The Concept of Autism in Autism Spectrum Disorder and Schizophrenia Spectrum Disorder: Historical Divergence and Phenomenological Rapprochement

Abstract

This study aims to trace the historical origins and conceptual divergence of “autism” as employed in autism spectrum disorder (ASD) and schizophrenia spectrum disorder (SSD), and to examine their recent rapprochement through the lens of phenomenological psychopathology. A narrative review was conducted to analyze primary historical sources, including works by Bleuler, Kanner, and their predecessors, along with contemporary literature on neurodevelopmental perspectives, social cognition, and phenomenological psychopathology. The analysis focused on comparing the structures of self-experience between patients with ASD and those with SSD using frameworks such as ipseity disturbance and anomalous self-experience. Bleuler’s “Autismus” (1911) denoted active withdrawal from reality and construction of an inner fantasy world in schizophrenia, whereas Kanner’s “infantile autism” (1943) described innate deficits in forming affective bonds. Despite strict diagnostic separation since DSM-III, recent research reveals shared genetic pathways, social cognitive impairments, and clinical presentations. Phenomenological analysis revealed that while both conditions share common predicaments in being-in-the-world, they manifest qualitatively distinct patterns of self-disorder. Patients with SSD exhibit ipseity disturbance characterized by instability of the minimal self, diminished self-affection, and hyperreflexivity, whereas patients with ASD generally show preserved minimal self but deficient intersubjective attunement. Social withdrawal in SSD represents a defensive retreat against ontological anxiety and self-dissolution, whereas in ASD it reflects involuntary isolation arising from impaired intuitive connections with others. ASD and SSD share common predicaments in being-in-the-world, yet manifest qualitatively distinct forms of self-disorder. This phenomenological framework offers a promising transdiagnostic approach for clarifying the relationship between these two conditions and understanding the essence of “autism.”

INTRODUCTION

In contemporary usage, the term “autism” commonly refers to autism spectrum disorder (ASD). However, in the history of psychiatry, this term originally designated an entirely different concept. When Eugen Bleuler coined “Autismus” in 1911 as one of the four cardinal symptoms of schizophrenia, he intended it to denote a structural transformation in which patients sever their relationship with external reality and become absorbed in an inner world of fantasy. In contrast, when Leo Kanner first employed the term “infantile autism” in his seminal paper published three decades later, he defined it as a developmental disorder characterized by the inability to form affective bonds with other people. Despite the fundamental distinction between acquired withdrawal from reality and innate deficit, the use of the same term for these two concepts has engendered conceptual confusion and heated debates throughout the history of psychiatry [1,2].

Bleuler’s “Autismus” (hereafter, his concept of autism will be designated as “Autismus”) and Kanner’s “autism” have been separated both conceptually and diagnostically since the 1970s. However, they have been increasingly investigated through shared theoretical frameworks encompassing social cognition, theory of mind (ToM), intersubjectivity, and the embodied self. This tendency has become particularly pronounced as the diagnostic categories of both conditions have expanded into ASD and schizophrenia spectrum disorder (SSD), respectively.

This trend raises the question of whether ASD and SSD genuinely overlap at a more fundamental level, or whether confusion has simply arisen from the conflation of the term “autism.” Moreover, as infantile autism came to overshadow the concept of Autismus, the latter was marginalized from scholarly attention, and the phenomenological pathology Bleuler sought to capture—namely, the relational collapse between reality, world, and self—remained insufficiently explored [3]. Recent research trends, however, suggest that the two meanings of “autism” are once again converging. Studies in genetics, neurobiochemistry, and neurophysiology have highlighted shared pathophysiological substrates, whereas research on social cognition and ToM has revealed considerable overlap between the two conditions. Furthermore, with the emergence of “self-disorder” as a concept in phenomenological psychopathology, the possibility has been raised that ASD, like SSD, may not represent a mere deficit in sociality but rather a differently structured self-world relationship [4].

The present study aimed to examine, from a genealogical perspective, how Bleuler’s and Kanner’s concepts of autism were born, diverged, and have recently undergone rapprochement. Through this investigation, we seek to clarify these two concepts of autism and attempt to reinterpret the similarities and differences between ASD and SSD through the lens of anomalous self-experiences.

METHODS

This study was conducted as part of a narrative review. The original idea was drawn from two key sources: Henriksen et al. [3], who reappraised Bleuler’s concept of Autismus through the lens of phenomenological psychopathology, and Jeličić et al. [5], who examined self-disorder as a transdiagnostic construct bridging ASD and SSD. These works served as the point of departure, and their reference lists provided an initial corpus of relevant literature.

Literature was identified primarily through PubMed using combinations of the following search terms: “autism,” “autistic disorder,” “schizophrenia,” “Bleuler,” “Kanner,” “phenomenology,” and “self.” No formal date restrictions were imposed. The search was supplemented by backward citation tracking: references cited in the seed articles were retrieved, and the bibliographies of those secondary sources were examined iteratively, thereby expanding the corpus of the reviewed literature.

Tracing the conceptual development process for more than a century, the source material extends beyond indexed journal articles. Book chapters, monographs, and other scholarly texts that were not indexed in PubMed were also consulted when they constituted primary or authoritative sources of historical claims. Although the review draws predominantly on English-language publications, selected works in German and French were included where necessary to document the original citations of key historical figures (e.g., Bleuler, Minkowski, Lévinas).

No formal inclusion or exclusion criteria, quality appraisal procedures, or systematic search protocols were applied, which is consistent with narrative review methodology. The selection and synthesis of literature were guided by the overarching purpose of the study: tracing the genealogy of the concept of “autism” across ASD and SSD, and examining their convergence and divergence through phenomenological constructs. Sources were prioritized based on their conceptual relevance, historical significance, and contribution to understanding the phenomenological dimensions of both conditions.

THE BIRTH AND DIVERGENCE OF THE TWO AUTISMS

Bleuler’s Autismus

The origins of the Autismus

The late 19th and early 20th centuries marked tumultuous periods for both biological and dynamic psychiatry. In this era, Emil Kraepelin delineated “dementia praecox” with a focus on the course and prognosis of the illness. Bleuler, however, directed his attention to the “content” and “meaning” of symptoms, proposing the diagnostic term “schizophrenia.” His 1911 monograph, “Dementia Praecox or the Group of Schizophrenias,” introduced the concept of “Autismus” alongside the term schizophrenia [6].

In this monograph, Bleuler explicitly acknowledged that “Autismus” was derived from “auto-erotism,” a term proposed by British sexologist Havelock Ellis [6]. In his 1898 paper [7], Ellis defined auto-erotism as “sexual emotion or excitement arising spontaneously from within, without external stimulus from an object.” In 1905, Freud adopted Ellis’ concept as the cornerstone of his theory of infantile sexuality, explicating auto-erotism as a stage preceding primary narcissism [8].

Bleuler inherited this term from Freud, yet he did not follow Freud’s overemphasis on sexuality [9]. Instead, he embraced Jung’s view that withdrawal from reality might stem from “feeling-toned complexes” [9,10]. Accordingly, Bleuler coined the term “Autismus” by removing “erotism” to diminish the sexual connotation and appending the suffix “-ismus.”

“The detachment from reality, together with the relative or absolute predominance of the inner life, we term autism (Autismus)” [6].

Bleuler was profoundly influenced by the French psychologist Pierre Janet, to the extent that he named “schizophrenia” drawing upon Janet’s concept of “dissociated consciousness.” Concurrently, he adopted Janet’s concept of “Fonction du Réel (function of the real),” which denotes “the function of integrating perceptual stimuli from the external world to construct reality” [9,10]. Bleuler explained Autismus as “the function of actively constructing an alternative reality to evade maladaptation to reality.” He believed that patients possess the capacity to perceive reality; rather, because reality is excessively painful, they actively generate fantasies. This alternative reality coexists with the actual reality, but patients remain unaware of the contradiction between the two realities. French psychiatrist Eugène Minkowski described this situation as “double bookkeeping (double comptabilité)” [11].

Refinement of the concept

Bleuler devoted considerable efforts to refining this concept. Gündel and Rudolf [1] argued that Bleuler distinguished two types of autism. The first is “normal autism,” encompassing daydreaming, children’s play, artistic fantasy, and religious meditation. This represents a temporary and controlled departure from reality, and may function as a resource for creative capacity and psychological resilience. The second is “schizophrenic autism (Autismus),” which refers to a pathological state in which the reality principle collapses and fantasy and delusion overwhelm external reality. While the former aligns with Jung’s concept of “introversion,” the latter is pathological in that its connection with reality is fundamentally severed. Accordingly, autism should be understood not as a mere individual symptom or personality trait, but as a global deformation of self-structure [12].

Researchers have attempted to integrate Bleuler’s concept of Autismus with the tradition of phenomenological psychopathology [3]. In a patient’s subjective world, reality does not disappear; rather, the capacity to engage with reality is impaired. This echoes French philosopher Emmanuel Lévinas’s remark: “The [other’s] face is present in its refusal to be comprehended…” [13]. Patients cannot decode others’ intentions or find themselves in a state of anti-empathy or aempathy [3]. This fundamental alienation was subsequently taken up by phenomenological psychiatrists, notably Minkowski, through the concept of “self-disorder,” and has been reestablished as a core phenotype of the schizophrenia spectrum [3,12,14].

Kanner and infantile autism

Pioneering figures

Hans Asperger of Austria and Leo Kanner of the United States have long been regarded as the first to provide clinical descriptions of infantile autism; however, a closer examination of the historical records reveals the pioneering researchers who preceded them. The German psychiatrist, Fritz Künkel, analyzed the developmental histories of 100 pediatric patients diagnosed with childhood schizophrenia and categorized them into four patterns: pedantic, asocial, hypersensitive, and autistic types [15,16]. He particularly emphasized “disturbance in the affective domain” manifested in the autistic group to be the core pathology. Meanwhile, the Soviet psychiatrist Grunya Sukhareva reported the clinical cases of six boys who met the diagnostic criteria for what is now recognized as ASD. This study was written in Russian in 1925 and translated into German the following year; however, owing to linguistic barriers and gender biases prevalent in academia, it received scant attention outside the Soviet Union [17-19].

Sukhareva judged that a diagnosis of schizophrenia was inappropriate for these children and proposed that the condition should be termed “schizoid psychopathy.” Under the section titled “An autistic attitude” in her 1926 paper, she described: “All affected children keep themselves apart from their peers, find it hard to adapt to, and are never fully themselves among other children… All these children manifest a tendency towards solitude and avoidance of other people from early childhood onwards” [17,20]. It was not until 1959 that Sukhareva renamed the condition from “schizoid psychopathy” to “autistic psychopathy” [21].

The state of child psychiatry

Despite Sukhareva’s contributions, child psychiatry at the time relied heavily on the broad and ambiguous diagnostic categories of “childhood schizophrenia.” This diagnosis has been broadly applied to children exhibiting social withdrawal, stereotyped behaviors, inappropriate affect, and hallucinatory or delusional thinking. As a result, heterogeneous conditions including what we now recognize as ASD were subsumed under “childhood schizophrenia.” For instance, the American psychiatrist Lauretta Bender, in her paper “Clinical Study of One Hundred Schizophrenic Children” [22], described children with varied presentations of schizophrenia, many of whom would today meet the criteria for Kanner’s infantile autism.

J. Lous Despert distinguished patients with childhood schizophrenia with acute onset from those with insidious onset [23], with the latter bearing a striking resemblance to the clinical presentation of infantile autism. However, Despert maintained that, although these children may have displayed autistic tendencies prior to onset, they had clearly undergone a period of normal development. In his seminal paper [24], Kanner challenged this opinion. A careful examination of his developmental history revealed no evidence of a prior period of normal development. He became convinced that these children had been autistic since birth and that their condition could be clearly distinguished from childhood schizophrenia.

The emergence of infantile autism

Despite the geographical distance and wartime circumstances that separated Austria and the United States in the 1940s, Asperger and Kanner were able to formulate the concept of ASD almost simultaneously. This was made possible by Georg Frankl, who served as a link between them [16,25]. In the early 1930s, when Asperger was training under Frankl’s supervision, Frankl was conducting research on children who exhibited deficits in social interactions. In his 1933 paper “Ordering and Obeying” [26], Frankl reported that certain children comprehend the semantic content of language but fail to understand its affective nuances [27].

Based on this intellectual background, Asperger’s syndrome emerged. Asperger had already employed the term “Autistic Psychopathy” in a lecture delivered in 1938 [25], and the same terminology appeared in his 1944 paper “Autistic Psychopathy in Childhood” [28]. In 1937, Frankl emigrated to the United States and subsequently worked with Kanner at Johns Hopkins Hospital. In 1943, the journal “Nervous Child” published papers by Frankl and Kanner in succession: Frankl’s paper was entitled “Language and Affective Contact” [29], and Kanner’s “Autistic Disturbances of Affective Contact” [24]. This similarity in titles suggests that Kanner drew upon Frankl’s ideas.

Kanner does not directly cite the works of Sukhareva and Asperger. However, considering the scholarly context, it is reasonable to assume that Sukhareva’s “autistic tendency” and Asperger’s “autistic psychopathy” combined with Frankl’s “affective contact” to crystallize into “Autistic Disturbances of Affective Contact,” that is, infantile autism. In his 1943 paper, Kanner wrote the following:

“We must, therefore, assume that these children have come into the world with an innate inability to form the usual, biologically provided affective contact with people, just as other children come into the world with innate physical or intellectual handicaps. This is the essence of the condition, the ‘extreme autistic aloneness’” [24].

Kanner appears to have recognized that the phenomenon of “extreme autistic aloneness” could apply to both infantile autism and childhood schizophrenia. In his 1949 paper [30], he wrote, “The extreme emotional isolation from other people, which is the foremost characteristic of early infantile autism, bears so close a resemblance to the schizophrenic withdrawal that a relationship between the two conditions deserves serious consideration.” However, in a 1965 lecture, he noted, “This definition [Bleuler’s Autismus] is not adequate to explain the condition of our patients. Withdrawal refers to a retreat from previous participation, but these children have never participated in the first place,” thus pointing to the limitations encountered in applying the concept of autism to infantile autism [31].

Independence from childhood schizophrenia

However, not all child psychiatrists fully endorsed Kanner’s views. British psychoanalysts, notably Melanie Klein, understood the fantasy world prior to the development of logical thinking as an “autistic” state, viewing childhood psychosis as a process in which the child withdraws into autistic thinking [10]. Klein presented the case of a 4-year-old patient, arguing that schizophrenia could develop even at this age and that children regress to autistic defenses due to anxiety about their internal sadistic fantasies [32].

However, a critical turning point occurred during the 1960s. As mental health legislation was enacted and deinstitutionalization progressed, primarily in Britain and the United States, the need for objective statistical data on mental illness emerged. This development prompted a departure from ambiguous psychoanalytic concepts toward objectively assessable behavioral signs. For example, Lotter [33] restructured autism as a constellation of indicators measured by external observers. However, more rigorous criteria are required for infantile autism to achieve independence from childhood schizophrenia. At that time, clinicians tended to assume that children were hearing voices or absorbed in fantasies if they exhibited behaviors such as difficulty maintaining attention in stimulating environments or staring in space. Israel Kolvin [34] challenged this practice, arguing: “Behavior that merely appears to involve hearing voices cannot be diagnosed as a hallucination. The child must report hallucinations verbally; otherwise, the presence of hallucinations should not be assumed.” Accordingly, he argued that the concept of “psychosis” should no longer be applied to pediatric patients with insufficient language development.

The introduction of DSM-III marked a definitive rupture. DSM-III positioned infantile autism as a subcategory of “pervasive developmental disorder” and explicitly specified the age of onset as prior to 30 months, thereby abandoning the tradition of diagnosing this condition as early-onset childhood schizophrenia. Simultaneously, by requiring childhood schizophrenia to have an onset no earlier than 5 years and the required presence of hallucinations or delusions, the DSM-III definitively established the boundary between the two diagnoses. Thus, the two conditions were separated into distinct entities across all dimensions: developmental trajectory, pathological mechanism, core symptoms, and therapeutic approach.

RAPPROCHEMENT BETWEEN ASD AND SSD

Since the DSM-III, the concept of infantile autism has undergone successive expansion through a proliferation of diagnostic labels such as autistic disorder, Asperger’s disorder, pervasive developmental disorder-not otherwise specified (PDD-NOS), and others; however, ASD and SSD have remained consistently separated into distinct categories. This began to shift when DSM-5 introduced the spectrum concept, and the two diagnostic categories have now entered a stage reminiscent of Margaret Mahler’s “rapprochement” phase: neither fully separated nor fully integrated, the two categories cautiously approach one another.

ASD and SSD overlap considerably at both the biological and clinical levels, including shared genetic vulnerability pathways, phenotypic similarities, and high rates of comorbidity [35,36]. Furthermore, various frameworks for understanding social cognition—such as ToM, mirror neuron system dysfunction, and impairments in common sense—have been actively explored in both conditions, bringing previously overlooked commonalities back into focus [37]. Additionally, with the rise of “self-disorder” as a concept in phenomenological psychopathology, both ASD and SSD have come to be discussed within a shared framework of structural alterations in subjectivity and self-experience.

Reappraisal from a neurodevelopmental perspective

Kanner emphasized that infantile autism is innate, and sought to distinguish it from childhood schizophrenia, which he regarded as an acquired condition. However, this demarcation has progressively weakened with the emergence of the neurodevelopmental hypothesis, which traces the origin of schizophrenia to abnormalities in fetal or early postnatal brain development [38,39]. If schizophrenia is indeed rooted in early development, age-based distinctions become untenable. The implicated risk factors, genetic abnormalities, maternal infections, and perinatal complications overlap substantially with those of autism [40].

Genetic overlap and shared etiology

The close relationship between these two conditions is supported by the presence of overlapping genetic risk factors. Large-scale genomic studies have shown that shared genetic variants can simultaneously increase the risk of ASD and SSD [41]. Genome-wide association studies have identified significant genetic correlations and common variants at single loci that affect both disorders [42].

This overlap was particularly pronounced for the rare variants and copy number variations. Rare variants that increase neurodevelopmental risk, such as 16p11.2 duplications—occur at nearly identical rates (approximately 0.3%) in both the ASD and SSD populations [36]. Moreover, single variants such as 22q11.2 microdeletion syndrome can manifest as autistic features in childhood and psychotic features from young adulthood onward [43]. This suggests that the same genetic factors may produce divergent phenotypes depending on developmental timing or environmental context.

Neurobiological commonalities are unlikely to coincide. Some investigators have proposed that SSD reflects reduced connectivity due to excessive synaptic pruning, whereas ASD reflects hyperconnectivity due to insufficient pruning [44,45]. Although the directionality differs, both conditions share the mechanisms underlying synaptic formation and maintenance [46,47]. Similarly, 17q21.31 variants occur in both disorders but exert opposing regulatory effects on brain development, illustrating that shared genetic foundations can yield distinct clinical phenotypes [42].

Symptomatic similarities and high comorbidity

In clinical practice, distinguishing ASD from SSD based solely on symptoms and behavior is far from straightforward [48]. Patients with ASD diagnosed in adulthood display social interaction deficits that are difficult to differentiate from those with SSD [49]. While an impaired capacity to perceive others’ emotions and engage in affective exchange constitutes the cardinal feature of ASD, prominent deficits in social cognition and mentalizing are often observed in SSD [50]. Both the ASD and SSD patient groups demonstrate significantly impaired performance on tasks involving facial affect recognition, empathy, and intention inference compared to that of normal controls, with comparable degrees of impairment [50].

The autism spectrum quotient (AQ), originally developed to measure autistic traits in high-functioning individuals with autism [51], has also been employed to assess quality of life in individuals with SSD. Patients with SSD score significantly higher on total AQ than do healthy individuals, though somewhat lower than patients with ASD. However, reliably distinguishing the two conditions using this scale alone is practically impossible [52,53].

The Autism Diagnostic Observation Schedule (ADOS-2), the gold standard for ASD diagnosis, demonstrates reasonably high sensitivity and specificity when Modules 1 or 2 are applied to individuals with limited verbal ability. However, Module 4, designed for verbally fluent adults, shows considerably diminished diagnostic accuracy [54,55]. Notably, a study attempting to distinguish adult ASD from SSD using Module 4 found that the current ADOS-2 scoring algorithm failed to adequately differentiate between the two groups [56]. Meanwhile, Kästner et al. [57] devised the “PANSS Autism Severity Score” by selecting and recombining PANSS items, arguing that this measure can identify an “autistic schizophrenia” subtype within SSD. This suggests that autistic features in schizophrenia should not be regarded as exceptional but as a principal clinical characteristic.

Such symptomatic overlap is reflected in the high comorbidity rates. The odds ratio for comorbid schizophrenia in patients with ASD is approximately 3.55 (95% confidence interval [CI] 2.08–6.05) compared to that in controls [58], while the odds ratio for ASD diagnosis in patients with schizophrenia is 7.01 (95% CI 2.98–16.43) [59].

Social cognitive function

Since its emergence alongside the cognitive revolution of the 1960s and the 1970s, social cognition has been a central research topic in both ASD and SSD [50,60]. In 1985, Baron-Cohen et al. [61] first reported that children with autism exhibit deficits in ToM tasks. By the mid-1990s, Corcoran et al. [62] and Frith and Corcoran [63] applied the same framework to patients with SSD with notable findings. Likewise, patients with SSD distort others’ intentions, form persecutory delusions, and struggle with interpersonal relationships due to their inability to interpret subtle social cues. On ToM tasks such as the “Reading the Mind in the Eyes Test,” patients with ASD and SSD demonstrated nearly indistinguishable patterns of impairment [50]. Consequently, mindreading difficulty has become established as a transdiagnostic concept explaining social cognitive impairment across multiple psychiatric conditions rather than as an ASD-specific symptom.

The “mirror neuron” hypothesis has been actively examined in both conditions. In 2006, Ramachandran and Oberman [64] proposed the “Broken Mirror Hypothesis,” positing that mirror neuron system dysfunction underlies the social deficits in ASD [64,65]. This hypothesis has been swiftly applied in SSD research, in which similar neurological abnormalities have been reported [66]. Mirror neuron system abnormalities may lead to difficulty in predicting others’ behavior and weaken self-other boundaries, thereby contributing to abnormal self-experience in SSD [66].

The concept of “deficiency in common sense” also applies to both conditions. Blankenburg and Mishara [67] observed that patients with SSD “lose their natural common sense,” rendering them unable to intuitively grasp social contexts. Though traditionally employed to explain detachment from intersubjectivity in patients with SSD, this mechanism has recently been applied to ASD as well [37]. Patients with ASD struggle with social conventions and implicit rules and are impaired in context-dependent meaning inference. Phenomenological comparative studies confirm that “deficits in implicit understanding” and “difficulties with spontaneous empathy” are commonly observed in both ASD and SSD, with both populations reporting similar subjective experiences of lacking social intuition [37,68,69].

Transition to the spectrum disorder concept

Changes in diagnostic systems have played a pivotal role in the rapprochement of ASD and SSD. The DSM-5 redefines ASD boundaries by consolidating previously separate diagnoses—“Asperger’s syndrome” and “PDD-NOS”—into a single label of ASD [70]. While this change solidified the continuum concept of the “autism spectrum,” it simultaneously blurred diagnostic boundaries with other conditions [71].

As the prevalence of ASD without intellectual disability has increased in clinical practice, the similarities between its presentation and schizophrenia symptoms have received renewed attention [72]. This population may exhibit social withdrawal, blunted affect, restricted interests, and other features that phenomenologically resemble the negative symptoms of schizophrenia [73,74]. Indeed, a considerable proportion of newly diagnosed adult ASD cases have previously been classified as having a schizoid personality disorder or atypical psychosis [75,76]. Conversely, social withdrawal in patients with schizotypal personality disorder or mild psychotic symptoms may reflect autistic characteristics [77,78].

Another significant DSM-5 change is that the comorbid diagnosis of schizophrenia has become permissible. Although the ASD diagnostic criteria specify that symptoms must manifest during the “early developmental period,” this change represents a substantial paradigm shift, given that schizophrenia and infantile autism have been mutually exclusive diagnoses for half a century. This has alleviated the burden on clinicians who previously faced the either-or dilemma of selecting only one diagnosis during assessment [79].

Phenomenological turn and self-disorder

Limitations of the behavioral approach for autism diagnosis

During the 1960s and the 1970s, psychiatry undertook a behavioral turn, redefining infantile autism as a behavioral phenotype amenable to objective measurement [80]. However, this approach encountered some fundamental limitations. The behavioral approach has been criticized for focusing exclusively on externally manifested behaviors, while excluding patients’ subjective experiences [5]. Because ASD and SSD share similar behavioral patterns, behavioral signs alone cannot reveal the underlying experiential structures, presenting practical limitations for differential diagnoses [3].

As early as the 1960s, Creak [81] argued that capturing the essence of autism based solely on behavioral signs was fundamentally inadequate. Subsequently, phenomenological psychopathologists sought to comprehend autism not as mere behavioral deficit but as a qualitative difference in relation to self, others, and the world. Fuchs [82] characterized autism as a pathology of intersubjectivity, identifying the absence of embodied attunement as its core mechanism, while Zahavi and Parnas [83] sought to distinguish ASD and SSD on the grounds that SSD represents a collapse of the minimal self, while ASD constitutes a developmental problem of the social self.

Additionally, sociologist Damian Milton, himself autistic, raised the “double empathy problem,” emphasizing that the everyday difficulties experienced by patients with ASD arise not only from patients’ lack of empathy but also from a reciprocal mismatch in communication, wherein neurotypicals fail to empathize with them [84]. Building on this argument, a growing movement alongside neurodiversity advocacy has emerged to reinterpret autism as a difference rather than a mere pathology [85]. Simultaneously, affected individuals have begun to demand that society understands their subjective experiences. This has shifted the research focus toward how patients experience and constitute the self and world [83,86,87].

The structure of phenomenological self-experience

Human self-experience is a totality integrating multidimensional aspects such as “self-presence,” “being-in-the-world,” “temporal identity,” and “intersubjectivity.” Therefore, understanding phenomenological psychopathology requires a survey of how these core concepts are defined and employed.

Phenomenologically, experience comprises the subject and object of the experience, the intentionality directed toward the object, and experiential content. The core experiential subject that persists when object and content are bracketed is termed the “minimal self.” Also termed “ipseity (selfhood or ownness),” it signifies the first-person perspective through which experience is given as “mine” at a pre-reflective level.

The minimal self functions as the “primordial medium” pervading all experiences, not only in perception but also in encounters with others (intersubjectivity) and the constitution of identity (narrative self). It plays a role akin to that of a transparent ether that sustains these processes. When functioning normally, this medium remains transparent and the subject perceives the world without being conscious of the minimal self. When impaired, this causes the subject to become excessively self-conscious (hyperreflexivity) or to pathologically doubt their self-evident surroundings. In normal perception, the subject does not view objects as mere things, but always cognizes them “as something.” This characteristic is termed intentionality, and Heidegger named the relationship wherein objects are grasped as equipment “Zuhandenheit (ready-to-hand).” An object’s instrumental properties cannot be determined arbitrarily without considering social conventions and rules. Therefore, fully understanding an object requires understanding the inter-subjective context in which it is situated. Furthermore, by influencing the world through tools, the individual acquires a sense of agency and efficacy, which are essential prerequisites for participating in an intersubjective world.

When the stability of the self is compromised, entry into an intersubjective world becomes difficult. As the sense of “I” becomes diluted and the feeling that experience belongs to me grows faint, other people transform from objects of communion into opaque and intrusive presences, while things are perceived as alien objects stripped of meaning. Simultaneously, the loss of agency engenders powerlessness and the individual may be plagued by a fear of annihilation.

The narrative self emerges through a process in which the minimal self integrates itself through time and repeated experiences, mediated by the gaze of others. However, when the minimal self’s foundation is shaken, the narrative connecting past, present, and future cannot properly form. The confusion of self-identity or the peculiar philosophical rumination experienced by patients may be interpreted as a distorted attempt to reconstruct a fragmented narrative self.

Self-disorder in SSD

Interpretation of schizophrenia through self-experience has deep historical roots. In the early 20th century, Joseph Berze and Hans Walter Gruhle identified “ego disorder (Ichstörung)” as the primary symptom of schizophrenia [88]. Gruhle argued that disturbance of “self-feeling” or “self-awareness” constitutes the fundamental pathology [89]. The most influential scholar was Eugène Minkowski. Elaborating on the concept of autism, he defined schizophrenia’s essence as “loss of vital contact with reality” signifying not mere introversion or withdrawal but structural collapse at the most fundamental level of the self.

Contemporary phenomenological psychopathologists such as Parnas, Sass, and Stanghellini have conceptualized schizophrenia as a pathology of the minimal self: “ipseity disturbance” [90,91]. As criticism against the DSM checklist diagnostic system has been leveled, scholarly interest in phenomenological psychopathology has intensified. The minimal self endows all conscious experience with the sense of “mineness” or “for-me-ness,” guaranteeing the unity of experience and maintaining the boundary between “I” and “not-I.” However, the minimal self becomes unstable in patients, manifesting as two interrelated phenomena [90,91].

1) Diminished self-affection: the vitality and unity felt as subjects of experience were attenuated. Patients reported a weakened sense of presence and feelings of unreality or alienation, wherein their thoughts and actions seemed to unfold without agency.

2) Hyper-reflexivity: as the sense of presence weakens, unconscious and automatic processes such as breathing, walking, and the flow of thought become highly conscious. In this state, patients observe their bodily and mental functions as external objects. This process consumes excess cognitive resources and impedes daily functioning.

This discussion is not merely a philosophical debate but has been supported by empirical research accumulated over the past decade. A meta-analysis by Raballo et al. [92] using the “Examination of Anomalous Self-Experience (EASE)” scale showed that patients with ASD exhibited significantly higher levels of self-disorder, not only compared to that of healthy controls but also compared to that of patients with other psychiatric disorders. Notably, high levels of self-disorder were confirmed even in high-risk clinical groups at the prodromal stage and in patients with schizotypal personality disorder.

Self-disorder in ASD

Recently, a sense of self and the capacity for self-integration have emerged as core pathologies of ASD [93]. The sensory integration deficits observed in ASD suggest that embodied self-experience, the manner in which the body is experienced as a unified subject, is unstable [94,95]. Such phenomena raise the possibility that patients with ASD also exhibit fundamental disturbances in the self–world relationship [96].

Traditionally, SSD has been characterized by the dissolution of self-other boundaries, and ASD by excessive rigidity [96,97]. Unlike neurotypicals, who flexibly regulate boundaries according to the context, patients with ASD exhibit deficits in context-dependent modulation [98]. In contrast, patients with SSD readily project their own emotions onto others, or report anxiety that others will intrude upon their thoughts and feelings. These findings suggest that although ASD and SSD exhibit opposite patterns, they share a common pathology of self–other boundaries [87,96].

Recent research on self-experience in ASD has expanded, underscoring the importance of self-structure. Impairments in sensory integration [99], attenuation of embodied sense of self [100], and abnormalities in self–other boundaries [94,97] may be interpreted not as independent symptoms but as indicators of instability at the level of self-experience [5,37].

PHENOMENOLOGICAL COMPARISON OF ASD AND SSD

From a phenomenological perspective, ASD and SSD share common predicaments regarding the essential processes of being-in-the-world. However, even when both are discussed under the rubric of “self-disorder,” qualitative differences remain. Nilsson et al. [101] compared self-disorder patterns between patients with ASD and SSD using the EASE scale. The mean total EASE score was 25 points for SSD but only 7 points for ASD. Specifically, patients with ASD exhibited a disturbed sense of “mineness,” whereas patients with ASD did not question their pre-reflective sense of “I.” While both groups manifested problems in intersubjectivity, patients with SSD failed because of a collapse of the self-structure that grounds experience, whereas patients with ASD failed because of a deficit in the intuitive capacity to reach others, while the foundation of self-experience remained intact.

The minimal self

The “ipseity disturbance” often manifests as thought insertion, thought withdrawal, or sensations of one’s existence becoming transparent. However, these symptoms are rarely observed in patients with ASD. They may report alienation as if they were “aliens who have landed on the wrong planet,”; however, this alienation does not seem to reflect ipseity disturbance [5,37].

According to French psychiatrist Arthur Tatossian, schizophrenia symptoms emerge from a breakdown of the balance between the constituting self that composes the experience and the observing self that reflectively monitors it [102]. In a healthy state, these two selves are not in conflict, rendering the dual structure imperceptible. However, in SSD, observing oneself objectifies and perceives the constituting self as if it were another subject. This pathological self-duplication erodes the sense of mineness, wherein thoughts, emotions, and perceptions become detached and one feels alien. This “split within the self,” which precedes the precarious relationship with the external world, structurally distinguishes SSD from ASD.

The embodied self

SSD is often characterized by “disembodiment” [103]. This term refers to the experience wherein the patient’s body is no longer perceived as naturally inhabiting the world, but as an objectified thing or machine. This alienation leads to selfother boundaries becoming ambiguous or porous [104].

Patients with ASD also exhibit deficits in motor coordination and sensory processing. Motor dysfunction is observed in approximately 80% of children with ASD and manifests as fine and gross motor deficits, abnormal eye movements, postural instability, and balance and coordination problems. Because fluent control of one’s body is essential for maintaining a sense of self, such motor dysfunction may disrupt the embodied self [105]. Hypersensitivity or hyposensitivity to sensory stimuli is prominent in the sensory domains. Autobiographical accounts by ASD individuals with ASD frequently emphasize intense sensory experiences. They may become captivated by specific stimuli or experience distress from minor stimuli that neurotypicals can easily overlook. Furthermore, the significantly higher prevalence of synesthesia suggests that they experience a perceptual world qualitatively different from that of neurotypicals [106].

Recently, research on proprioception and interoception has been actively pursued [107]. Body signals from muscles, joints, and internal organs serve as mechanisms linking emotions and self-awareness, thereby sculpting the embodied self [105]. Interoception abnormalities have been reported in both SSD and ASD, although these findings vary across studies [108,109]. Such interoceptive deficits may lead to alexithymia, an inability to recognize one’s own emotions and a diminished capacity to resonate with others’ emotions [110,111]. This may partially explain the empathic difficulties observed in patients with SSD and ASD.

The narrative self

Patients with SSD experience a disruption of temporal continuity, which impedes maintenance of the narrative self. Patients encounter difficulties integrating the past with the present or projecting themselves onto the future, and may deny ownership of past memories or report that their personality was completely transformed at a specific point in time. This relates to the phenomenon of experiencing time not as a continuous flow, but as a fragmented collection of isolated moments [112,113].

Patients with ASD may exhibit similar difficulties in constituting the narrative self, although these primarily stem from a lack of understanding of social contexts or a diminished capacity to integrate others’ perspectives [114]. Ordinarily, forging the narrative self by weaving together memories involves incorporating the perspectives of others, especially that of parents. Patients with ASD who lack this capacity may describe their lives as a mere list of factual and concrete events. However, the capacity to recognize past memories as one’s own is generally preserved and complaints of identity discontinuity at a specific point in time are extremely rare [115].

Intersubjectivity

The intersubjectivity disturbance in SSD is closely related to the ambiguity of self-boundaries. Patients fear that the gaze or presence of others may invade or annihilate them, prompting a defensive withdrawal from social relationships. Many patients exhibit “double bookkeeping,” appearing to navigate social life adequately on the surface while maintaining an inner fantasy world, a schizoid pattern in which shared social reality and a private psychotic world coexist without integration [116].

By contrast, patients with ASD lack the means of entry into the intersubjective world [81]. As intuitive embodied attunement with others is impaired, social interaction becomes a task that demands constant cognitive effort. Social avoidance in patients with ASD stems from cognitive and sensory exhaustion rather than fear of self-loss due to the difficulty in decoding social signals. These individuals tend to rely on explicit rules rather than intuition to grasp others’ intentions.

Difference between ASD and SSD

From a phenomenological perspective, ASD and SSD share common deficits in being-in-the-world: impaired contact with others, withdrawal from the inner world, and compromised social cognition. However, even though both conditions are discussed under the category of “self-disorder,” qualitative differences cannot be overlooked.

Jeličić et al. [5] summarized these structural differences. The SSD group primarily reported that the boundary between the self and the world became ambiguous or eroded, consistent with the concept of ipseity disturbance. By contrast, the ASD group reported difficulties with “connection”—grasping others’ affects, intentions, and implicit expectations. Their most prominent characteristic was the sensation that the world was approaching rapidly and in a complex manner, leaving insufficient time for integration.

These findings suggest that the two conditions should be understood across multiple, more refined dimensions such as the regulation of self-structure, flexibility of boundaries, and the modality of sensory-cognitive integration (Table 1).

Table 1.

Phenomenological comparison of autistic features in autism spectrum disorder and schizophrenia spectrum disorder

Feature	Autism spectrum disorder (Kanner’s autism)	Schizophrenia spectrum disorder (Bleuler’s Autismus)
Core deficit	Deficit in social cognition/intuition (lack of intersubjectivity)	Instability of the minimal self (ipseity disturbance)
Self-experience	Generally preserved minimal self; stable sense of “I”	Diminished self-affection, depersonalization, ambiguity of boundaries
Cause of social withdrawal	Inability to process social signals (“mind-blindness”)	Ontological instability & hyper-reflexivity
Relationship with the world	Literal engagement; failure to grasp abstract/social nuances	Loss of natural self-evidence; “double bookkeeping” (real world and fantasy world)
Age of onset	Early developmental period (congenital), observed as “delay” or “deviation”	Primarily post-adolescence (prodromal), experienced as “change” or “rupture”

CONCLUSION

This study has undertaken a diachronic and genealogical examination of how Bleuler’s “Autismus” and Kanner’s “infantile autism” diverged historically, and how they are now converging through recent neuroscientific and clinical research. Bleuler’s Autismus signifies an active withdrawal from painful reality and the construction of an inner world, whereas Kanner’s autism denotes an innate deficit in forming affective bonds. Following the DSM, schizophrenia and infantile autism are strictly demarcated as psychosis and developmental disorders, respectively. However, recent genetic and neurobiological evidence has confirmed a considerable etiological overlap. Deficits in social cognition, ToM impairment, and clinical similarities between ASD without intellectual disability, and the negative symptoms of SSD call for a reconsideration of the dichotomy that regards these conditions as entirely separate.

Such exploration is particularly fruitful in phenomenological psychopathology. This phenomenological framework has long been applied to SSD with considerable success. However, its application to ASD is relatively recent. Nevertheless, both conditions share the predicament of being-in-the-world within the broad category of “self-disorder.”

The core pathology of SSD may be summarized as an ipseity disturbance or the collapse of the minimal self. Patients lose ownership of their experiences, undergo hyperreflexivity, observe their own functions as external objects, and experience ontological anxiety as their self-boundaries disintegrate. In contrast, in ASD, the minimal self is generally preserved, and the motivation to approach others remains intact. However, these individuals lack intuitive attunement and rely on logic and algorithms. Thus, although social withdrawal may appear superficially similar, SSD represents a defensive withdrawal to prevent self-collapse, whereas ASD constitutes involuntary isolation because of the inability to connect qualitatively distinct manifestations.

As a narrative review, this study has some limitations. First, it is not a systematic review and may present a biased perspective by relying primarily on Western psychiatric literature and phenomenological discourse. There is no basis for asserting that subjective experiences in ASD and SSD must be elucidated solely through phenomenology; a multifaceted analysis through diverse philosophical, psychological, and psychiatric perspectives is required.

Second, the content examined was largely confined to adult patients with ASD, but without intellectual disabilities. For those with limited language function, severe stereotypies with challenging behaviors or profound intellectual disabilities, the phenomenological speculations discussed here cannot be applied. Novel assessment methods must be devised to investigate self-experiences across a broader patient population. Similarly, instruments, such as the EASE, for assessing self-disorder in SSD are applicable only to patients who are capable of introspection and verbal articulation. Phenomenological assessments are difficult in patients with severe thought disorders or prominent negative symptoms. Finally, how overlapping genetic and neurobiological etiologies differentiate into distinct phenomenological manifestations remains largely unknown. Despite the many commonalities between ASD and SSD, we cannot claim to understand them properly without understanding the origins of their clinical differences.

Despite these limitations, this paper emphasizes the necessity of a transdiagnostic approach along a continuous dimension of “social brain” and “self-experience.” The term “autism” has been a source of misunderstanding within psychiatry; however, it now requires renewed attention as a key concept that enables the exploration of human subjective experience and the essence of the self. This finding does not suggest that ASD or SSD can be reduced in patients with the same disease. However, we argue that they are in a rapprochement phase, neither complete integration nor thorough separation, but are cautiously drawing together while preserving each condition’s unique identity.