In recent years, there has been much focus on the apparent heterogeneity of schizophrenic symptoms. By contrast, this article proposes a unifying account emphasizing basic abnormalities of consciousness that underlie and also antecede a disparate assortment of signs and symptoms. Schizophrenia, we argue, is fundamentally a self-disorder or ipseity disturbance that is characterized by complementary distortions of the act of awareness: hyperreflexivity and diminished self-affection. Hyperreflexivity refers to forms of exaggerated self-consciousness in which aspects of oneself are experienced as (...) akin to external objects. Diminished self-affection or self-presence refers to a weakened sense of existing as a vital and self-coinciding source of awareness and action. This article integrates recent psychiatric research and European phenomenological psychiatry with some current work in cognitive science and phenomenological philosophy. After introducing the phenomenological approach along with a theoretical account of normal consciousness and self-awareness, we turn to a variety of schizophrenic syndromes. We examine positive, then negative, and finally disorganization symptoms—attempting in each case to illuminate shared distortions of consciousness and the sense of self. We conclude by discussing the possible relevance of this approach for identifying early schizophrenic symptoms. (shrink)

Patients with schizophrenia have a higher risk of cardiovascular diseases and higher mortality from them than does the general population; however, the underlying mechanism remains unclear. Impaired cerebral autoregulation is associated with cerebrovascular diseases and their mortality. Increased or decreased cerebral blood flow in different brain regions has been reported in patients with schizophrenia, which implies impaired cerebral autoregulation. This study investigated the cerebral autoregulation in 21 patients with schizophrenia and 23 age- and sex-matched healthy controls. None (...) of the participants had a history of cardiovascular diseases, hypertension, or diabetes. All participants underwent 10-min blood pressure and cerebral blood flow recording through finger plethysmography and Doppler ultrasonography, respectively. Cerebral autoregulation was assessed by analyzing two autoregulation indices: the mean blood pressure and cerebral blood flow correlation coefficient (Mx), and the phase shift between the waveforms of blood pressure and cerebral blood flow determined using transfer function analysis. Compared with the controls, the patients had a significantly higher Mx (0.257 vs. 0.399, p = 0.036) and lower phase shift (44.3° vs. 38.7° in the 0.07–0.20 Hz frequency band, p = 0.019), which indicated impaired maintenance of constant cerebral blood flow and a delayed cerebrovascular autoregulatory response. Impaired cerebral autoregulation may be caused by schizophrenia and may not be an artifact of coexisting medical conditions. The mechanism underlying impaired cerebral autoregulation in schizophrenia and its probable role in the development of cerebrovascular diseases require further investigation. (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)

Wittgenstein’s concepts shed light on the phenomenon of schizophrenia in at least three different ways: with a view to empathy, scientific explanation, or philosophical clarification. I consider two different “positive” wittgensteinian accounts―Campbell’s idea that delusions involve a mechanism of which different framework propositions are parts, Sass’ proposal that the schizophrenic patient can be described as a solipsist, and a Rhodes’ and Gipp’s account, where epistemic aspects of schizophrenia are explained as failures in the ordinary background of certainties. I (...) argue that none of them amounts to empathic-phenomenological understanding, but they provide examples of how philosophical concepts can contribute to scientific explanation, and to philosophical clarification respectively. (shrink)

Schizophrenia is a disturbance of the self, of which the attribution of agency is a major component. In this article, we review current theories of the Sense of Agency, their relevance to schizophrenia, and propose a novel framework for future research. We explore some of the models of agency, in which both bottom-up and top-down processes are implicated in the genesis of agency. We further this line of inquiry by suggesting that ongoing neurological activity (the brain’s resting state) (...) in self-referential regions of the brain can provide a deeper level of influence beyond what the current models capture. Based on neuroimaging studies, we suggest that aberrant activity in regions such as the default mode network of individuals with schizophrenia can lead to a misattribution of internally/externally generated stimuli. This can result in symptoms such as thought insertion and delusions of control. Consequently, neuroimaging can contribute to a more comprehensive conceptualization and measurement of agency and potential treatment implications. (shrink)

Do self‐monitoring accounts, a dominant account of the positive symptoms of schizophrenia, explain auditory verbal hallucination? In this essay, I argue that the account fails to answer crucial questions any explanation of auditory verbal hallucination must address. Where the account provides a plausible answer, I make the case for an alternative explanation: auditory verbal hallucination is not the result of a failed control mechanism, namely failed self‐monitoring, but, rather, of the persistent automaticity of auditory experience of a voice. My (...) argument emphasizes the importance of careful examination of phenomenology as providing substantive constraints on causal models of the positive symptoms in schizophrenia. (shrink)

A family of recent externalist approaches in philosophy of mind argues that our psychological capacities are synchronically and diachronically “scaffolded” by external (i.e., beyond-the-brain) resources. I consider how these “scaffolded” approaches might inform debates in phenomenological psychopathology. I first introduce the idea of “affective scaffolding” and make some taxonomic distinctions. Next, I use schizophrenia as a case study to argue — along with others in phenomenological psychopathology — that schizophrenia is fundamentally a self-disturbance. However, I offer a subtle (...) reconfiguration of these approaches. I argue that schizophrenia is not simply a disruption of ipseity or minimal self-consciousness but rather a disruption of the scaffolded self, established and regulated via its ongoing engagement with the world and others. I conclude by considering how this scaffolded framework indicates the need to consider new forms of intervention and treatment. (shrink)

In this article I ask whether elaborated and systematized delusions emerging in the context of schizophrenia have the potential for epistemic innocence. Cognitions are epistemically innocent if they have significant epistemic benefits that could not be attained otherwise. In particular, I propose that a cognition is epistemically innocent if it delivers some significant epistemic benefit to a given agent at a given time, and if alternative cognitions delivering the same epistemic benefit are unavailable to that agent at that time. (...) Elaborated and systematized delusions in schizophrenia are typically false and exemplify failures of rationality and self-knowledge. Empirical studies suggest that they may have psychological benefits by relieving anxiety and enhancing meaningfulness. Moreover, these delusions have been considered as adaptive in virtue of the fact that they enable automated learning to resume after a significant disruption caused by incorrect prediction-error signalling. I argue that such psychological benefits and adaptive features also have positive epistemic consequences. More precisely, delusions can be a means to restoring epistemic functionality in agents who are overwhelmed by hypersalient experiences in the prodromal stage of psychosis. The analysis leads to a more complex view of the epistemic status of delusions than is found in the contemporary philosophical literature and has some implications for clinical practice. 1 Introduction2 Types of Delusions3 What Is Wrong with Elaborated and Systematized Delusions?4 Finding Life Meaningful5 Learning Resumed6 Epistemic Innocence7 Epistemic Benefit8 No Alternatives9 Conclusions and Implications. (shrink)

Recent work on the mechanisms underlying auditory verbal hallucination (AVH) has been heavily informed by self-monitoring accounts that postulate defects in an internal monitoring mechanism as the basis of AVH. A more neglected alternative is an account focusing on defects in auditory processing, namely a spontaneous activation account of auditory activity underlying AVH. Science is often aided by putting theories in competition. Accordingly, a discussion that systematically contrasts the two models of AVH can generate sharper questions that will lead to (...) new avenues of investigation. In this paper, we provide such a theoretical discussion of the two models, drawing strong contrasts between them. We identify a set of challenges for the self-monitoring account and argue that the spontaneous activation account has much in favor of it and should be the default account. Our theoretical overview leads to new questions and issues regarding the explanation of AVH as a subjective phenomenon and its neural basis. Accordingly, we suggest a set of experimental strategies to dissect the underlying mechanisms of AVH in light of the two competing models. (shrink)

In this comparative study, we examine experiential disruptions of embodiment and affectivity in Moebius Syndrome and schizophrenia. We suggest that using phenomenological resources to explore these experiences may help us better understand what it’s like to live with these conditions, and that such an understanding may have significant therapeutic value. Additionally, we suggest that this sort of phenomenologically-informed comparative analysis can shed light on the importance of embodiment and affectivity for the constitution of a sense of self and interpersonal (...) relatedness in normal conditions. (shrink)

So far, the value dimension underlying affectivity disorders has remained out of focus in phenomenological psychopathology. As early as at the beginning of the 20th century, however, German phenomenologist Max Scheler examined in depth the relationship between affectivity and value dimension through the concept of valueception (Wertnehmung). In this sense, a recent noteworthy contribution has been provided by John Cutting, who has drawn attention to the importance of Scheler’s analyses for psychiatry. In this work I take into consideration only two (...) aspects of Cutting’s proposal: 1) the relationship between the impairments of valueception and the perception of certain value classes; and 2) the interpretation of Scheler’s phenomenological reduction and its juxtaposition with the modus vivendi of schizophrenia. According to Cutting, in the modus vivendi of schizophrenia the valueception impairment entails putting vital values in brackets and focusing on personal values, with a process that recalls Scheler’s phenomenological reduction. Regarding the first aspect, I share Cutting’s starting point, but then shift the focus on how important the valueception is for the intersubjective dimension. In particular, I maintain that rather than compromising the perception of vital values, valueception impairments in the modus vivendi of schizophrenia interfere with the intersubjective dimension and are interwoven with a process of disembodiment. My thesis is that the modus vivendi of schizophrenia involves a disturbance of the intersubjective dimension that arises from the level of valueception and that determines the person’s self-referential closure. With regard to the second point, by analyzing Scheler’s phenomenological reduction, I sustain that its main objective is to increase both the interaction with otherness and the openness to the world (Weltoffenheit). As a consequence, the modus vivendi of schizophrenia, in my opinion, is not comparable, as Cutting claims, with Scheler’s phenomenological reduction, but goes in a different direction. (shrink)

This article examines the supposedly incomprehensibility of schizophrenic delusions. According to the contemporary classificatory systems (DSM-IV-TR and ICD-10), some delusions typically found in schizophrenia are considered bizarre and incomprehensible. The aim of this article is to discuss the notion of understanding that deems these delusions incomprehensible and to see if it is possible to comprehend these delusions if we apply another notion of understanding. First, I discuss the contemporary schizophrenia definitions and their inherent problems, and I argue that (...) the notion of incomprehensibility in these definitions rests heavily on Jaspers’ notions of understanding and empathy. Secondly, I discuss two Wittgensteinian attempts to comprehend bizarre delusions: (a) Campbell’s proposal to conceive delusions as framework propositions and (b) Sass’s suggestion to interpret delusions in the light of solipsism. Finally, I discuss the phenomenological conception of schizophrenia, which conceives delusion formation as resulting from alterations of the structure of experiencing and from underlying self-disorders. I argue that although a psychological understanding that seeks to grasp meaning in terms of motivations, desires, and other more straightforward psychological connections between mental states is impossible in schizophrenia, we can in fact have a philosophical understanding of the schizophrenic world and of the emergence of delusions typically found in 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)

BackgroundCommunity engagement within biomedical research is broadly defined as a collaborative relationship between a research team and a group of individuals targeted for research. A Community Advisory Board is one mechanism of engaging the community. Within genomics research CABs may be particularly relevant due to the potential implications of research findings drawn from individual participants on the larger communities they represent. Within such research, CABs seek to meet instrumental goals such as protecting research participants and their community from research-related risks, (...) as well as intrinsic goals such as promoting the respect of participants and their community. However, successful community engagement depends on the degree to which CABs legitimately represent and engage with communities targeted for research. Currently, there is little literature describing the use of CABs in genomics research taking place in developing countries, and even less in the field of genomics research relating to mental illness. The aim of this article is to describe and consider the contributions made by a researcher-driven, population-specific CAB in a genomics of schizophrenia research project taking place in South Africa, from the perspective of the research team.DiscussionFour broad discussion topics emerged during the CAB meetings namely: 1) informed consent procedures, 2) recruitment strategies, 3) patient illness beliefs and stigma experiences, and 4) specific ethical concerns relating to the project. The authors consider these discussions in terms of their contributions to instrumental and intrinsic goals of community engagement.SummaryThe CAB gave valuable input on the consent processes and materials, recruitment strategies and suggested ways of minimizing the potential for stigma and discrimination. All of these contributions were of an instrumental nature, and helped improve the way in which the research took place. In addition, and perhaps more importantly, the CAB made a unique and important contribution relating to intrinsic functions such as promoting the respect and dignity of research participants and their community. This was particularly evident in ensuring sensitivity and respect of the community’s traditional beliefs about schizophrenia and its treatment, and in this way promoting a respectful relationship between the research team and the participants. (shrink)

The notion of embodiment is central to the phenomenological approach to schizophrenia. This paper argues that fundamental concepts for the understanding of schizophrenia have a bodily dimension. We present two single cases of first-onset schizophrenic patients and analyze the reports of their experiences. Problems such as loss of self, loss of common sense, and intentionality disorders reveal a disconnectedness that can be traced back to a detachment from the lived body. Hyperreflectivity and hyperautomaticity are used as coping mechanisms, (...) but reflect the same problem of the split between body and mind. It is argued that the sole focus on cognitive impairments leads to a distorted image of schizophrenia, and that the acknowledgment of its fundamental bodily roots enables one to see the coherence between the diverse symptoms. As for the practical implications of the phenomenological approach, further research is needed to investigate if and how body- and movement-oriented therapies might strengthen the embodiment of schizophrenic patients. (shrink)

We argue that a phenomenological approach to social space, as well as its relation to embodiment and affectivity, is crucial for understanding how the social world shows up as social in the first place—that is, as affording different forms of sharing, connection, and relatedness. We explore this idea by considering two cases where social space is experientially disrupted: Moebius Syndrome and schizophrenia. We show how this altered sense of social space emerges from subtle disruptions of embodiment and affectivity characteristic (...) of these conditions. These disruptions are instructive, we suggest, in that they highlight the foundational role that body and affect play in organizing social space—the lived context in which we first encounter one another as social agents. (shrink)

Michael Stocker’s “The Schizophrenia of Modern Ethical Theories” attacks versions of consequentialism and deontological ethics on the grounds that they are self-effacing. While it is often thought that Stocker’s argument gives us a reason to favour virtue ethics over those other theories, Simon Keller has argued that this is a mistake. He claims that virtue ethics is also self-effacing, and is therefore afflicted with the self-effacement- related problems that Stocker identifies in consequentialism and deontology. This paper defends virtue ethics (...) against this claim. Although there is a kind of self-effacement invol- ved in the exercise of virtue, this is quite different from the so-called schizophrenia that Stocker thinks is induced by modern ethical theory. Importantly, manifesting virtue does not require one to embrace mutually inconsistent moral commitments, as is at times encouraged by consequentialists and deontologists. This paper also considers a reading of the virtue-ethical criterion of right action that is encouraged by Bernard Williams’s distinction between a de re and a de dicto interpretation of the phrase “acting as the virtuous person would.” I argue that such a reading addresses concerns that a virtue-ethi- cal criterion of right action inevitably generates a problematic form of self-effacement. (shrink)

Scientists, philosophers, and even the lay public commonly accept that schizophrenia stems from a biological or internal ‘dysfunction.’ However, this assessment is typically accompanied neither by well-defined criteria for determining that something is dysfunctional nor empirical evidence that schizophrenia satisfies those criteria. In the following, a concept of biological function is developed and applied to a neurobiological model of schizophrenia. It concludes that current evidence does not warrant the claim that schizophrenia stems from a biological dysfunction, (...) and, in fact, that unusual neural structures associated with schizophrenia may have functional or adaptive significance. The fact that current evidence is ambivalent between these two possibilities (dysfunction versus adaptive function) implies that schizophrenia researchers should be much more cautious in using the ‘dysfunction’ label than they currently are. This has implications for both psychiatric treatment as well as public perception of mental disorders. (shrink)

This paper explores the question concerning the relationship between basic and higher layers of experience and self-experience. The latter distinction implicitly presupposes the idea of a univocal foundation. After explaining the formal ontological law of foundation, an attempt is made to clarify how the idea of foundation may be suitable to understand the relationship among moments, or layers, of self-experience. To this aim, the phenomenological descriptions of self- and world-experience in dementia and schizophrenia are compared. The comparison between these (...) two, in many ways radically different, pathologies allows us to highlight both the potentialities and the limits of resorting to the foundational relationship for the description of lived experience. Taking the challenges coming from the description of dementia and schizophrenia into serious consideration, the meaning of the “stratified” account of self-experience will be eventually reassessed, and a way to complement the idea of foundation among layers will be proposed. (shrink)

Whether or not conscious recollection in autobiographical memory is affected in schizophrenia is unknown. The aim of this study was to address this issue using an experiential approach. An autobiographical memory enquiry was used in combination with the Remember/Know procedure. Twenty-two patients with schizophrenia and 22 normal subjects were asked to recall specific autobiographical memories from four lifetime periods and to indicate the subjective states of awareness associated with the recall of what happened, when and where. They gave (...) Remember, Know or Guess responses according to whether they recalled these aspects of the event on the basis of conscious recollection, simply knowing, or guessing. Results showed that the frequency and consistency of Remember responses was significantly lower in patients than in comparison subjects. In contrast, the frequency of Know responses was not significantly different, whereas the frequency of patients’ Guess responses was significantly enhanced. It is concluded that the frequency and consistency of conscious recollection in autobiographical memory is reduced in patients with 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)

Schizophrenia involves profound but enigmatic disturbances of affective or emotional life. The affective responses as well as expression of many patients in the schizophrenia spectrum can seem odd, incongruent, inadequate, or otherwise off-the-mark. Such patients are, in fact, often described in rather contradictory terms: as being prone both to exaggerated and to diminished levels of emotional or affective response. According to Ernst Kretschmer, they actually tend to have both kinds of experience at the same time. This paper attempts (...) to explain what might be termed this 'Kretschmerian paradox'. Some relevant concepts and vocabulary for affect and emotion are discussed . The need for a phenomenological approach focusing on subjective experience is suggested. Three modes of abnormal experience in schizophrenia are investigated in light of their implications for affect or emotion: alienation of the lived body ; fragmented perception and loss of affordances ; and preoccupation with a quasi-delusional world created by the self. (shrink)

Empirical approaches on topics such as consciousness, self-awareness, or introspective perspective, need a conceptual framework so that the emerging, still unconnected findings can be integrated and put into perspective. We introduce a model of self-consciousness derived from phenomenology, philosophy, the cognitive, and neurosciences. We will then give an overview of research data on one particular aspect of our model, self-agency, trying to link findings from cognitive psychology and neuroscience. Finally, we will expand on pathological aspects of self-agency, and in particular (...) on psychosis in schizophrenia. We show, that a deficient self-monitoring system underlies, in part, hallucinations and formal thought (language) disorder in schizophrenia. We argue, that self-consciousness is a valid construct and can be studied with the instruments of cognitive and neuroscience. (shrink)

This article provides an introduction to a special issue of the journal Philosophy, Psychiatry and Psychology, On Understanding and Explaining Schizophrenia. The article identifies a common thread running through the different contributions to this special issue, inspired by Jaspers's (1963) suggestion that a profound impairment in the ability to engage in interpersonal and social relations is a key factor in psychiatric disorders. It is argued that this suggestion can help solve a central dilemma in psychopathology, which is to make (...) intelligible the emergence and nature of psychiatric phenomena involving disturbances of rationality, intentionality and self-consciousness, whilst at the same time accounting for a sense in which such phenomena resist understanding. (shrink)

Based on recent insight into the thalamocortical system and its role in perception and conscious experience, a unified pathophysiological framework for hallucinations in neurological and psychiatric conditions is proposed, which integrates previously unrelated neurobiological and psychological findings. Gamma-frequency rhythms of discharge activity from thalamic and cortical neurons are facilitated by cholinergic arousal and resonate in networks of thalamocortical circuits, thereby transiently forming assemblies of coherent gamma oscillations under constraints of afferent sensory input and prefrontal attentional mechanisms. If perception is based (...) on synchronisation of intrinsic gamma activity in the thalamocortical system, then sensory input to specific thalamic nuclei may merely play a constraining role. Hallucinations can be regarded as underconstrained perceptions that arise when the impact of sensory input on activation of thalamocortical circuits and synchronisation of thalamocortical gamma activity is reduced. In conditions that are accompanied by hallucinations, factors such as cortical hyperexcitability, cortical attentional mechanisms, hyperarousal, increased noise in specific thalamic nuclei, and random sensory input to specific thalamic nuclei may, to a varying degree, contribute to underconstrained activation of thalamocortical circuits. The reticular thalamic nucleus plays an important role in suppressing random activity of relay cells in specific thalamic nuclei, and its dysfunction may be implicated in the biological vulnerability to hallucinations in schizophrenia. Combined with general activation during cholinergic arousal, this leads to excessive disinhibition in specific thalamic nuclei, which may allow cortical attentional mechanisms to recruit thalamic relay cells into resonant assemblies of gamma oscillations, regardless of their actual sensory input, thereby producing an underconstrained perceptual experience. Key Words: Charles Bonnet syndrome; gamma oscillations; hallucinations; late paraphrenia; Lewy body dementia; perception; schizophrenia; thalamocortical system. (shrink)

The paper discusses two recent approaches to schizophrenia, a phenomenological and a neuroscientific approach, illustrating how new directions in philosophy and cognitive science can elaborate accounts of psychopathologies of the self. It is argued that the notion of the minimal and bodily self underlying these approaches is still limited since it downplays the relevance of social interactions and relations for the formation of a coherent sense of self. These approaches also illustrate that we still lack an account of how (...) 1st and 3rd person observations can fruitfully go together in an embodied account of disorders of the self. Two concepts from enactive cognitive science are introduced, the notions of autonomy and sense-making. Based on these, a new proposal for an enactive approach to psychopathologies of the self is outlined that integrates 1st and 3rd person perspectives, while strongly emphasising the role of social interactions in the formation of self. It is shown how the enactive framework might serve as a basis for an alternative understanding of disorders of the self such as schizophrenia, as a particular form of socially constituted self-organisation. (shrink)

Suicide prevention is a National Health Service priority in the United Kingdom. People with mental illness are seen to represent one of the most vulnerable groups for suicide and recent British Government policy has focused on prevention and management of perceived risk. This approach to suicide prevention is constructed under a biomedical model of psychiatry, which maintains that suicidal persons suffer from some form of disease or irrational drive towards self-destruction. Many react to the idea of self-inflicted death with instinctive (...) revulsion, which has prevented serious discussion of the concept of rational suicide, particularly in relation to those with schizophrenia. The idea that there may be circumstances in which suicide can be viewed as rational is discussed within the biomedical approach to ethics and wider literature primarily in relation to physical disease, terminal states and chronic pain. It is not deemed a viable choice for those who are considered ‘non-autonomous’ due to the controlling forces of mental illness. I propose that suicide is not a consequence of mental illness per se, and that it may be seen as a rational response to a realistic perspective on the course and consequences of living with schizophrenia. The denial of dialogue about the validity of suicidal ideation for people with schizophrenia has led to negative consequences for people with serious mental illness in terms of justice and recognition of person-hood. (shrink)

We compared the processing of natural language quantifiers in a group of patients with schizophrenia and a healthy control group. In both groups, the difficulty of the quantifiers was consistent with computational predictions, and patients with schizophrenia took more time to solve the problems. However, they were significantly less accurate only with proportional quantifiers, like more than half. This can be explained by noting that, according to the complexity perspective, only proportional quantifiers require working memory engagement.

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)

In this paper, we use a phenomenological approach to compare the unusual ways in which language can be experienced by individuals with schizophrenia or severe mood disorders, specifically mania and melancholia. Our discussion follows a tripartite/dialectical format: first we describe traditionally observed distinctions ; then we consider some apparent similarities in the experience of language in these conditions. Finally, we explore more subtle, qualitative differences. These involve: 1, interpersonal orientation, 2, forms of attention and context-relevance, 3, underlying mutations of (...) experience, and 4, meta-attitudes toward language. Such distinctions appear to reflect significant differences in underlying forms of subjectivity; they are broadly consistent with work in phenomenological psychopathology on other aspects of experience, including body, self, and social world. An understanding of such distinctions may assist with difficult cases of differential diagnosis, while also contributing to a better understanding of suffering persons and of psychological factors underlying their disorders. (shrink)

In this paper, I give a Kantian answer to the question whether and why it would be inappropriate to blame people suffering from mental disorders that fall within the schizophrenia spectrum. I answer this question by reconstructing Kant’s account of mental disorder, in particular his explanation of psychotic symptoms. Kant explains these symptoms in terms of various types of cognitive impairment. I show that this explanation is plausible and discuss Kant’s claim that the unifying feature of the symptoms is (...) the patient’s inability to enter into an exchange of reasons with others. After developing a Kantian Quality of Will Thesis, I analyze some real life cases. Firstly, I argue that delusional patients who are unable to enter into an exchange of epistemic reasons are exempted from doxastic rather than moral responsibility. They are part of the moral community and exonerated from moral blame only if their actions do not express a lack of good will. Secondly, I argue that disorganized patients who are unable to form intentions and to make plans are exempted from moral responsibility because they do not satisfy the conditions for agency. (shrink)

In this paper I discuss an intriguing and relatively little studied symptomatic expression of schizophrenia known as experiences of activity in which patients form the delusion that they can control some external events by the sole means of their mind. I argue that experiences of activity result from patients being prone to aberrantly infer causal relations between unrelated events in a retrospective way owing to widespread predictive deficits. Moreover, I suggest that such deficits may, in addition, lead to an (...) aberrant intentional binding effect i.e., the subjective compression of the temporal interval between an intentional action and its external effects. In particular, it might be that patient’s thoughts are bound to the external events they aimed to control producing, arguably, a temporal contiguity between these two components. Such temporal contiguity would reinforce or sustain the feeling that the patient mind is directly causally efficient. (shrink)

Contemporary psychiatry is becoming more biologically oriented in the attempt to elicit a biological rationale of mental diseases. Although mental disorders comprise mostly functional abnormalities, there is a substantial overlap between neurology and psychiatry in addressing cognitive disturbances. In schizophrenia, the presence of cognitive impairment prior to the onset of psychosis and early after its manifestation suggests that some neurocognitive abnormalities precede the onset of psychosis and may represent a trait marker. These cognitive alterations may arise from functional disconnectivity, (...) as no significant brain damage has been found. In this review we aim to revise A.R. Luria’s systematic approach used in the neuropsychological evaluation of cognitive functions, which was primarily applied in patients with neurological disorders and in the cognitive evaluation in schizophrenia and other related disorders. As proposed by Luria, cognitive processes, associated with higher cortical functions, may represent functional systems that are not localized in narrow, circumscribed areas of the brain, but occur among groups of concertedly working brain structures, each of which makes its own particular contribution to the organization of the functional system. Current developments in neuroscience provide evidence of functional connectivity in the brain. Therefore, Luria’s approach may serve as a frame of reference for the analysis and interpretation of cognitive functions in general and their abnormalities in schizophrenia in particular. Having said that, modern technology, as well as experimental evidence, may help us to understand the brain better and lead us towards creating a new classification of cognitive functions. In schizophrenia research, multidisciplinary approaches must be utilized to address specific cognitive alterations. The relationships among the components of cognitive functions derived from the functional connectivity of the brain may provide an insight into cognitive machinery. (shrink)

Many with schizophrenia find social interactions a profound and terrifying threat to their sense of self. To better understand this we draw upon dialogical models of the self that suggest that those with schizophrenia have difficulty sustaining dialogues among diverse aspects of self. Because interpersonal exchanges solicit and evoke movement among diverse aspects of self, many with schizophrenia may consequently find those exchanges overwhelming, resulting in despair, the sensation of fusion with another, and/or self-dissolution. In short, compromised (...) dialogical capacities may be a contributing factor to social dysfunction in schizophrenia. (shrink)

BackgroundCognitive impairments are a core feature in schizophrenia and are linked to poor social functioning. Numerous studies have shown that cognitive remediation can enhance cognitive and functional abilities in patients with this pathology. The underlying mechanism of these behavioral improvements seems to be related to structural and functional changes in the brain. However, studies on neural correlates of such enhancement remain scarce.ObjectivesWe explored the neural correlates of cognitive enhancement following cognitive remediation interventions in schizophrenia and the differential effect (...) between cognitive training and other therapeutic interventions or patients’ usual care.MethodWe searched MEDLINE, PsycInfo, and ScienceDirect databases for studies on cognitive remediation therapy in schizophrenia that used neuroimaging techniques and a randomized design. Search terms included randomized controlled trial, cognitive remediation, cognitive training, rehabilitation, magnetic resonance imaging, po... (shrink)

I begin by examining how genetics drivesschizophrenia research, and raise both familiar andrelatively novel criticisms of the evidence putativelysupporting the genetic basis of schizophrenia. Inparticular, I call attention to a set of concernsabout the effects of placentation on concordance ratesof schizophrenia in monozygotic twins, which furtherweakens the case for schizophrenia''s so-called stronggenetic component. I then underscore two criticalpoints. First, I emphasize the importance of takingseriously considerations about the complexity of bothontogenesis and the development of hereditarydiseases. The recognition (...) of developmentalconstraints and supports is crucial, for attention todevelopment exposes the naivete of too many models ofgene action in the aetiology of disease. Secondly, Iattend to those schizophreniologists who ignoremethodological criticisms and thus presume a geneticbasis for schizophrenia, and then seek the schizophrenic genotype lacking an adequatephenotype. In response I attempt to demonstrate thenecessity of a sustained effort at characterizing thephenotype of schizophrenia as an enabling conditionfor the whole enterprise of psychiatric genetics – andfor psychiatry itself. Without the organism-levelphenotype, research at the level of genes will remainunproductive – assuming of course that research at thegenetic level is appropriate at all. (shrink)

Patients suffering from schizophrenia have an impaired meta-representation also known as Theory of Mind . Moreover, the presence of delusions or other positive symptoms of schizophrenia has been correlated to poor ToM performances. Lack of insight is a common symptom of schizophrenia and can be considered a critical manifestation of impaired ToM abilities. In particular, the present study addresses the role of perspective ToM ability in schizophrenic patients. Thirty severely delusional schizophrenic patients completely lack insight when interviewed (...) about their delusions. Seven subsequently gain insight about their mental state when perspective is shifted from the first person to third person. These data suggest that in some delusional schizophrenic patients, it may be possible to gain access to and modify their mental states. (shrink)

This paper seeks to demonstrate the structural difference in communication of schizophrenia and autism. For a normal adult, spontaneous communication is nothing but the transmission of phantasía (thought) by means of perceptual objects or language. This transmission is first observed in a make-believe play of child. Husserl named this function “perceptual phantasía,” and this function presupposes as its basis the “internalized affection of contact” (which functions empirically in eye contact, body contact, or voice calling me). Regarding autism, because of (...) the innate lack of affection of contact, intersubjective perceptual phantasía does not occur spontaneously. Consequently, autistics do not engage in make-believe play but in stereotyped and solipsistic play. Without the formation of perceptual phantasía, there is no differentiation between phantasía and perception. For this reason, people with Asperger's syndrome consider conversation not an immediate communication of thought but a logical transmission of concepts. Schizophrenia is characterized by a distortion in the internalized affection of contact, resulting in a disturbance of perceptual phantasía, and this later is covered by various symptoms—for example, delusion as a pathological kind of communication of thought. This delusion is based on the pathological internalized affection of contact represented by a terrifying Other. (shrink)

Recent studies have shown that schizophrenia may be a disease affecting the states of consciousness. The present study is aimed at investigating metamemory, i.e., the knowledge about one's own memory capabilities, in patients with schizophrenia. The accuracy of the Confidence level (CL) in the correctness of the answers provided during a recall phase, and the predictability of the Feeling of Knowing (FOK) when recall fails were measured using a task consisting of general information questions and assessing semantic memory. (...) Nineteen outpatients were paired with 19 control subjects with respect to age, sex, and education. Results showed that patients with schizophrenia exhibited an impaired semantic memory. CL ratings as well as CL and FOK accuracy were not significantly different in the schizophrenic and the control groups. However, FOK ratings were significantly reduced for the patient group, and discordant FOK judgments were also observed more frequently. Such results suggest that FOK judgments are impaired in patients with schizophrenia, which confirms that schizophrenia is an illness characterized by an impaired conscious awareness of one's own knowledge. (shrink)

Chlorpromazine efficacy in schizophrenia was observed 60 years ago. Advances in pharmacotherapy of this disorder have been modest with effectiveness still limited to the psychosis psychopathology and mechanism still dependent on dopamine antagonism. While a look backward may generate pessimism, future discovery may be far more robust. The near future will see significant changes in paradigms applied in discovery. Rather than viewing schizophrenia as a disease entity represented by psychosis, the construct will be deconstructed into component psychopathology domains. (...) Each domain will represent a clinical target for aetiologic and therapeutic discovery. Research on pathophysiology will shift to the neural circuit level in relation to specific behavioural constructs. Progress at the molecular, genetic, cellular and network levels will be more robust. The behavioural paradigm will map on to the deconstructed clinical paradigm and in the process discovery will cut across current classification boundaries. (shrink)

Conscious awareness comprises two distinct states, autonoetic and noetic awareness. Schizophrenia impairs autonoetic, but not noetic, awareness. We investigated the strategic regulation of relevant and irrelevant contents of conscious awareness in schizophrenia using a directed forgetting paradigm. Twenty-one patients with schizophrenia and 21 normal controls were presented with words and told to learn some of them and forget others. In a subsequent test, they were asked to recognize all the words they had seen previously and give remember, (...) know or guess responses according to whether they recognized words on the basis of autonoetic awareness, noetic awareness, or guessing. Overall, patients showed the same degree of a directed forgetting effect as normal subjects. However, whereas the effect was observed both for remember and know responses in normal subjects, it was observed for know, but not for remember, responses in patients. These results indicate that patients with schizophrenia exhibit an impaired strategic regulation of contents of autonetic awareness for relevant and irrelevant information. (shrink)

A diagnosis of schizophrenia is often taken to denote a state of global irrationality within the psychiatric paradigm, wherein psychotic phenomena are seen to equate with a lack of mental capacity. However, the little research that has been undertaken on mental capacity in psychiatric patients shows that people with schizophrenia are more likely to experience isolated, rather than constitutive, irrationality and are therefore not necessarily globally incapacitated. Rational suicide has not been accepted as a valid choice for people (...) with schizophrenia due in part to a belief that characteristic irrationality prevents autonomous decision-making. Since people with schizophrenia are often seen to lack insight into the nature of their disorder, both psychiatric and ethical perspectives generally presume that suicidal acts result directly from mental illness itself and not from second-order desires. In this article, I challenge notions of global irrationality conferred by a diagnosis of schizophrenia and argue that, where delusional beliefs are unifocal, schizophrenia does not necessarily lead to a state of mental incapacity. I then attempt to show that people with schizophrenia can sometimes be rational with regard to suicide, where this decision stems from a realistic appraisal of psychological suffering. (shrink)

The insight a patient shares into their own psychosis is fundamental to their condition - it goes to the heart of what we understand 'madness' to be. Can a person be expected to accept treatment for a condition that they deny they have? Can a person be held responsible for their actions if those actions are inspired by their own unique perceptions and beliefs - beliefs that no-one else shares? The topic of insight in schizophrenia and related disorders has (...) become a major focus of research in psychiatry and psychology. It has important clinical implications in terms of outcome, treatment adherence, competence, and forensic issues. In order to study 'insight' a broad perspective is required. This involves applying knowledge from the cognitive and brain sciences, as well as from philosophy and the social sciences. Insight and Psychosis comprises a series of in-depth, well-referenced, scholarly overviews from each of these perspectives with a strong empirical foundation - including in some cases the presentation of new data and meta-analysis of the published literature. These are integrated and synthesised by the editors, both acknowledged experts in the field. The scope is truly international and spans theoretical perspectives, clinical practice, and consumer views. The book will act as a source for students and researchers interested in pursuing any number of questions and controversies around lack of insight and awareness, and will guide clinical psychologists and psychiatrists who seek a broader view of the many facets of insight that might arise during their day-to-day work. (shrink)

This paper provides a concise description and discussion of bottom–up and top–down approaches to misattribution of agency in schizophrenia. It explores if first-person accounts of passivity phenomena can provide support for one of these approaches. The focus is on excerpts in which the writers specifically examine their experiences of external influence. None of the accounts provides arguments that fit easily with only one of the possible approaches, which is in line with current attempts to theoretical integration.

In the USA and England and Wales, involuntary treatment for mental illness is subject to the constraint that it must be necessary for the health or safety of the patient, if he poses no danger to others. I will argue against this necessary condition of administering treatment and propose that the category of individuals eligible for involuntary treatment should be extended. I begin by focusing on the common disorder of schizophrenia and proceed to demonstrate that it can be a (...) considerable harm to a person's life without causing the person to be a danger to himself. I illuminate this claim by constructing a thought experiment concerning a person who slips on a banana peel and falls into a malfunctioning version of Robert Nozick's experience machine. I propose that the reasons why we should remove the person from the machine are the same reasons why we should administer involuntary treatment to individuals with schizophrenia. I rebut three objections to the analogy and conclude that if we believe that we have a duty to provide treatment for reasons relating to a person's wellbeing, it follows that we should reject the health or safety requirement and instead broaden the category of individuals who are eligible for involuntary treatment. (shrink)

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)

The reorganization of psychiatric knowledge at the turn of the twentieth century derived from Emil Kraepelin’s clinical classification of psychoses. Surprisingly, within just few years, Kraepelin’s simple dichotomy between dementia praecox and manic-depressive psychosis succeeded in giving psychiatry a new framework that is still used until the present day. Unexpectedly, Kraepelin’s simple clinical scheme based on the dichotomy replaced the significantly more differentiated nosography that dominated psychiatric research in the last three decades of the nineteenth century. Moreover, although all the (...) components of the future development were already available shortly after 1868, the real course, which led to Kraepelin’s dichotomy, was unpredictable then. This paper explores the ways in which the unpredictability of psychiatric knowledge and the postulate of a rationality underlying psychopathological phenomena interacted in the debates regarding the classification of psychoses. It examines the “natural antagonism” between the practical aspirations of an increasingly specialized medical nosology and unitary conceptions, which, in a psychopathological countermovement, emphasized that no somatic criteria can be specified for the majority of psychic abnormalities and that all nosological distinctions are not binding. In this context, this paper investigates the revival of unitary theories of psychosis in postwar German psychiatry and seeks to understand why the forms of thinking that dominated nineteenth-century psychiatry have proved to be very lasting. Furthermore, this paper emphasizes the perspectivity underlying psychiatric research on psychoses and explores the ways in which writing the history of the schizophrenia concept involves inevitably writing the history of the entire psychiatry. (shrink)

Treatment-resistant symptoms complicate the clinical course of schizophrenia, and a large proportion of patients do not reach functional recovery. In consequence, polypharmacy is frequently used in treatment-refractory cases, addressing psychotic positive, negative and cognitive symptoms, treatment-emergent side effects caused by antipsychotics and comorbid depressive or obsessive-compulsive symptoms. To a large extent, such strategies are not covered by pharmacological guidelines which strongly suggest antipsychotic monotherapy. Add-on strategies comprise combinations of several antipsychotic agents and augmentations with mood stabilizers; moreover, antidepressants and (...) experimental substances are applied. Based on the accumulated evidence of clinical trials and meta-analyses, combinations of clozapine with certain second-generation antipsychotic agents and the augmentation of antipsychotics with antidepressants seem recommendable, while the augmentation with mood stabilizers cannot be considered superior to placebo. Forthcoming investigations will have to focus on innovative pharmacological agents, the clinical spectrum of cognitive deficits and the implementation of cognitive behavioral therapy. (shrink)

Activity-dependent neuroprotective protein, discovered in our laboratory in 1999, has been characterized as a master gene vital for mammalian brain formation. ADNP de novo mutations in humans result in a syndromic form of autism-like spectrum disorder, including cognitive and motor deficits, the ADNP syndrome. One of the most important cellular processes associated with ADNP is the autophagy pathway, recently discovered by us as a key player in the pathophysiology of schizophrenia. In this regard, given the link between the microtubule (...) and autophagy systems, the ADNP microtubule end binding protein motif, namely, the neuroprotective NAP, was found to enhance autophagy while protecting microtubules and augmenting ADNP's association with both systems. Thus, linking autophagy and ADNP is proposed as a major target for intervention in brain diseases from autism to Alzheimer's disease and our findings introduce autophagy as a possible novel target for treating schizophrenia. Activity-dependent neuroprotective protein binds to microtubule-associated protein light chain 3, which forms the membrane of the autophagosome, a key organelle in the autophagy process and regulates beclin1 formation, an inducer of autophagy. Autophagy plays a major role in Alzheimer's disease and as recently discovered in schizophrenia and autism. (shrink)