IntroductionSymptoms of schizophrenia are closely related to aberrant language comprehension and production. Macroscopic brain changes seen in some patients with schizophrenia are suspected to relate to impaired language production, but this is yet to be reliably characterized. Since heterogeneity in language dysfunctions, as well as brain structure, is suspected in schizophrenia, we aimed to first seek patient subgroups with different neurobiological signatures and then quantify linguistic indices that capture the symptoms of “negative formal thought disorder”.MethodsAtlas-based cortical thickness (...) values of 66 patients with first-episode psychosis and 36 healthy controls were analyzed with hierarchical clustering algorithms to produce neuroanatomical subtypes. We then examined the generated subtypes and investigated the quantitative differences in MRS-based glutamate levels [in the dorsal anterior cingulate cortex ] as well as in three aspects of language production features: fluency, syntactic complexity, and lexical cohesion.ResultsTwo neuroanatomical subtypes among patients were observed, one with near-normal cortical thickness patterns while the other with widespread cortical thinning. Compared to the subgroup of patients with relatively normal cortical thickness patterns, the subgroup with widespread cortical thinning was older, with higher glutamate concentration in dACC and produced speech with reduced mean length of T-units and lower repeats of content words, despite being equally fluent.ConclusionWe characterized a patient subgroup with thinner cortex in first-episode psychosis. This subgroup, identifiable through macroscopic changes, is also distinguishable in terms of neurochemistry and language behavior. This study supports the hypothesis that glutamate-mediated cortical thinning may contribute to a phenotype that is detectable using the tools of computational linguistics in schizophrenia. (shrink)

This essay selectively reviews, from an historical and philosophical perspective, the dopamine (DA) hypothesis of schizophrenia (DHS; Table 1 lists the abbreviations used in this essay). Our goal is not to adjudicate the validity of the theory—although we arrive at a generally skeptical conclusion—but to focus on the process whereby the DHS has evolved over time and been evaluated. Since its inception, the DHS has been the most prominent etiologic theory in psychiatry and is still referred to widely (...) in current textbooks (e.g., Buchanan and Carpenter, Jr. 2005, 1336; Cohen 2003, 225; Gazzaniga 2004, 1257;Kandel et al. 2000, 1200). Understanding its origins and evolution should help to clarify the nature of modern .. (shrink)

I defend the case for an evolutionary theory of schizophrenia and the social brain, arguing that such an exercise necessitates a broader methodology than that familiar to neuroscience. I propose a reworked evolutionary genetic model of schizophrenia, drawing on insights from commentators, buttressing my claim that psychosis is a costly consequence of sophisticated social cognition in humans. Expanded models of social brain anatomy and the spectrum of psychopathologies are presented in terms of upper and lower social brain and (...) top-down and bottom-up processes. Finally, I argue that cerebral asymmetry evolved as an emergent property of primary intrahemispheric reorganisation in hominoids. (shrink)

Crespi & Badcock (C&B) convincingly argue that autism and schizophrenia are diametric malfunctions of the social brain, but their core imprinting hypothesis is less persuasive. Much of the evidence they cite is unrelated to their hypothesis, is selective, or is overstated; their hypothesis lacks a clearly explained mechanism; and it is unclear how their explanation fits in with known aspects of the disorders.

We are gratified at the largely positive comments on our essay on the dopamine hypothesis of schizophrenia (DHS) by these two distinguished commentators from the fields of biological psychiatry (Dr. Tamminga) and the philosophy of psychiatry (Dr. Murphy). There is little that they have said with which we disagree. Rather, we want to expand briefly on their commentaries.We found Dr. Tamminga's reactions to be particularly fascinating because she has been an "insider" to the story of the DHS as (...) it has unfolded. She provides substantial insight into the "extra-scientific" reasons for the persistence of the DHS despite its poor empirical record.She validates our impression that the DHS was in its first years of .. (shrink)

A significant cluster of complaints of persons affected by schizophrenia, for example, their feeling ephemeral, lacking core identity, being affected by a diminished sense of existing as a self-present subject, point to the disruptions of structural aspects of the core self. These and similar disturbances aggregate significantly and selectively in the schizophrenia spectrum disorders, occur and are detectable in adolescents at risk of future schizophrenic disorder, and have a tendency to persist. All this led to the proposal that (...) the generative disorder in schizophrenia is a disorder of the self. The phenomenological notion of the self serves to investigate the fact that we live.. (shrink)

The claim that the disorganized subtype of schizophrenia results from glutamate hypofunction is enhanced by consideration of current subtypology of schizophrenia, symptom definition, interdependence of neurotransmitters, and the nature of the data needed to support the hypothesis. Careful specification clarifies the clinical reality of disorganization as a feature of schizophrenia and increases the utility of the subtype.

Schizophrenia is a worldwide, prevalent disorder with a multifactorial but highly genetic aetiology. A constant prevalence rate in the face of reduced fecundity has caused some to argue that an evolutionary advantage exists in unaffected relatives. Here, I critique this adaptationist approach, and review – and find wanting – Crow's “speciation” hypothesis. In keeping with available biological and psychological evidence, I propose an alternative theory of the origins of this disorder. Schizophrenia is a disorder of the social (...) brain, and it exists as a costly trade-off in the evolution of complex social cognition. Paleoanthropological and comparative primate research suggests that hominids evolved complex cortical interconnectivity (in particular, frontotemporal and frontoparietal circuits) to regulate social cognition and the intellectual demands of group living. I suggest that the ontogenetic mechanism underlying this cerebral adaptation was sequential hypermorphosis and that it rendered the hominid brain vulnerable to genetic and environmental insults. I argue that changes in genes regulating the timing of neurodevelopment occurred prior to the migration of Homo sapiens out of Africa 100,000–150,000 years ago, giving rise to the schizotypal spectrum. While some individuals within this spectrum may have exhibited unusual creativity and iconoclasm, this phenotype was not necessarily adaptive in reproductive terms. However, because the disorder shared a common genetic basis with the evolving circuitry of the social brain, it persisted. Thus schizophrenia emerged as a costly trade-off in the evolution of complex social cognition. Key Words: cortical connectivity; evolution; heterochrony; metarepresentation; primates; psychiatry; schizophrenia; social brain; social cognition. (shrink)

For more than 20 years now, the phenomenological approach to schizophrenia has developed a strong and influential hypothesis on the basic alterations of this disorder. Schizophrenia, it is claimed, is a disorder of subjectivity, and more specifically, a disorder of the minimal self. This ‘minimal self’ aims to describe the most basic or core self, which is considered to be foundational for every other kind of self. It is a form of minimal self-awareness that precedes every explicit (...) or reflective self-awareness. Based on this model, a semistructured interview has... (shrink)

The ongoing incidence of schizophrenia is considered a paradox, as the disorder has genetic basis yet confers survival handicaps. Researchers have not reached consensus regarding theories explaining this contradiction. Major evolutionary theories hypothesize that schizophrenia is: a byproduct of other evolutionary processes, linked to survival advantages that counteract disadvantages, associated with processes such as shamanism conferring advantages to groups, a consequence of modern environments, a result of random processes, such as mutations. A null hypothesis argues that philosophical (...) or methodological problems render evolutionary paradigms inappropriate. These arguments are reviewed in light of an experience-centered approach, which regards experiential accounts as data. A ritual healing theory, derived from this orientation, has bearing on evolutionary theories pertaining to schizophrenia. This theory explains the nature of shamanism, which has features coinciding with schizophrenia. The ritual healing theory is supported by folklore, medical, and anthropological evidence, is amenable to empirical evaluation, and has clinical applications. (shrink)

The disease construction of schizophrenia is no longer tenable. That construction originated during a period of rapid growth of biological science based on mechanistic principles. Crude diagnostis measures failed to differentiate absurd, unwanted conduct due to biological conditions from atypical conduct directed to solving existential or identity problems. The construction was communicated - in the absence of solid evidence - by medical practitioners by means of symbolic, rhetorical, and organizational acts. The patient came to be regarded as an object (...) without agency or goals. In spite of enormous research funding, no biological or psychological marker has been discovered that would differentiate diagnosed schizophrenics from normals without creating unacceptable proportions of false positives and false negatives. Employing a moral category, "unwanted conduct," as a criterion, and tacitly transforming moral judgments to the medical category, schizophrenia, leads to the use of schizophrenia/nonschizophrenia as the independent variable in research designs. The failure of eight decades of research to produce a reliable marker leads to the conclusion that schizophrenia is an obsolescent hypothesis and should be abandoned. (shrink)

In lieu of an abstract, here is a brief excerpt of the content:How Narrative Counts in Phenomenological Models of SchizophreniaThe author reports no conflicts of interest.Rosanna Wannberg (2024) offers an intriguing and novel critique of the predominant phenomenological model of schizophrenia, the ipseity disturbance hypothesis. According to this model, which was initially proposed by Sass and Parnas (2003), schizophrenia is best understood as arising from a disturbance or instability of minimal or basic self-hood, the sense of being (...) present to oneself and one's experiences (Henriksen, 2022). This disturbance appears as various experiential anomalies, sometimes termed "anomalous self (or world) experiences" or "self disorders," which include such phenomena as alienation from subjective processes, doubt in the existence of the world or one's own existence, fluidity of boundaries between self and others or self and world, and many other phenomena. Many of these have been captured in the Examination of Anomalous Self Experience (Parnas et al., 2005) and the Examination of Anomalous World Experience (Sass et al., 2017).At the same time, some research reveals the presence of self disorders in nonpsychotic conditions like panic disorder (Madeira et al., 2017) and depersonalization/derealization disorder (Sass et al., 2013). There are also competing phenomenological models that posit schizophrenia instead as a disturbance of dialogical self (Lysaker & Lysaker, 2002) or as a disruption of automatic perceptual processing (Uhlhaas & Mishara, 2007). Such works contain implicit critiques of the ipseity disturbance hypothesis that focus on the specificity of self disorders, or else on the specific nature of the underlying disturbance in schizophrenia.Wannberg's critique is distinct from these others: by considering the validity and function of recovery narratives, she raises crucial epistemological and ethical questions about the phenomenological approach to psychopathology, asking not only whose narrative counts, but how narrative counts. In particular, Wannberg questions a phenomenology that, she suggests, might find any ongoing symptoms as evidence of continued alterations of subjectivity, and that would then be dismissive of recovery narratives—a phenomenology that would prioritize the authority [End Page 71] of consciousness, as Wannberg puts it, over the authority of the person.It is worth stating here that the standard phenomenological response would not be to distrust or dismiss accounts of recovery. Ideally, phenomenological models, along with their ongoing theoretical developments and empirical work, are based on a deep respect for patients' experience and self-descriptions, striving to attend to experiences as they are lived without imposing pre-defined constructs that would limit or alter the experiences in a fundamental way (Nordgaard et al., 2013).Questions about the nature of recovery might be addressed within phenomenology by considering the difference between minimal (or basic) self and narrative (or extended) self, a more complex self-understanding or self-interpretation that is founded on the more basic, pre-reflective sense of being alive in the world (Gallagher, 2000; Parnas, 2007). According to proponents of the ipseity disturbance hypothesis, disturbances of basic self-hood can contribute to disturbances of narrative self, such as confusion about one's future goals or difficulties making sense of one's life history, though it is unlikely for disruptions that originate in the narrative self to trickle down to the minimal self (Henriksen, 2022). Such a view might similarly suggest that it would be unlikely for work on the level of the narrative self to lead to improvements in minimal self. Recovery, according to this approach, might best be viewed as an understanding of and compensation for alterations in basic self-hood, such that a person can develop a relatively solid narrative self that accounts for and manages disturbances of minimal self—while the minimal self may also grow more solid through various therapeutic interventions (Skodlar & Henriksen, 2019).Wannberg finds a more transformative possibility in Wittgenstein's grammatical approach, which is concerned with the function and rules of discourse. According to her grammar of recovery, recovery narratives are not only the product of a process of meaning-making and self-understanding, but they can create meaning and new realities. Furthermore, this process, according to Wannberg, has an inherently social and normative quality to it: the self-work that occurs in recovery and the recovery narrative involves the development of agency, autonomy, and responsibility in a social world... (shrink)

Evidence for a dysfunction in cognitive coordination in schizophrenia is emerging, but it is not specific enough to prove (or disprove) this long-standing hypothesis. Many aspects of the external world are spatially mapped in the brain. A comprehensive internal representation relies on integration of information across space. Focus on spatial integration in the perceptual and cognitive processes will generate empirical data that shed light on the pathophysiology of schizophrenia.

This paper evaluates the ongoing Finnish Adoptive Family Study of Schizophrenia. The Tienari, Lahti et al. study is the most recent attempt to use adoptees as a way of testing the hypothesis that schizophrenia carries a genetic component, and the purpose here is to present what is probably the first in-depth critical analysis of its findings. The published reports of Tienari and associates are the primary focus of analysis, while problems with other schizophrenia adoption studies using (...) similar research designs are also discussed. Because of factors including the selective placement of adoptees, the low variance explained by the two major hypothesized predictor variables for schizophrenia, the invalidity of the schizophrenia spectrum concept, and the failure to find an index schizophrenia rate greater than general population expectations, it is concluded that the Finnish study cannot be regarded as having produced evidence in favor of the genetic theory of schizophrenia. (shrink)

The concept of locally specialized functions dominates research on higher brain function and its disorders. Locally specialized functions must be complemented by processes that coordinate those functions, however, and impairment of coordinating processes may be central to some psychotic conditions. Evidence for processes that coordinate activity is provided by neurobiological and psychological studies of contextual disambiguation and dynamic grouping. Mechanisms by which this important class of cognitive functions could be achieved include those long-range connections within and between cortical regions that (...) activate synaptic channels via NMDA-receptors, and which control gain through their voltage-dependent mode of operation. An impairment of these mechanisms is central to PCP-psychosis, and the cognitive capabilities that they could provide are impaired in some forms of schizophrenia. We conclude that impaired cognitive coordination due to reduced ion flow through NMDA-channels is involved in schizophrenia, and we suggest that it may also be involved in other disorders. This perspective suggests several ways in which further research could enhance our understanding of cognitive coordination, its neural basis, and its relevance to psychopathology. Key Words: attention; cerebral cortex; cognitive coordination; cognitive neuropsychiatry; cognitive neuropsychology; context disorganization; Gamma rhythms; Gestalt theory; glutamate; grouping; memory; NMDA-receptors; PCP-psychosis; perceptual organization; schizophrenia. (shrink)

Intersubjectivity impairment has been considered the main pathogenic nucleus of schizophrenia. Enriching this concept with references to Scheler’s phenomenology, our hypothesis is that schizophrenic subjects are affected by a deeper impairment: the inability to resonate with unipathic affectivity. Fragmentation of the Leibschema, valueception impairment, and the lack of vital impulse are, in our hypothesis, the original alterations of the schizophrenic bodily experience from which all relational impairments originate. Our proposal is, therefore, to enhance a psychotherapy that does (...) not only focus on the verbal level, but endeavors to touch the patient’s Leib, focusing on emotional sharing and on the development of a sense of cohesion of one’s body as the starting point for accessing intersubjectivity. (shrink)

Merleau-Ponty finds a philosophical interest in the psychoanalytical clinic, especially in the the clinic of children and hallucinating people, which can support the concepts of flesh and Ineinander. But in the philosophy of Merleau-Ponty there is also a clinical interest, residing in the link he establishes between the flesh, conceived as the origin of existence, and the pathologies that Freud described as “narcissistic” and nowadays called “psychotic” or “borderline” states. To support this hypothesis, we will link Merleau-Ponty’s own “clinic (...) of the origins” and Harold Searles’ theory of narcissistic pathologies based on his clinical experience with schizophrenics. This confrontation will reveal how a philosophy of flesh provides us not only with theoretical points of reference relevant to the clinic of schizophrenia, but also fruitful technical indications regarding the direction towards a cure of such a pathology, indications that join those provided by Searles. (shrink)

Objective: The dopamine hypothesis is one of the most influential theories of the neurobiological background of schizophrenia (SCZ). However, direct evidence for abnormal dopamine-related subcortical-cortical circuitry disconnectivity is still lacking. The aim of this study was therefore to test dopamine-related substantia nigra (SN)-based striato-thalamo-cortical resting-state functional connectivity (FC) in SCZ. Method: Based on our a priori hypothesis, we analyzed a large sample resting-state functional magnetic resonance imaging (fMRI) dataset from first-episode drug-naïve SCZ patients (n = 112) and (...) healthy controls (n = 82) using the SN as the seed region for an investigation of striato-thalamo-cortical FC. This was done in the standard band of slow frequency oscillations and then in its subfrequency bands (Slow4 and Slow5). Results: The analysis showed in SCZ: (1) reciprocal functional hypo-connectivity between SN and striatum, with differential patterns for Slow5 and Slow4; (2) functional hypo-connectivity between striatum and thalamus, as well as functional hyper-connectivity between thalamus and sensorimotor cortical areas, specifically in Slow4; (3) correlation of thalamo-sensorimotor functional hyper-connectivity with psychopathological symptoms. Conclusions: We demonstrate abnormal dopamine-related SN-based striato-thalamo-cortical FC in slow frequency oscillations in first-episode drug-naive SCZ. This suggests that altered dopaminergic function in the SN leads to abnormal neuronal synchronization (as indexed by FC) within subcortical-cortical circuitry, complementing the dopamine hypothesis in SCZ on the regional level of resting-state activity. (shrink)

A number of studies have demonstrated pragmatic language difficulties in people with Schizophrenia Spectrum and Other Psychotic Disorders. However, research about how people with schizophrenia spectrum and other psychotic disorders understand scalar implicatures is surprisingly rare, since SIs have generated much of the most recent literature. Scalar implicatures are pragmatic inferences, based on linguistic expressions like some, must, or, which are part of a scale of informativeness. Logically, the less informative expressions imply the more informative ones, but pragmatically (...) people usually infer that the presence of a less informative term implies that the more informative term was not applicable. In one of the few existing studies with people with schizophrenia spectrum and other psychotic disorders, Wampers et al. observed that in general, people with schizophrenia spectrum and other psychotic disorders were less likely to derive SIs than controls. The current study has three main aims. First, we want to replicate the original finding with the scalar terms some-all. Second, we want to investigate how these patients deal with different scalar terms, that is, we want to investigate if scalar diversity is also observed in this clinical group. Third, we investigate the role of working memory, often seen as another important mechanism to enable inferring SIs. Twenty-one individuals with a psychotic disorder and 21 matched controls answered 54 under-informative statements, in which seven different pairs of scalar terms were used. In addition, working memory capacity was measured. Patients with schizophrenia spectrum and other psychotic disorders did not make more logical interpretations when processing quantifiers, disconfirming Wampers et al.. However, certain scalar scales elicited more pragmatic interpretations than others, which is in line with the scalar diversity hypothesis. Additionally, we observed only partial evidence for the role of working memory. Only for the scalar scale and-or, a significant effect of working memory was observed. The implications of these results for patients with schizophrenia spectrum and other psychotic disorders are discussed, but also the role of working memory for pragmatic inferences, as well as the place of SIs in experimental pragmatics. (shrink)

The influence of emotion on episodic and autobiographical memory in schizophrenia was investigated. Using an experiential approach, the states of awareness accompanying recollection of pictures from the IAPS and of associated autobiographical memories was recorded. Results show that schizophrenia impairs episodic and autobiographical memories in their critical feature: autonoetic awareness, i.e., the type of awareness experienced when mentally reliving events from one’s past. Schizophrenia was also associated with a reduction of specific autobiographical memories. The impact of stimulus (...) valence on memory performance was moderated by clinical status. Patients with schizophrenia recognized more positive than negative pictures, and recalled more positive than negative autobiographical memories while controls displayed the opposite pattern. A hypothesis in terms of a fundamental executive deficit underlying these impairments is proposed. (shrink)

This commentary challenges the argument that the diathesis for hallucinations is equivalent to that for schizophrenia. Evidence against this comes from data on the prevalence of hallucinations in schizophrenia, their nonspecificity, and their relationships with moderating variables. We also highlight, however, the manner in which the Behrendt & Young (B&Y) hypothesis extends recent neuroscientific theories of schizophrenia, and its potential treatment applications.

Phillips & Silverstein offer an exciting synthesis of ongoing efforts to link the clinical and cognitive manifestations of schizophrenia with cellular accounts of its pathophysiology. We applaud their efforts but wonder whether the highly inclusive notion of “context” adequately captures some important details regarding schizophrenia and NMDA/glutamate function that are suggested by work on language processing and cognitive electrophysiology.

In psychiatry, pharmacological drugs play an important experimental role in attempts to identify the neurobiological causes of mental disorders. Besides being developed in applied contexts as potential treatments for patients with mental disorders, pharmacological drugs play a crucial role in research contexts as experimental instruments that facilitate the formulation and revision of neurobiological theories of psychopathology. This paper examines the various epistemic functions that pharmacological drugs serve in the discovery, refinement, testing, and elaboration of neurobiological theories of mental disorders. I (...) articulate this thesis with reference to the history of antipsychotic drugs and the evolution of the dopamine hypothesis of schizophrenia in the second half of the twentieth century. I argue that interventions with psychiatric patients through the medium of antipsychotic drugs provide researchers with information and evidence about the neurobiological causes of schizophrenia. This analysis highlights the importance of pharmacological drugs as research tools in the generation of psychiatric knowledge and the dynamic relationship between practical and theoretical contexts in psychiatry. (shrink)

This hypothesis proposes that increased extracellular glutamate in Amyotrophic Lateral Sclerosis (ALS) and cerebral ischemia, currently viewed as a trigger for excitotoxicity, is actually beneficial as it stimulates the utilization of glutamate as metabolic fuel. Renewed appreciation of glutamate oxidation by ischemic neurons has raised questions regarding the role of extracellular glutamate in ischemia. Is it detrimental, as suggested by excitotoxicity in early in vitro studies, or beneficial, as suggested by its oxidation in later in (...) vivo studies? The answer may depend on the activity of N‐methyl‐D‐aspartate (NMDA) glutamate receptors. Early in vitro procedures co‐activated NMDA receptors (NMDARs) containing 2A (GluN2A) and 2B (GluN2B) subunits, an event now believed to trigger excitotoxicity; however, during in vivo ischemia D‐serine and zinc molecules are released and these ensure only GluN2B receptors are stimulated. This not only prevents excitotoxicity but also initiates signaling cascades that allow ischemic neurons to import and oxidize glutamate. (shrink)

RESUMEN Desde 1980, C. D. Frith investiga la esquizofrenia, y explica sus síntomas centrales como las alucinaciones, con miras a aclarar cuál es el déficit originario de este trastorno mental. Frith propone una hipótesis centrada en el concepto de conciencia, que ha elaborado como parte del desarrollo científico contemporáneo. En primer lugar, como parte de la aplicación de modelos neurocognitivos de control motor, según los cuales el déficit se atribuye al concepto de copia eferente y su función. En segundo lugar, (...) la actualiza y complementa con evidencia de imagen cerebral de la atenuación de la actividad cortical parietal, como efecto derivado de la copia eferente. En tercer lugar, adiciona el concepto de sentido de agencia, y el componente de cognición social, intentando integrar la experiencia del paciente y la relevancia del ámbito intersubjetivo a su propuesta. Este artículo hace una revisión crítica de la hipótesis de Frith y se divide en cuatro partes: primero, se presenta una síntesis de la evolución de la hipótesis; segundo, se sintetiza su argumentación; tercero, se presentan los principales puntos críticos y, por último, se derivan unas conclusiones generales. ABSTRACT Since 1980, C. D. Frith has been working on schizophrenia, and explaining central symptoms such as hallucinations, in an attempt to clarify the basic deficits of this mental disorder. Frith has put forth a hypothesis based on the concept of consciousness, and has been adjusting it alongside contemporary scientific developments. In first place, it begins with the use of neurocognitive models of motor control, according to which the deficit is attributable to the concept of efferent copy and its function. In second place, he updated the model by including neuroimaging evidence of attenuation in parietal activity, as a consequence of the efferent copy. In third place, he added the concept of sense of agency, and the social cognition component, trying to integrate to his proposal the patient's experience and the relevance of the inter-subjective aspect. The current paper, which critically reviews Frith's hypothesis, it's divided in four parts: First, the hypothesis' evolution is synthesized; second, the main arguments are summarized; third, the main critical points are presented; and, finally, some general conclusions are drawn. (shrink)

Phillips & Silverstein's focus on schizophrenia as a failure of “cognitive coordination” is welcome. They note that a simple hypothesis of reduced Gamma synchronisation subserving impaired coordination does not fully account for recent observations. We suggest that schizophrenia reflects a dynamic compensation to a core deficit of coordination, expressed either as hyper- or hyposynchronisation, with neurotransmitter systems and arousal as modulatory mechanisms.

Abstract:In this paper, I argue for a social conception of subjectivity, via a philosophical reading of first-person accounts of recovery from schizophrenia, published in the Schizophrenia Bulletin. Following the hypothesis that these accounts exemplify a more general tension between, on the one hand, normative and social dimensions of the self, and on the other, experiential and psychological dimensions, the first section of the paper formulates the problem from a philosophical perspective inspired by Ludwig Wittgenstein's grammatical approach. The (...) second section explores and rejects different possible readings (sociologistic, phenomenological, or narrativist readings), as conceiving the subject in too passive a relationship with him or herself, and as leading to overly skeptical conclusions about the claims in the first-person accounts insisting on the notion of recovery as a restoration of a sense of self and as empowerment. The third section suggests that a more positive answer can be given via the idea of a certain grammar of recovery governing these narratives, and sketches out how this relates to the more general philosophical question on subjectivity. (shrink)

Disorders of consciousness and the self are at the forefront of schizophrenia symptomatology. Patients are impaired in feeling themselves as the authors of their thoughts and actions. In addition, their flow of consciousness is disrupted, and thought fragmentation has been suggested to be involved in the patients’ difficulties in feeling as being one unique, unchanging self across time. Both impairments are related to self disorders, and both have been investigated at the experimental level. Here we review evidence that both (...) mechanisms of motor control and the temporal structure of signal processing are impaired in schizophrenia patients. Based on this review, we propose that the sequencing of action and perception plays a key role in the patients’ impairments. Furthermore, the millisecond time scale of the disorders, as well as the impaired sequencing, highlights the cooperation between brain networks including the cerebellum, as proposed by Andreasen (1999). We examine this possibility in the light of recent knowledge on the anatomical and physiological properties of the cerebellum, its role in timing, and its involvement in known physiological impairments in patients with schizophrenia, e.g., resting states and brain dynamics. A disruption in communication between networks involving the cerebellum, related to known impairments in dopamine, glutamate and GABA transmission, may help to better explain why patients experience reduced attunement with the external world and possibly with themselves. (shrink)

Life, whatsoever it is, is a temporal flux. Everything is doomed to change often apparently beyond our awareness. My body appears totally different now, so does my mind. I have gained new attitudes and new ambitions, and a substantial number of old ones have been discarded. But, I am still the same person in an ongoing manner. Besides, recent neuroscientific and psychological evidence has shown that our conscious perception happens as a series of discrete or bounded instants—it emerges in temporally (...) scattered, gappy, and discrete forms. But, if it is so, how does the brain persevere our self-continuity in this gappy setting? How is it possible that despite moment-to-moment changes in my appearance and mind, I am still feeling that I am that person? How can we tackle with this second by second gap and resurrection in our existence which leads to a foundation of wholeness and continuity of our self? How is continuity of self that results in a feeling that one’s life has purpose and meaning preserved? To answer these questions, the problem has been comprehended from a philosophical, psychological, and neuroscientific perspective. I realize that first and foremost fact lies in the temporal nature of identity. Having equipped with these thoughts, in this article, it is hypothesized that according to two principles self-continuity is maintained. It is supposed that there should be a precise temporal integration mechanism in the CNS with the outside world that provides us this smooth, ungappy flow of the Self. However, we are often taken for granted the importance of self-continuity, but it can be challenged by life transitions such as entering adulthood, retirement, senility, emigration, and societal changes such as immigration, globalization, and in much unfortunate and extreme cases of mental illnesses such as schizophrenia. (shrink)

There has recently been emphasis put on providing two-factor accounts of monothematic delusions. Such accounts would explain (1) whether a delusional hypothesis (e.g. someone else is inserting thoughts into my mind) can be understood as a prima facie reasonable response to an experience and (2) why such a delusional hypothesis is believed and maintained given its implausibility and evidence against it. I argue that if we are to avoid obfuscating the cognitive mechanisms involved in monothematic delusion formation we (...) should split the first factor (1 above) into two factors: how abnormal experience can give rise to a delusional ‘proto-hypothesis’ and how a ‘proto-hypothesis’ in consort with normal experiences and background information, can be developed into a delusional hypothesis. In particular I will argue that a schizophrenic is faced with the unusual requirement of having to identify an introspectively accessible thought as one's own, and that this requirement of identification is the central experiential abnormality of thought insertion, auditory verbal hallucination, and alien control (i.e. passivity symptoms). Additionally, I will consider non-experiential factors which are required for the formation of a delusional hypothesis. (shrink)

Phillips & Silverstein (P&S, 2003) propose that NMDA-receptor dysfunction may be the fundamental neurobiological mechanism underlying and associating impaired holistic perception and cognitive coordination with schizophrenic psychopathology. We discuss how the P&S hypothesis shares different aspects of the weak central coherence account of autism from both theoretical and experimental perspectives. Specifically, we believe that neither those persons with autism nor those with schizophrenia integrate visuo-perceptual information efficiently, resulting in incongruous internal representations of their external world. However, although NMDA-hypofunction (...) may be responsible for perceptual impairments in schizophrenia and possibly autism, we suggest that it is highly unlikely that NMDA-hypofunction is specifically responsible for the autistic behavioral symptomology, as described by P&S in their target article. (shrink)

Early-Onset Schizophrenia (EOS) and Attention Deficit-Hyperactivity Disorder (ADHD) are early- onset neurodevelopmental disorders associated with cognitive deficits. The current study represents the first attempt to compare these groups on a comprehensive cognitive test battery in a longitudinal design over 25 years in order to enhance our knowledge of particular patterns resulting from the interaction between normal maturational processes and different illness processes of these disorders. In the baseline study, 19 adolescents with schizophrenia were compared to 20 adolescents with (...) ADHD and 30 healthy controls (HC), all between 12 and 18 years of age. After 13 years (T2) and after 25 years (T3) they were re-evaluated with the cognitive test battery. A cognitive Composite Score was used in a linear mixed model. The EOS group had a significant cognitive stagnation or deterioration from T1 to T2 compared to HC. However, the EOS group had the most positive change from T2 to T3, supporting a stable level of cognitive performance over the 25 year span. The ADHD group improved or had similar development as the HC group from T1 to T2. They continued to improve significantly compared to the HC group from T2 to T3. Individuals in the EOS group performed more impaired on the cognitive composite score compared to the HC group and the ADHD group at all three time points. Results might indicate a neurodevelopmental pathway of EOS with subnormal cognitive development specific in adolescence. In comparison, the ADHD group had a more consistent cognitive maturation supporting a maturational delay hypothesis of ADHD. (shrink)

A number of differences between the dreams of schizophrenia patients and those of healthy participants have been linked to changes in waking life that schizophrenia may cause. This way, the “continuity hypothesis” has become a standard way to relate dreaming and waking experiences in schizophrenia. Nevertheless, some of the findings in dream literature are not compatible with the continuity hypothesis and suggest some other ways how dream content and waking experiences could interact. Conceptually, the continuity (...) hypothesis could be sharpened into the “waking-to-dreaming” and the “dreaming-to-waking” hypotheses, whereas a less explored type of “discontinuity” could embrace the “compensated waking” and the “compensated dreaming” hypotheses. A careful consideration and empirical testing of each of those hypotheses may reveal a multiplicity of the ways how dreaming and waking life interact in schizophrenia. (shrink)

Given the contemporary ambivalent standpoints toward the future of artificial intelligence, recently denoted as the phenomenon of Singularitarianism, Gregory Bateson’s core theories of ecology of mind, schismogenesis, and double bind, are hereby revisited, taken out of their respective sociological, anthropological, and psychotherapeutic contexts and recontextualized in the field of Roboethics as to a twofold aim: the proposal of a rigid ethical standpoint toward both artificial and non-artificial agents, and an explanatory analysis of the reasons bringing about such a polarized outcome (...) of contradictory views in regard to the future of robots. Firstly, the paper applies the Batesonian ecology of mind for constructing a unified roboethical framework which endorses a flat ontology embracing multiple forms of agency, borrowing elements from Floridi’s information ethics, classic virtue ethics, Felix Guattari’s ecosophy, Braidotti’s posthumanism, and the Japanese animist doctrine of Rinri. The proposed framework wishes to act as a pragmatic solution to the endless dispute regarding the nature of consciousness or the natural/artificial dichotomy and as a further argumentation against the recognition of future artificial agency as a potential existential threat. Secondly, schismogenic analysis is employed to describe the emergence of the hostile human–robot cultural contact, tracing its origins in the early scientific discourse of man–machine symbiosis up to the contemporary countermeasures against superintelligent agents. Thirdly, Bateson’s double bind theory is utilized as an analytic methodological tool of humanity’s collective agency, leading to the hypothesis of collective schizophrenic symptomatology, due to the constancy and intensity of confronting messages emitted by either proponents or opponents of artificial intelligence. The double bind’s treatment is the mirroring “therapeutic double bind,” and the article concludes in proposing the conceptual pragmatic imperative necessary for such a condition to follow: humanity’s conscience of habitualizing danger and familiarization with its possible future extinction, as the result of a progressive blurrification between natural and artificial agency, succeeded by a totally non-organic intelligent form of agency. (shrink)

To understand schizophrenia, a linking hypothesis is needed that shows how brain mechanisms lead to behavioral functions in normals, and also how breakdowns in these mechanisms lead to behavioral symptoms of schizophrenia. Such a linking hypothesis is now available that complements the discussion offered by Phillips & Silverstein (P&S).

Drawing on previous models of anxiety, intermediate memory, the positive symptoms of schizophrenia, and goal-directed behaviour, a neuropsychological hypothesis is proposed for the generation of the contents of consciousness. It is suggested that these correspond to the outputs of a comparator that, on a moment-by-moment basis, compares the current state of the organism's perceptual world with a predicted state. An outline is given of the information-processing functions of the comparator system and of the neural systems which mediate them. (...) The hypothesis appears to be able to account for a number of key features of the contents of consciousness. However, it is argued that neitherthis nor any existing comparable hypothesis is yet able to explain why the brain should generate conscious experience of any kind at all. (shrink)

We argue that thought insertion primarily involves a disruption of the sense of ownership for thoughts and that the lack of a sense of agency is but a consequence of this disruption. We defend the hypothesis that this disruption of the sense of ownership stems from a fail- ure in the online integration of the contextual information related to a thought, in partic- ular contextual information concerning the different causal factors that may be implicated in their production. Loss of (...) unity of consciousness, manifested by incoherent subjective experiences is a general phenomenal characteristic of schizophrenia. This loss of coherence has been hypothesized to reflect a generalized deficit of contextual information integration not conveyed by, but related to, a target event. This deficit is manifested across many cog- nitive domains. We argue that it is also manifested in the process of thinking itself, result- ing in causally decontextualized thoughts that are experienced as inserted thoughts. (shrink)

The paper analyzes S.N. Spielrein’s scientific contribution to development K.G. Jung’s ideas. It starts with a list of areas pioneered by S.N. Spielrein’s and a review of literature which, as the author points out, is often biased, focusing not on the ideas of one of the first women in psychoanalysis, but on her personal life and individual characteristics. Further the paper analyzes several principal conceptions (with the exception of the original conception of destruction) where S.N. Spielrein’s contribution was essential. She (...) tried to give a more strict definition to C.G. Jung’s theory of the complex which played a key part in development of analytical psychology. S.N. Spielrein was the first to prove empirically in her dissertation the potential of the theory which contradicted classical psychoanalysis. S.N. Spielrein also played a part in development of C.G. Jung’s notions of philo- and ontogenesis of the mind in the process of the so called ‘complex intergrowth’ and gradually developing a common core in the form of I-consciousness. She also worked to define genesis of schizophrenia as a process of replacement of the personal content of the mind by collective contents. She contributed to development of the notion of the collective unconscious. The author analyzes her conception of ‘ancestral soul’ in the context of later achievements of analytical psychology, pointing out similarities in definitions. The author suggests a hypothesis on reasons why, after her separation from C.G. Jung, all mention of the collective unconscious disappeared from S.N. Spielrein’s publications. In conclusion, on the basis of characteristics of the female mind, identified by S.N. Shpilrein, the author hypothesizes on why actuality of her ideas has not been appreciated. Статья посвящена оценке научного вклада С.Н. Шпильрейн в развитие идей К.Г. Юнга. Основной текст предваряется указанием областей, в которых Шпильрейн оказалась первопроходцем, а также библиографическим обзором с выявлением слабых мест сложившейся традиции, сторонники которой предпочитают фокусироваться не на идеях одной из первых женщин-психоаналитиков, а на ее личной жизни и психологических особенностях. В основной части подробно рассматриваются несколько ключевых для аналитической психологии концепций (за исключением оригинальной концепции деструкции), вклад С.Н. Шпильрейн в развитие которых оказался наиболее существенным. Во-первых, анализируются ее усилия по уточнению сформулированной К.Г. Юнгом теории комплекса, сыгравшей ключевую роль в становлении аналитической психологии. С.Н. Шпильрейн стала первым исследователем, который в своей диссертации на конкретном эмпирическом материале доказал приемлемость этой теории, идущей вразрез с классическим психоанализом. Во-вторых, эксплицируется вклад С.Н. Шпильрейн в развитие представлений К.Г. Юнга о филогенезе и онтогенезе психики в результате так называемого комплексного срастания и постепенного обретения единого стержня в форме Я-сознания. В-третьих, отмечается роль Шпильрейн в уточнении генезиса шизофрении как процесса замещения личностных содержаний психики коллективными психическими содержаниями. В-четвертых, рассматривается вклад С.Н. Шпильрейн в развитие понятия коллективного бессознательного. В частности, анализируется ее учение о «душе рода» или «родовой душе» в контексте более поздних открытий аналитической психологии, указываются сходства формулировок. Кроме того, выдвигается гипотеза, почему после разрыва с К.Г. Юнгом в трудах С.Н. Шпильрейн полностью исчезают концепты, близкие понятию коллективного бессознательного. В заключение на основании выявленных С.Н. Шпильрейн особенностей женской психики строится предположение, почему ее идеи только сегодня стали по-настоящему актуальными. (shrink)

This study compares 20 subjects, in each of three different settings, with serious psychotic disorder who hear voices, and compares their voice-hearing experience. We find that while there is much that is similar, there are notable differences in the kinds of voices that people seem to experience. In a California sample, people were more likely to describe their voices as intrusive unreal thoughts; in the South Indian sample, they were more likely to describe them as providing useful guidance; and in (...) our West African sample, they were more likely to describe them as morally good and causally powerful. What we think we may be observing is that people who fall ill with serious psychotic disorder pay selective attention to a constant stream of many different auditory and quasi-auditory events because of different “cultural invitations”—variations in ways of thinking about minds, persons, spirits and so forth. Such a process is consistent with processes described in the cognitive psychology and psychiatric anthropology literature, but not yet described or understood with respect to cultural variations in auditory hallucinations. We call this process “social kindling.”. (shrink)

Glutamate is the major excitatory neurotransmitter in the mammalian brain, with receptors on every neuron in the central nervous system; it has major roles in fast synaptic transmission and in the establishment of certain forms of memory. More than 20 years ago Olney and his colleagues(1) described the [Excitotoxic Hypothesis] which postulates that, in addition to its normal function in the healthy brain, glutamate can kill neurons by prolonged, receptorsmediated depolarization resulting in irreversible disturbances in ion homeostasis. (...) Therefore, glutamate is a two‐edged sword; in certain undefined, adverse conditions it undergoes a transition from neurotransmitter to neurotoxin. Its toxicity has been implicated in the death of neurons in ischemia, epilepsy, and the neurodegenerative disorders such as Alzheimer's, Huntington's, and Parkinson's diseases(2–5). Recent advances in the molecular cloning of the genes for the glutamate family of receptors has revealed a plethora of receptor subtypes and an unexpected level of complexity in the mechanisms of receptor expression and function. (shrink)

Recent years have witnessed an intensification of historical and philosophical research on the link between psychotropic drugs and psychiatric theories. For example, Kendler and Schaffner detailed how the dopamine hypothesis of schizophrenia was intimately linked to the dopamine theory of antipsychotic drug action. Here, a related case is explored: the use of antidepressants' neurochemical effects to speculate about the pathophysiology of depression.This rationale was central to American psychiatrist Schildkraut's landmark article on the catecholamine hypothesis of affective disorders. (...) Accordingly, the paper's hypothesis—that depressions may relate to decreased... (shrink)

Explanation of logic of psychoses: schizophrenia and bi-polar, with empirical confirmation - e.g. IQ decreases the likelihood of psychosis, and bi-polar is more likely than schizophrenia... MA thesis in 1998 (Comenius University), Presented at Art exhibition "From Animation", London, Holland Park (W8 6LU), Conferences in Santorini, Daejon, Adelaide 2016.

Introduction: More than half a century after the introduction of effective pharmacotherapy for the illness, in most patients schizophrenia remains a chronic, relapsing condition with poor long-term outcomes. Methods: We examine the pharmacological treatment of schizophrenia from different perspectives to understand why there have not been significant advances, and to consider what the future might hold in store. Results: We argue that the treatment of schizophrenia addresses the phenotype and not the cause; that the causes may not (...) be treatable even if identifiable; that secondary prevention approaches involving treating the phenotype before full-fledged illness develops have, so far, not yielded promising results; and that shifting the focus of treatment from dopamine to other neurotransmitter systems is merely a tertiary prevention approach which will not reverse the extensive structural and functional pathology of schizophrenia. Conclusions: We believe that, given the current state of our knowledge of the illness, the future of the pharmacotherapy of schizophrenia looks bleak. (shrink)

Each of us enjoys a special awareness of (some) of her mental states. The adverbial model of first-person awareness claims that to be aware of a mental state is for it to be conscious, where ‘conscious’ describes the kind of state it is, rather than denoting a form of awareness directed at it. Here, I present an argument for construing first-person awareness of intentions adverbially, by showing that this model can meet a serious challenge posed by the simulation hypothesis, (...) which draws on data about schizophrenia. (shrink)

Recent studies have provided evidence of associations between neurochemistry and reading (dis)ability (Pugh et al., 2014). Based on a long history of studies indicating that fluent reading entails the automatic convergence of the written and spoken forms of language and our recently proposed Neural Noise Hypothesis (Hancock et al., 2017), we hypothesized that individual differences in cross-modal integration would mediate, at least partially, the relationship between neurochemical concentrations and reading. Cross-modal integration was measured in 231 children using a two-alternative (...) forced choice cross-modal matching task with three language conditions (letters, words, and pseudowords) and two levels of difficulty within each language condition. Neurometabolite concentrations of Choline (Cho), Glutamate (Glu), gamma-Aminobutyric (GABA), and N- acetyl-aspartate (NAA) were then measured in a subset of this sample (n = 70) with Magnetic Resonance Spectroscopy (MRS). A structural equation mediation model revealed that the effect of cross-modal word matching mediated the relationship between increased Glu (which has been proposed to be an index of neural noise) and poorer reading ability. In addition, the effect of cross-modal word matching fully mediated a relationship between increased Cho and poorer reading ability. Multilevel mixed effects models confirmed that lower Cho predicted faster cross-modal matching reaction time, specifically in the hard word condition. These Cho... (shrink)

There are strong resemblances between the neurobiological characteristics of hallucinations occurring in the particular case of schizophrenia and the hallucinatory activity observed during the rapid-eye-movement (dreaming) sleep stage: the same prefrontal dorsolateral deactivation; forebrain disconnectivity and disinhibition; sensory deprivation; and acetylcholine, monoamine, and glutamate modifications.