidious onset. Symptoms such as social withdrawal, decreased motivation, and subtle cognitive changes often precede the onset of full-blown psychosis by months or even years. This prodromal phase is less commonly observed in SIP, where the onset of psychosis is more closely tied to substance use. Additionally, individuals with primary psychotic disorders often exhibit a more chronic and relapsing course, with periods of symptom exacerbation and remission [31,32].
The course and prognosis of SIP and primary psychotic disorders also differ significantly. SIP is generally considered to be a more transient condition, with symptoms typically resolving with sustained abstinence from the offending substance. However, there is growing evidence that a significant proportion of individuals with SIP may go on to develop persistent psychosis or schizophrenia [33,34]. This transition is particularly common in cases of cannabis-induced psychosis, where high-potency cannabis use has been linked to an increased risk of developing chronic psychotic disorders [5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,23,24,25,26,27,28,29,30,31,32,33,34,35].
In contrast, primary psychotic disorders like schizophrenia are characterized by a chronic and often debilitating course. Despite advances in pharmacological and psychosocial treatments, many individuals with schizophrenia continue to experience significant symptoms and functional impairments throughout their lives. Early intervention and sustained treatment can improve outcomes, but the prognosis remains guarded for many patients [36]. The main characteristics regarding the differences between substance-related psychoses and endogenous psychoses are presented in Table 1.

2.2. Phenomenological Approach

A phenomenological approach to understanding psychosis emphasizes the subjective experience of individuals undergoing psychotic episodes. This approach can provide insights into the qualitative differences between substance-induced psychosis (SIP) and primary psychotic disorders. Researchers with a phenomenological orientation suggest that disturbances in the basic sense of self may serve as a marker of vulnerability to psychosis [37]. This hypothesis integrates both empirical findings and philosophical perspectives. The self-disturbance thought to be central in schizophrenia affects the pre-reflective level of selfhood, also known as ipseity. As psychotic symptoms evolve, these self-disorders become more pronounced and manifest in the form of delusions, hallucinations, and passivity experiences. However, when substance use significantly contributes to the onset of psychotic experiences, this model needs to be expanded. Many individuals with prolonged and heavy substance use display persistent psychotic symptoms, prompting questions about the link between substance use and the development of a chronic, atypical form of psychosis. In this context, De Clerambault’s mental automatism and twilight states can serve as constructive diagnostic tools for clinicians working with substance users experiencing psychosis.

2.2.1. Gaetan de Clerambault and Mental Automatism

Gaëtan Gatian de Clérambault (1872–1934) began working at the Special Infirmary for the Insane in Paris in 1905 and became its head in 1920. During his tenure, he evaluated thousands of individuals experiencing acute intoxication from alcohol and drugs. Starting in 1909, he published a series of papers on mental automatism, a concept he refined throughout his career. By 1925, he described it as a clinical syndrome characterized by involuntary phenomena in the motor, sensory, and ideo-verbal domains, where individuals perceive intrusive thoughts, sensations, or actions as alien to themselves. These experiences disrupt cognitive processes, causing confusion and distress without necessarily involving strong emotions. He differentiated between minor automatism, which is less noticeable and often goes undetected, and major automatism, which significantly impairs functioning. De Clérambault’s perspective diverged from conventional psychiatry by emphasizing mental automatism as a core process in psychosis rather than focusing solely on symptoms like hallucinations or delusions. He considered automatic phenomena as crucial indicators of psychosis, regardless of the presence of other symptoms. His theory was built on the work of earlier French psychiatrists like Jules Baillarger and Jules Séglas, but he broadened the concept to include a wider array of intrusive experiences [38]. He linked mental automatism to various psychotic disorders, such as paranoia and hallucinatory psychoses, and attributed these phenomena to neurological disturbances like infections or intoxications, rejecting psychological explanations. Although he adhered to an organicist view, he did not dwell on the specific causes, instead using the concept of “mechanism” as a metaphor to describe the clinical patterns he observed.
According to de Clérambault, mental automatism is the core mechanism of psychosis, with other symptoms like delusions emerging as secondary responses. He viewed delusions as the mind’s attempt to make sense of the confusing automatic phenomena, describing them as extensions of these experiences that compel the individual to find an external explanation: “the intensity, unexpected nature, persistence, and strangeness of the sensation lead the person to seek an external cause” (de Clérambault, 1925) [38]. These delusional interpretations may eventually give rise to a distinct delusional identity after an “incubation period” of confusion and conflicting thoughts. He distinguished between productive symptoms such as hallucinations and the more subtle psychic phenomena of mental automatism, which he described as “non-sensory” disruptions in thought, lacking clear sensory content and often isolated from delusions. He explained that these experiences, like intrusive thoughts and anticipatory thinking, create a “thought echo”, where the individual’s thoughts are duplicated in time and space without initially causing significant distress.
These characteristics are clinically important, as some patients present similar phenomena independently of their primary condition. Such symptoms may emerge early or during treatment, sometimes identified by patients as barriers to recovery, or noticed by clinicians. The autonomous nature of these phenomena can be a precursor to the development of delusions. Building on Jacksonian theories, de Clérambault believed that intoxications could disrupt the control exerted by higher inhibitory centers, unleashing activities that would manifest as automatisms, appearing spontaneous or unwanted. He was convinced that these automatisms had a strong organic basis due to their mechanistic nature. He developed these insights through his work at the Paris Prefecture, where he frequently observed individuals intoxicated with substances like absinthe, ether, and chloral hydrate. For de Clérambault, automatisms were deeply linked to the biological substrate. The patient’s critical self-awareness helplessly observes the automatism, while delusions form as an overlay in response to these experiences [37]. In this context, patients become aware of “unfamiliar or disturbed thoughts” within their own minds and recognize these as unusual experiences beyond their conscious control. This state is often accompanied by vivid visual and kinesthetic hallucinations, delusional perceptions, and frequently significant agitation and aggression. Occasionally, more structured but limited delusional thoughts may also emerge. Despite these cognitive disturbances, the individual’s sense of self remains partially intact, retaining some degree of awareness and control over their experience. Inizio moduloFine modulo [38]. The main characteristics of mental automatism are presented in Table 2.

2.2.2. Role of the “Twilight State” of Consciousness

After defining mental automatism as a necessary psychopathological element in the development of substance-related psychoses, we now turn to the primary alteration of consciousness: the twilight state, characterized by heightened sensory experiences and a detachment from reality. Auditory and visual hallucinations are common, with individuals experiencing a deep sense of unreality and altered self-perception [39].
In primary psychotic disorders, such as schizophrenia, the phenomenological experience is often more deeply rooted in the individual’s sense of self and identity. Delusions and hallucinations typically reflect ingrained beliefs and perceptions resistant to change. A disrupted or fragmented self is a frequent theme, where individuals experience a loss of coherence and continuity in thoughts and perceptions. This significant alteration in the existential framework is a hallmark of primary psychoses and aids in differential diagnosis. The twilight state plays a crucial role in the transition from substance use to psychosis, impacting spatiality, intersubjectivity, and temporality [40]. This complex path challenges traditional diagnostic models and emphasizes the need for a deeper understanding of substance-induced psychopathological experiences. The twilight state is a transitional phase of consciousness, bridging wakefulness and sleep, reality and fantasy. It is marked by a narrowing of the individual’s consciousness, leading to heightened sensory perceptions and altered awareness. Often induced by psychoactive substances, this state disrupts normal cognitive processes, creating a unique phenomenological experience [41], altering the perception of space, time, and consequently intersubjectivity.
Spatial awareness is particularly affected in this state, becoming compressed and distorted, often resulting in disorientation, a sense of bodily dissociation, or a feeling of merging with the environment. These spatial distortions are especially pronounced with hallucinogens like LSD and psilocybin, which can cause vivid visual hallucinations and blur the boundaries between the self and the surroundings [40]. These changes in spatial perception hinder the individual’s interaction with their environment, making even simple tasks challenging due to impaired spatial judgment and coordination. Unlike primary psychotic disorders, where spatial distortions are less prominent, these alterations are key features of substance-induced psychosis [39].
Intersubjectivity, or the ability to understand and engage with others, is also severely disrupted in the twilight state. Substance use can cause a breakdown in social interactions, leading to feelings of isolation, paranoia, and mistrust [42,43]. Paranoid delusions and ideas of reference, where benign actions are perceived as threatening or personally significant, are common in this phase [44]. This breakdown of intersubjectivity, a core feature of psychosis, can lead to social withdrawal, increased aggression, and further complications in the clinical picture [39,44,45].
Temporality, or the perception of time, is another key aspect affected by the twilight state. Psychoactive substances frequently distort the sense of time, causing either time dilation or contraction. Moments may seem endlessly prolonged, or entire hours may pass unnoticed, contributing to the sense of unreality and disorientation typical of substance-induced psychosis. In the twilight state, time is fragmented, disrupting the flow of thoughts and memories, which makes it difficult for individuals to maintain a coherent narrative of past, present, and future events. While this temporal disintegration is central to the psychotic experience, temporal continuity often returns after the substance’s effects subside, in contrast to endogenous psychoses, where the loss of temporal structure tends to persist [46,47]. The main characteristics of mental automatism are presented in Table 3.

2.2.3. Implications and Clinical Significance

During twilight, there is a notable narrowing of the subject’s conscious awareness, often focusing on just a few or even a single aspect of their experience. Crucially, this narrowing does not mean a significant reduction in alertness, as individuals maintain the ability to perform purposeful and goal-oriented actions within their immediate surroundings. The field of consciousness can expand again, especially in response to sudden and stimulating events. This phase acts as a transitional point, similar to the change from day to night at sunset or from night to day at dawn.
The objects that capture attention are limited in number and characteristics. Consciousness envelops these objects in their essential phenomenological forms, leading to a dynamic interplay of essences. Surfaces intersect, and shapes become distinct in the fading light, merging until they blend together. Focusing intensely on specific objects, as opposed to others, can create genuine illusions of movement. This illusion, or the perceived motion of a stationary object, can cause it to gradually disperse, disintegrate, and ultimately vanish from the visual field (negative hallucination) [48]. As the object fades, it leaves an empty space that is quickly occupied by another figure, indicating the beginning of true hallucination. Productive psychopathological phenomena, often seen in individuals with specific sensory deficits (such as auditory or visual hallucinations in the deaf and blind, or tactile hallucinations in those with sensory disorders), demonstrate the brain’s tendency to compensate for deficiencies by creating alternative experiences. The twilight state of consciousness, characterized by its deficit, restricts the perceptual field and reduces the focus of consciousness. This emphasis on a select few elements facilitates the emergence of hallucinations and delusions. This state can be viewed as a transitional phase, a critical point relevant to various clinical psychiatric conditions like schizophrenia, mania, and melancholia. It marks a moment of suspension between the organic and the psychic or between the organic and the inorganic in the context of substance use. This transitional phase is marked by a shifting interplay between light and darkness.
Certain states, not only of a psychopathological nature, can be defined as true twilight states: Empirical studies have elucidated the concept of “reverie”, for example, describing the ability to engage in fantasy and immerse oneself in the ecstasy and sorrow of mental images. This point is characterized by a sense of amazement and wonder, an encounter where consciousness yields a profound unity with the cosmos [49].
This fleeting and intense moment is a juncture where everything holds the potential to begin and end, where the creative act can either give rise to an artistic form or dismantle the spontaneity of occurrence. It embodies a “daydream” where the subject is consciously aware and actively participates in the imaginative process, in contrast to a dream where the subject takes a passive role, experiencing the content without conscious vigilance. This unique state of consciousness allows for an active shaping of imaginative processes, blurring the lines between creation and dissolution. The twilight state of consciousness is also associated with the pharmacologically induced state resulting from various psychopharmacological treatments. This state characterizes the maintenance condition for individuals with psychiatric symptoms responsive to treatment. Psychotropic medications, including benzodiazepines, neuroleptics, antidepressants, and lithium, tend to return the subject’s consciousness to the twilight condition and effectively anchor it in this state. Essentially, these medications position the subject within a metaphorical twilight zone, where they remain unless specific critical factors intervene [40].
The sensation of being “high” can be likened to a twilight state, as it does not necessarily involve a severe alteration in arousal. In substance users, this twilight state of consciousness represents a borderland between reality and the dream world. Beyond this border, individuals may encounter illusions, hallucinations, delusions, as well as visual and auditory distortions. Their responses to external stimuli may seem irrational or disconnected from conventional reality. Depersonalization and derealization are commonly experienced during the twilight state of consciousness, which serves as a transitional phase facilitating the progression from basic symptoms to more advanced manifestations, as indicated by the transient phenomena described by Klosterkötter [50]. Consequently, the consciousness of individual substance users often exhibits a discontinuous and fragmented nature. It oscillates between phases characterized by a synthetic and clear perception of reality and phases marked by fragmentation and a loss of coherence in the overall experience.
In clinical practice, events such as rave parties and techno-music gatherings can be viewed as examples of “collective” twilight states. The term “rave” refers to an experience characterized by deviation and delirium, marked by heightened enthusiasm culminating in exhilaration and ecstasy. The intensified state induced rapidly and consistently during these events, often through chemical substances, can lead to a liminal state, similar to a trance or psychosis. Exiting this state frequently results in a downturn or low phase, emphasizing the dynamic nature of the experience and its potential impact on mood and consciousness. The combination of music, communal energy, and chemical influences creates a distinct collective twilight state, with both euphoric and challenging aspects within the realm of human experience.
Understanding the twilight state is vital for clinicians in diagnosing and treating substance-induced psychosis. Traditional diagnostic models often fail to capture the complexity of this state, leading to misdiagnosis and inadequate treatment. Recognizing the unique spatial, intersubjective, and temporal alterations in the twilight state can help clinicians develop more accurate diagnostic criteria and tailored interventions. For example, interventions that focus on grounding individuals in reality, such as cognitive–behavioral techniques and sensory integration therapies, may be particularly effective in addressing the spatial and temporal distortions of the twilight state. Additionally, social support and therapeutic strategies that enhance intersubjectivity, such as group therapy and family interventions, can help mitigate the social isolation and paranoia associated with this state [51].

3. Discussion

Substance-induced psychosis (SIP) represents a significant and growing concern in the field of mental health, driven by the increasing prevalence of novel psychoactive substances (NPSs) and potent traditional compounds like cannabis and cocaine. For instance, our study highlights two critical aspects of the psychopathology associated with substance-induced psychosis (SIP), which are essential for understanding this condition: De Clérambault’s mental automatism and the twilight state. These phenomena not only deepen our understanding of substance-induced psychotic processes but also provide a novel contribution to the existing literature. In particular, we have revived a fundamental concept in the development of psychosis: mental automatism, which is even more relevant when applied to the genesis of substance-induced psychosis, where the external element of the substance triggers a psychotic cascade. It represents a core mechanism in psychosis, where individuals experience thoughts, sensations, or actions as foreign to their own will, serving as the foundation for the development of delusions. This psychotic process unfolds within the framework of the twilight state, characterized by profound alterations in consciousness, with distortions in the perception of space, time, and social interactions, acting as a transitional phase between reality and substance-induced psychosis.
The differentiation between substance-induced psychosis (SIP) and primary psychotic disorders, such as schizophrenia, is crucial for effective clinical management. While both conditions share overlapping symptoms, they differ significantly in their etiology, pathophysiology, and clinical course. Understanding the clinical mechanisms driving the development of substance-related psychoses provides valuable insights into the subjective experiences of affected individuals. For example, from a clinical perspective, mental automatism offers a framework for understanding how individuals experience thoughts, sensations, or actions as foreign or alien, a process that is exacerbated by intoxication. These automatic phenomena, often driven by the neurobiological effects of substances, result in a greater sense of estrangement rather than passivity in psychotic experiences. Similarly, the twilight state can be a necessary condition for the transition from substance use to psychosis. This state acts as a threshold between the clarity of reality and the obscurity of dreams and psychosis, fostering illusions, delusions, and hallucinations. Depersonalization and derealization are common experiences within the twilight state, where Klosterkötter’s transitional phenomena are more likely to occur, evolving from basic symptoms into fully developed psychotic features. These patients may live with this fragile condition on a daily, monthly, or yearly basis, where their perception of reality becomes fragmented and incomplete, making the twilight state feel like a normal part of life. This state of consciousness functions like a flickering screen, with brief flashes of perception appearing and disappearing. More specifically, this “twilight psychosis” appears as a cluster of basic symptoms affecting mood, cognition, thought, and perception. In this twilight state, a specific form of psychosis, termed “Basic Psychosis”, can develop. “Basic Psychosis” is characterized by a blending of cognitive, perceptual, and mood symptoms. The recognition and assessment of this condition can be conducted using the Basic Symptoms Interview (BSI), as described by Huber, Gross [52], and Klosterkötter [50]. Basic symptoms are subjective alterations that indicate the onset of psychosis, and according to Klosterkötter, these transitions lead from basic symptoms to fully developed psychotic features. Multiple basic symptoms combine to form a psychopathological condition known as the “basic stage”, which serves as the foundation for “Basic Psychosis”. Diagnosing and treating “Basic Psychosis” in substance users is particularly challenging, as psychiatrists may fail to recognize it, leading to severe discomfort for the individuals and often resulting in the continued use of substances. The impaired mental functioning caused by these basic symptoms can make it difficult for many addicts to cease substance use, as they experience acute discomfort during drug-free periods. In such cases, substances both mask and exacerbate “Basic Psychosis”.

4. Conclusions

This study contributes to the existing literature on substance-induced psychoses, a condition whose diagnosis and treatment often lack precise criteria, leading to significant confusion. It is crucial to underscore the importance of this topic, especially given that many substances are readily available, affordable, and possess neurobiological properties that strongly impact dopaminergic neurons, making them highly psychotogenic. From a diagnostic perspective, this work emphasizes the need to recognize often-overlooked clinical features such as the twilight state of consciousness and mental automatism, which involve alterations in temporality and spatiality, the sensory nature of hallucinatory phenomena, and the persistence of some awareness of one’s psychotic state. The fundamental aim is to provide a theoretical and diagnostic framework that is useful for clinicians, enabling them to engage with addicted patients in an empathic and informed manner. For instance, recognizing these aspects enhances the clinician’s ability to distinguish between acute substance-induced psychoses and endogenous forms, a task that is often complicated by the widespread use of substances, many of which are undetectable in blood or urine due to the absence of appropriate testing methods.

5. Future Directions

Our research operates within a clinical–phenomenological framework, which we believe is the most effective approach for engaging empathically with substance-dependent patients while providing precise tools for interpreting substance-induced psychoses [53,54,55]. However, a significant unresolved issue remains the high transition rate from substance-induced psychosis (SIP) to persistent psychosis, particularly in cases involving high-potency substances. This highlights the urgent need for early intervention and comprehensive treatment strategies, particularly through enhanced clinical understanding. The detailed clinical data presented in our study can assist clinicians in better identifying individuals at risk of developing chronic psychosis. For instance, the recognition of mental automatism, its persistence over time, and the progressive dissolution of the patient’s critical self-awareness can serve as an early marker in the transition to persistent psychosis. Similarly, the persistence of the twilight state, even after the effects of the substance have worn off, and the consequent alteration of consciousness, may signal the development of chronic psychosis, closely resembling endogenous schizophrenic psychoses.
Public health initiatives should therefore focus on raising awareness about the risks associated with substance-induced psychosis and expanding access to mental health services for high-risk groups, including adolescents and young adults. Early identification of at-risk individuals, along with integrated treatment plans addressing both substance use and psychotic symptoms, could prevent the progression to chronic psychosis and improve long-term outcomes [56]. Further research into these clinical phenomena is essential. Understanding which individuals are at risk of developing SIP and how this condition may progress into chronicity is crucial. Investigating personal vulnerability factors, combined with the use of clinical assessment tools, could help clinicians identify at-risk patients earlier. However, this selection process remains complex and diagnostically challenging. Previous studies have already identified several risk factors for the development of chronic psychosis, including male sex, young age, regular and daily use of psychoactive substances with strong dopaminergic effects (such as cannabinoids and amphetamines), previous hospitalizations, and, in the case of synthetic cannabinoids, significantly increased THC (Tetrahydrocannbinol) levels [6,57,58,59,60]. Although the time frame for the progression to chronic psychosis is not well-defined, the presence of multiple risk factors accelerates this transition. Neuroimaging studies, such as functional magnetic resonance imaging (fMRI), could provide important insights into the brain regions most affected during SIP, particularly those involved in spatial, intersubjective, and temporal processing. These findings could offer a neurobiological counterpart to clinical data and help identify opportunities for timely pharmacological intervention. Longitudinal studies should also investigate how these altered states of consciousness evolve over time and their impact on long-term mental health outcomes.
From a therapeutic perspective, the diagnostic insight into a substance-induced psychosis can guide clinicians in selecting new-generation antipsychotics, which are more suitable for these novel and sometimes unknown forms of psychosis due to their psychodynamic properties and lower incidence of side effects [61,62]. Moreover, this study opens up avenues for considering psychotherapeutic approaches that aim to expand temporal horizons (often contracted in substance-induced psychoses) by restoring future-oriented planning and intersubjective spaces.

Author Contributions

Conceptualization, V.R. and G.M. (Giuseppe Maina); methodology, V.R.; validation, V.R. and G.M. (Giuseppe Maina); formal analysis, V.R. and G.M. (Giovanni Martinotti); investigation, V.R. and G.M. (Giuseppe Maina); resources, V.R.; data curation, V.R.; writing—original draft preparation V.R. and G.M. (Giovanni Martinotti); writing—review and editing, V.R.; visualization, supervision, G.M. (Giovanni Martinotti). All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Data Availability Statement

The data presented in this study are available on request from the corresponding author. The data are not publicly available due to privacy reasons.

Conflicts of Interest

Giuseppe Maina has been a consultant and/or a speaker and/or has received research grants from Angelini, Doc Generici, Janssen-Cilag, Lundbeck, Otsuka, Pfizer, Servier, Recordati. Valerio Ricci has been consultant for Lundbeck, Pfizer, Angelini.

References

  1. Corazza, O.; Assi, S.; Simonato, P.; Corkery, J.; Bersani, F.S.; Demetrovics, Z.; Stair, J.; Fergus, S.; Pezzolesi, C.; Pasinetti, M.; et al. Promoting Innovation and Excellence to Face the Rapid Diffusion of Novel Psychoactive Substances in the EU: The Outcomes of the ReDNet Project. Hum. Psychopharmacol. 2013, 28, 317–323. [Google Scholar] [CrossRef] [PubMed]
  2. Assi, S.; Keenan, A.; Al Hamid, A. Exploring e-psychonauts perspectives towards cocaine effects and toxicity. Subst. Abus. Treat. Prev. Policy 2022, 17, 48. [Google Scholar] [CrossRef] [PubMed]
  3. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 5th ed.; text rev.; American Psychiatric Association: Washington, DC, USA, 2022. [Google Scholar] [CrossRef]
  4. Bloomfield, M.A.; Ashok, A.H.; Volkow, N.D.; Howes, O.D. The effects of Δ9-tetrahydrocannabinol on the dopamine system. Nature 2016, 539, 369–377. [Google Scholar] [CrossRef] [PubMed]
  5. Bloomfield, M.A.; Morgan, C.J.; Egerton, A.; Kapur, S.; Curran, H.V.; Howes, O.D. Dopaminergic function in cannabis users and its relationship to cannabis-induced psychotic symptoms. Biol. Psychiatry 2014, 75, 470–478. [Google Scholar] [CrossRef] [PubMed]
  6. Rognli, E.B.; Heiberg, I.H.; Jacobsen, B.K.; Høye, A.; Bramness, J.G. Transition from Substance-Induced Psychosis to Schizophrenia Spectrum Disorder or Bipolar Disorder. Am. J. Psychiatry 2023, 180, 437–444. [Google Scholar] [CrossRef]
  7. Crebbin, K.; Mitford, E.; Paxton, R.; Turkington, D. First-episode psychosis and cannabis use: Different long-term outcomes for men and women? Schizophr. Res. 2009, 107, 303–308. [Google Scholar] [CrossRef]
  8. Ricci, V.; Ceci, F.; Di Carlo, F.; Lalli, A.; Ciavoni, L.; Mosca, A.; Sepede, G.; Salone, A.; Quattrone, D.; Fraticelli, S.; et al. Cannabis Use Disorder and Dissociation: A Report from a Prospective First-Episode Psychosis Study. Drug Alcohol Depend. 2021, 229 Pt A, 109118. [Google Scholar] [CrossRef]
  9. Weibell, M.A.; Joa, I.; Bramness, J.; Johannessen, J.O.; McGorry, P.D.; Ten Velden Hegelstad, W.; Larsen, T.K. Treated incidence and baseline characteristics of substance induced psychosis in a Norwegian catchment area. BMC Psychiatry 2013, 13, 319. [Google Scholar] [CrossRef]
  10. Mendrek, A.; Fattore, L. Sex differences in drug-induced psychosis. Curr. Opin. Behav. Sci. 2017, 13, 152–157. [Google Scholar] [CrossRef]
  11. Starzer, M.S.K.; Nordentoft, M.; Hjorthøj, C. Rates and Predictors of Conversion to Schizophrenia or Bipolar Disorder Following Substance-Induced Psychosis. Am. J. Psychiatry 2018, 175, 343–350. [Google Scholar] [CrossRef]
  12. Curran, H.V.; Freeman, T.P.; Mokrysz, C.; Lewis, D.A.; Morgan, C.J.; Parsons, L.H. Keep off the grass? Cannabis, cognition and addiction. Nat. Rev. Neurosci. 2016, 17, 293–306. [Google Scholar] [CrossRef] [PubMed]
  13. Mathias, S.; Lubman, D.I.; Hides, L. Substance-induced psychosis: A diagnostic conundrum. J. Clin. Psychiatry 2008, 69, 358–367. [Google Scholar] [CrossRef] [PubMed]
  14. Wolf, R.C.; Werler, F.; Schmitgen, M.M.; Wolf, N.D.; Wittemann, M.; Reith, W.; Hirjak, D. Functional correlates of neurological soft signs in heavy cannabis users. Addict. Biol. 2023, 28, e13270. [Google Scholar] [CrossRef]
  15. Beheshti, I. Cocaine Destroys Gray Matter Brain Cells and Accelerates Brain Aging. Biology 2023, 12, 752. [Google Scholar] [CrossRef]
  16. Thomas, D.M.; Walker, P.D.; Benjamins, J.A.; Geddes, T.J.; Kuhn, D.M. Methamphetamine neurotoxicity in dopamine nerve endings of the striatum is associated with microglial activation. J. Pharmacol. Exp. Ther. 2004, 311, 1–7. [Google Scholar] [CrossRef] [PubMed]
  17. Murnane, K.S.; Edinoff, A.N.; Cornett, E.M.; Kaye, A.D. Updated Perspectives on the Neurobiology of Substance Use Disorders Using Neuroimaging. Subst. Abus. Rehabil. 2023, 14, 99–111. [Google Scholar] [CrossRef]
  18. Hines, L.A.; Freeman, T.P.; Gage, S.H.; Zammit, S.; Hickman, M.; Cannon, M.; Munafo, M.; MacLeod, J.; Heron, J. Association of high-potency cannabis use with mental health and substance use in adolescence. JAMA Psychiatry 2020, 77, 1044–1051. [Google Scholar] [CrossRef]
  19. Baptiste-Roberts, K.; Hossain, M. Socioeconomic Disparities and Self-reported Substance Abuse-related Problems. Addict. Health 2018, 10, 112–122. [Google Scholar] [CrossRef]
  20. Smeland, O.B.; Frei, O.; Dale, A.M.; Andreassen, O.A. The polygenic architecture of schizophrenia-rethinking pathogenesis and nosology. Nat. Rev. Neurol. 2020, 16, 366–379. [Google Scholar] [CrossRef]
  21. Smeland, O.B.; Bahrami, S.; Frei, O.; Shadrin, A.; O’Connell, K.; Savage, J.; Watanabe, K.; Krull, F.; Bettella, F.; Steen, N.E.; et al. Genome-wide analysis reveals extensive genetic overlap between schizophrenia, bipolar disorder, and intelligence. Mol. Psychiatry 2020, 25, 844–853. [Google Scholar] [CrossRef]
  22. Karlsgodt, K.H.; Sun, D.; Cannon, T.D. Structural and Functional Brain Abnormalities in Schizophrenia. Curr. Dir. Psychol. Sci. 2010, 19, 226–231. [Google Scholar] [CrossRef] [PubMed]
  23. Ho, N.F.; Li Hui Chong, P.; Lee, D.R.; Chew, Q.H.; Chen, G.; Sim, K. The Amygdala in Schizophrenia and Bipolar Disorder: A Synthesis of Structural MRI, Diffusion Tensor Imaging, and Resting-State Functional Connectivity Findings. Harv. Rev. Psychiatry 2019, 27, 150–164. [Google Scholar] [CrossRef] [PubMed]
  24. Karlsgodt, K.H.; Sun, D.; Jimenez, A.M.; Lutkenhoff, E.S.; Willhite, R.; van Erp, T.G.; Cannon, T.D. Developmental disruptions in neural connectivity in the pathophysiology of schizophrenia. Dev. Psychopathol. 2008, 20, 1297–1327. [Google Scholar] [CrossRef] [PubMed]
  25. Fiorentini, A.; Volonteri, L.S.; Dragogna, F.; Rovera, C.; Maffini, M.; Mauri, M.C.; Altamura, C.A. Substance-induced psychoses: A critical review of the literature. Curr. Drug Abus. Rev. 2011, 4, 228–240. [Google Scholar] [CrossRef] [PubMed]
  26. Widing, L.; Simonsen, C.; Flaaten, C.B.; Haatveit, B.; Vik, R.K.; Wold, K.F.; Åsbø, G.; Ueland, T.; Melle, I. Symptom Profiles in Psychotic Disorder Not Otherwise Specified. Front. Psychiatry 2020, 11, 580444. [Google Scholar] [CrossRef] [PubMed]
  27. Stokes, P.R.; Mehta, M.A.; Curran, H.V.; Breen, G.; Grasby, P.M. Can recreational doses of THC produce significant dopamine release in the human striatum? NeuroImage 2009, 48, 186–190. [Google Scholar] [CrossRef]
  28. Weinstein, A.M. A brain imaging study of dopamine receptor D2 availability in cannabis dependent users after recovery from cannabis-induced psychosis. Front. Psychiatry 2023, 14, 1230760. [Google Scholar] [CrossRef] [PubMed]
  29. Kohno, M.; Dennis, L.E.; McCready, H.; Hoffman, W.F. Dopamine dysfunction in stimulant use disorders: Mechanistic comparisons and implications for treatment. Mol. Psychiatry 2022, 27, 220–229. [Google Scholar] [CrossRef]
  30. Hides, L.; Dawe, S.; McKetin, R.; Kavanagh, D.J.; Young, R.M.; Teesson, M.; Saunders, J.B. Primary and substance-induced psychotic disorders in methamphetamine users. Psychiatry Res. 2015, 226, 91–96. [Google Scholar] [CrossRef]
  31. van Dee, V.; Kia, S.M.; Winter-van Rossum, I.; Kahn, R.S.; Cahn, W.; Schnack, H.G. Revealing the impact of psychiatric comorbidities on treatment outcome in early psychosis using counterfactual model explanation. Front. Psychiatry 2023, 14, 1237490. [Google Scholar] [CrossRef]
  32. Urits, I.; Gress, K.; Charipova, K.; Li, N.; Berger, A.A.; Cornett, E.M.; Hasoon, J.; Kassem, H.; Kaye, A.D.; Viswanath, O. Cannabis Use and its Association with Psychological Disorders. Psychopharmacol. Bull. 2020, 50, 56–67. [Google Scholar] [PubMed]
  33. Blanco, C.; Hasin, D.S.; Wall, M.M.; Flórez-Salamanca, L.; Hoertel, N.; Wang, S.; Kerridge, B.T.; Olfson, M. Cannabis Use and Risk of Psychiatric Disorders: Prospective Evidence from a US National Longitudinal Study. JAMA Psychiatry 2016, 73, 388–395. [Google Scholar] [CrossRef] [PubMed]
  34. Murrie, B.; Lappin, J.; Large, M.; Sara, G. Transition of Substance-Induced, Brief, and Atypical Psychoses to Schizophrenia: A Systematic Review and Meta-analysis. Schizophr. Bull. 2020, 46, 505–516. [Google Scholar] [CrossRef] [PubMed]
  35. Myran, D.T.; Harrison, L.D.; Pugliese, M.; Solmi, M.; Anderson, K.K.; Fiedorowicz, J.G.; Perlman, C.M.; Webber, C.; Finkelstein, Y.; Tanuseputro, P. Transition to Schizophrenia Spectrum Disorder Following Emergency Department Visits Due to Substance Use with and without Psychosis. JAMA Psychiatry 2023, 80, 1169–1174. [Google Scholar] [CrossRef] [PubMed]
  36. Sara, G.E.; Burgess, P.M.; Malhi, G.S.; Whiteford, H.A.; Hall, W.C. The impact of cannabis and stimulant disorders on diagnostic stability in psychosis. J. Clin. Psychiatry 2014, 75, 349–356. [Google Scholar] [CrossRef]
  37. Sass, L.A.; Parnas, J. Schizophrenia, Consciousness, and the Self. Schizophr. Bull. 2003, 29, 427–444. [Google Scholar] [CrossRef]
  38. de Clérambault, G.G. Automatisme mental et scission du moi. In Oeuvres Psychiatriques; Frénésie Éditions: Paris, France, 1987; pp. 457–467. [Google Scholar]
  39. Messas, G. Plea for Using Dialectical Phenomenological Psychopathology as an Approach for Substance-Use Disorders. Clin. Neuropsychiatry 2021, 18, 185–187. [Google Scholar]
  40. Di Petta, G.; Tittarelli, D. Le Psicosi Sintetiche. Il Contributo Della Psicopatologia Fenomenologica Italiana Alle Psicosi Indotte da Sostanze; Giovanni Fioriti Editore: Roma, Italy, 2016. [Google Scholar]
  41. Ricci, V.; Maina, G.; Martinotti, G. The Loss of Spatiality and Temporality in Twilight Consciousness: The Emergence of Exogenous Psychosis Induced by Novel Psychoactive Substances. Psychopathology 2024, 57, 248–258. [Google Scholar] [CrossRef]
  42. Hasson-Ohayon, I.; Gumley, A.; McLeod, H.; Lysaker, P.H. Metacognition and Intersubjectivity: Reconsidering Their Relationship Following Advances from the Study of Persons with Psychosis. Front. Psychol. 2020, 11, 567. [Google Scholar] [CrossRef]
  43. Lysaker, P.H.; Cheli, S.; Dimaggio, G.; Buck, B.; Bonfils, K.A.; Huling, K.; Wiesepape, C.; Lysaker, J.T. Metacognition, social cognition, and mentalizing in psychosis: Are these distinct constructs when it comes to subjective experience or are we just splitting hairs? BMC Psychiatry 2021, 21, 329. [Google Scholar] [CrossRef]
  44. Fett, A.J.; Hanssen, E.; Eemers, M.; Peters, E.; Shergill, S.S. Social isolation and psychosis: An investigation of social interactions and paranoia in daily life. Eur. Arch. Psychiatry Clin. Neurosci. 2022, 272, 119–129. [Google Scholar] [CrossRef] [PubMed]
  45. Strauss, L.; Brink, C.B.; Möller, M.; Stein, D.J.; Harvey, B.H. Late-life effects of chronic methamphetamine exposure during puberty on behaviour and corticostriatal monoamines in social isolation-reared rats. Dev. Neurosci. 2014, 36, 18–28. [Google Scholar] [CrossRef] [PubMed]
  46. Wright, A.C.; Browne, J.; Cather, C.; Meyer-Kalos, P.; Mueser, K.T. Relationship between patterns of cannabis use and functional and symptomatic trajectories in first-episode psychosis. Eur. Arch. Psychiatry Clin. Neurosci. 2023, 273, 765–778. [Google Scholar] [CrossRef] [PubMed]
  47. Ricci, V.; Maina, G.; Martinotti, G. Dissociation and Temporality in Substance Abuse: A Clinical Phenomenological Overview. Psychopathology 2024, 57, 219–228. [Google Scholar] [CrossRef] [PubMed]
  48. Ricci, V.; Maina, G.; Di Petta, G.; Martinotti, G. The Resurgence of Exogenous Psychosis: A Phenomenological Examination of Substance-Induced Psychopathology. J. Nerv. Ment. Dis. 2024, 212, 457–459. [Google Scholar] [CrossRef]
  49. Masih, S. Madness and Otherness: Moments of Possibility. Psychoanal. Rev. 2020, 107, 175–195. [Google Scholar] [CrossRef]
  50. Klosterkötter, J. Früherkennung und Frühbehandlung von Psychosen [Early recognition and prevention of psychoses]. Fortschritte Der Neurol. Psychiatr. 2009, 77, 431. [Google Scholar] [CrossRef]
  51. Windt, J.M.; Noreika, V. How to integrate dreaming into a general theory of consciousness—A critical review of existing positions and suggestions for future research. Conscious. Cogn. 2011, 20, 1091–1107. [Google Scholar] [CrossRef]
  52. Huber, G.; Gross, G. The concept of basic symptoms in schizophrenic and schizoaffective psychoses. Recent. Progress. Med. 1989, 80, 646–652. [Google Scholar]
  53. Nelson, B.; McGorry, P.D.; Fernandez, A.V. Integrating clinical staging and phenomenological psychopathology to add depth, nuance, and utility to clinical phenotyping: A heuristic challenge. Lancet Psychiatry 2021, 8, 162–168. [Google Scholar] [CrossRef]
  54. Messas, G.; Tamelini, M.; Mancini, M.; Stanghellini, G. New Perspectives in Phenomenological Psychopathology: Its Use in Psychiatric Treatment. Front. Psychiatry 2018, 9, 466. [Google Scholar] [CrossRef] [PubMed]
  55. Papaseit, E.; Farré, M.; Schifano, F.; Torrens, M. Emerging drugs in Europe. Curr. Opin. Psychiatry 2014, 27, 243–250. [Google Scholar] [CrossRef] [PubMed]
  56. Raballo, A.; Poletti, M.; Preti, A. The temporal dynamics of transition to psychosis in individuals at clinical high-risk (CHR-P) shows negative prognostic effects of baseline antipsychotic exposure: A meta-analysis. Transl. Psychiatry 2023, 13, 112. [Google Scholar] [CrossRef] [PubMed]
  57. Rognli, E.B.; Taipale, H.; Hjorthøj, C.; Mittendorfer-Rutz, E.; Bramness, J.G.; Heiberg, I.H.; Niemelä, S. Annual incidence of substance-induced psychoses in Scandinavia from 2000 to 2016. Psychol. Med. 2023, 53, 5246–5255. [Google Scholar] [CrossRef] [PubMed]
  58. Dudley, R.; Dodgson, G.; Common, S.; O’Grady, L.; Watson, F.; Gibbs, C.; Arnott, B.; Fernyhough, C.; Alderson-Day, B.; Ogundimu, E.; et al. Managing Unusual Sensory Experiences in People with First-Episode Psychosis (MUSE FEP): A study protocol for a single-blind parallel-group randomised controlled feasibility trial. BMJ Open 2022, 12, e061827. [Google Scholar] [CrossRef]
  59. Murray, R.M.; Quigley, H.; Quattrone, D.; Englund, A.; Di Forti, M. Traditional marijuana, high-potency cannabis and synthetic cannabinoids: Increasing risk for psychosis. World Psychiatry Off. J. World Psychiatr. Assoc. (WPA) 2016, 15, 195–204. [Google Scholar] [CrossRef]
  60. Schoeler, T.; Monk, A.; Sami, M.B.; Klamerus, E.; Foglia, E.; Brown, R.; Camuri, G.; Altamura, A.C.; Murray, R.; Bhattacharyya, S. Continued versus discontinued cannabis use in patients with psychosis: A systematic review and meta-analysis. Lancet Psychiatry 2016, 3, 215–225. [Google Scholar] [CrossRef]
  61. Ricci, V.; De Berardis, D.; Maina, G. Third-Generation Antipsychotics and Lurasidone in the Treatment of Substance-Induced Psychoses: A Narrative Review. Healthcare 2024, 12, 339. [Google Scholar] [CrossRef]
  62. Chiappini, S.; Cavallotto, C.; Mosca, A.; Di Carlo, F.; Piro, T.; Giovannetti, G.; Pasino, A.; Vicinelli, M.; Lorenzini, C.; Di Paolo, M.; et al. Investigating the Effectiveness of Brexpiprazole in Subjects with Schizophrenia Spectrum Illness and Co-Occurring Substance Use Disorder: A Prospective, Multicentric, Real-World Study. Pharmaceuticals 2024, 17, 535. [Google Scholar] [CrossRef]
Table 1. Comparative overview of substance-induced psychosis (SIP) and primary psychotic disorders.
Table 1. Comparative overview of substance-induced psychosis (SIP) and primary psychotic disorders.
Primary Psychotic DisordersSubstance-Induced Psychosis (SIP)
EtiologyComplex interplay of genetic, neurodevelopmental, and environmental factors [21]Direct effects of acute or chronic use of psychoactive substances (cannabis, cocaine, LSD, etc.) [36]
NeurobiologyPersistent alterations in dopamine, glutamate, and GABA circuits and long-term structural and functional abnormalities (e.g., reduced gray matter in the brain) [20]Temporary disruptions in dopamine and serotonin pathways due to substance use. Transient neurobiological effects linked to substance use that can become chronic with persistent use [15]
Clinical presentationGradual onset with a prodromal phase (social withdrawal, cognitive decline). Hallucinations auditive, delusions, disorganized thinking, chronic cognitive deficits [20]Rapid onset of psychotic symptoms following substance use, with variable intensity depending on the substance, predominantly characterized by agitation, aggression, paranoid delusions, and intense and transient visual hallucinations [6]
Self-awarenessPoor self-awareness, with passivity towards symptoms [37,38]Partial self-awareness with insight [37,38]
Course of illnessChronic and relapsing course, with phases of exacerbation and remission [39]Generally transient, with symptoms resolving after abstinence [39]
PrognosisGuarded prognosis, even with pharmacological and psychosocial interventions [39}Good with abstinence [39]
Risk factors for chronicityGenetic predisposition, persistent neurobiological changes, number of relapses, and duration of untreated illness [6]Young age at first intake, frequency of use, and type of substances consumed (particularly those with strong psychostimulant effects) [6]
Table 2. Overview of the key features of mental automatism as described by de Clérambault, categorized into ideo-verbal, sensory, motor, and psychic automatisms in psychosis-related substances.
Table 2. Overview of the key features of mental automatism as described by de Clérambault, categorized into ideo-verbal, sensory, motor, and psychic automatisms in psychosis-related substances.
CategoryKey Features
Ideo-Verbal Automatism- Core or “nuclear” syndrome
- Voices, often threatening, auditory–verbal hallucinations
- Full range of hallucinations and pseudo-hallucinations, including thought echo, thought withdrawal, and thought insertion
- These intrusive thoughts are perceived as alien and disruptive to normal cognitive processes, leading to confusion and distress parasitism and restriction of thought processes (coarctation)
- Passivity, interference, thought alienation, and ideation imposed by external forces [38]
Sensory Automatism- Visual, gustatory, olfactory, and kinesthetic (bodily) hallucinations—tingling, itching, or sensations perceived as being externally imposed (parasitism of abnormal perceptions)
- Kinesthetic disturbances, where patients feel their body is acting or moving without their control [37,38]
Motor Automatism- Motor phenomena, such as involuntary movements or forced actions
- Sudden movements or jerks that are experienced as being imposed by an external force
- Patients may feel helpless as these actions unfold without their control, often leading to agitation and distress [38]
Delusional Interpretations- Delusions often emerge as a secondary response to automatic phenomena. Patients attempt to make sense of the strange, involuntary experiences by attributing them to external causes (e.g., thought insertion)
- Delusional identities can form after an “incubation period” of confusion and conflicting thoughts [38,39,40,41,42,43,44,45,46,47]
Psychic Automatism- Includes non-sensory disruptions in thought, where patients experience duplications of their thoughts in time and space (thought echo) without initially feeling distress
- Often, these subtle psychic disturbances precede more overt psychotic symptoms like delusions or hallucinations [38]
Clinical Significance- Mental automatism is the core mechanism of psychosis according to de Clérambault. These automatisms are seen as a precursor to the emergence of delusions and other psychotic features
- The patient’s awareness of their automatism contrasts with their lack of control, often resulting in heightened anxiety, aggression, or social withdrawal [38,39,40,41,42,43,44,45,46,47,48,49,50,51,52,53,54,55,56,57]
Table 3. Phenomenological dimensions of the twilight state of consciousness, a transitional phase induced by psychoactive substances.
Table 3. Phenomenological dimensions of the twilight state of consciousness, a transitional phase induced by psychoactive substances.
DimensionsKey Features
DefinitionA transitional phase of consciousness between wakefulness and sleep, reality and fantasy, often induced by psychoactive substances [40]
ConsciousnessNarrowing of consciousness with heightened sensory awareness. Individuals may experience a focused but altered perception of reality [40]
SpatialitySpatial perception becomes distorted, often resulting in disorientation or a sense of bodily dissociation, sometimes leading to feelings of merging with the environment [41]
TemporalityTime perception is often fragmented, with experiences of time fixed in a single moment. Modes of the intrafestum [46,47]
IntersubjectivitySeverely impaired social interactions, with individuals often feeling isolated, paranoid, or mistrustful. Paranoid delusions and ideas of reference are common [42,43,44,45]
HallucinationsAuditory and visual hallucinations are prevalent, often accompanied by a profound sense of unreality [54]
Clinical SignificanceThe twilight state plays a crucial role in the progression from substance use to psychosis, marking a key transition in the development of symptoms [40,41]
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Ricci, V.; Martinotti, G.; Maina, G. Substance-Induced Psychosis: Diagnostic Challenges and Phenomenological Insights. Psychiatry Int. 2024, 5, 759-772. https://doi.org/10.3390/psychiatryint5040052

AMA Style

Ricci V, Martinotti G, Maina G. Substance-Induced Psychosis: Diagnostic Challenges and Phenomenological Insights. Psychiatry International. 2024; 5(4):759-772. https://doi.org/10.3390/psychiatryint5040052

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Ricci, Valerio, Giovanni Martinotti, and Giuseppe Maina. 2024. "Substance-Induced Psychosis: Diagnostic Challenges and Phenomenological Insights" Psychiatry International 5, no. 4: 759-772. https://doi.org/10.3390/psychiatryint5040052

APA Style

Ricci, V., Martinotti, G., & Maina, G. (2024). Substance-Induced Psychosis: Diagnostic Challenges and Phenomenological Insights. Psychiatry International, 5(4), 759-772. https://doi.org/10.3390/psychiatryint5040052

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