Cognitive neuropsychiatry attempts to understand psychiatric disorders as disturbances to the normal function of human cognitive organisation, and it attempts to link this functional framework to relevant brain structures and their pathology. This recent scientific discipline is the natural extension of cognitive neuroscience into the domain of psychiatry. We present two examples of recent research in cognitive neuropsychiatry: delusions of control in schizophrenia, and affective disorders. The examples demonstrate how the cognitive approach is (...) a fruitful and necessary supplement to the otherwise successful biological psychiatry paradigm, which tend to bypass the cognitive level. Philosophy concerns some of the core concepts involved in psychiatric illness, particularly concerning rationality, thought and action, reality testing, and the self. We present concrete examples that illustrate how philosophical conceptual tools can be particularly important for the construction and interpretation of the cognitive models relevant to the understanding of psychiatric illness. We conclude that cognitive neuropsychiatry is a fruitful and necessary supplement to biological psychiatry. Furthermore, cognitive neuropsychiatry itself may benefit significantly from employing philosophical conceptual tools in the interpretation and construction of its cognitive models. The cognitive and philosophical approaches may thus be further steps towards a scientific psychopathology. (shrink)

The field of philosophical psychopathology is basically the philosophical study of mental disorders such as schizophrenia, bipolar disorder, depression, autism, as well as more specific symptoms and signs such as Capgras’ delusion (the delusion that your spouse, for example, is an impostor) or the anarchic hand sign (where your hand seems to act on its own intentions). This simple epithet covers a multitude of approaches: how can philosophy help to explain mental disorder? What does mental disorder tell us about consciousness, (...) cognition, emotion and ‘self’? What does the study of mental disorder tell us about phenomenology? What does philosophical phenomenology tell us about mental disorder? What do mental disorders tell us about reasoning, rationality and belief formation? What are the particular ethical aspects of mental disorder and its treatment? If philosophical.. (shrink)

The excellent and highly interesting commentaries address the following concerns: (1) neuroanatomy and neurophysiology of catatonia; (2) cognitive-motor deficits in catatonia; (3) conceptual issues; (4) general methodology in neuropsychiatric research; and (5) neurophilosophical implications. The specific problems, issues, and aspects raised by the different commentators are grouped under these categories in Table R1 presented below. These five areas of concern are then discussed in the order listed in the five sections of the Response.

The last 25 years have seen advances in our understanding of the neuroscience and neuropsychiatry of fear. From the basic brain mechanisms of fear to new evidence-based treatments for the pathologies of fear, the field has experienced progress towards an understanding of the underpinnings of fear in the brain and its influence on behaviors. Yet, to date, there has been less than ideal incorporation of these new findings, insights and models into the public policy and economic domains. Even when (...) notions of risk, uncertainty, and emotional decision-making are discussed, these discussions may not access insights from the latest contemporary neuroscience of fear, or clinical techniques in changing pathological fear responses. This paper will explore how a more complete incorporation of these advances may contribute to our understanding of fear and its management. Applying these advances in specific amenable policy areas may lead to new, more effective approaches to public and economic policies. (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)

This article focuses on both daily forms of weakness of will as discussed in the philosophical debate and psychopathological phenomena as impairments of decision making. We argue that both descriptions of dysfunctional decision making can be organized within a common theoretical framework that divides the decision making process in three different stages: option generation, option selection, and action initiation. We first discuss our theoretical framework, focusing on option generation as an aspect that has been neglected by previous models. In the (...) main body of this article, we review how both philosophy and neuropsychiatry have provided accounts of dysfunction in each decision-making stage, as well as where these accounts can be integrated. Also, the neural underpinnings of dysfunction in the three different stages are discussed. We conclude by discussing advantages and limitations of our integrative approach. (shrink)

For the new generation of cognitive neuroscientists, the mind-brain problem is no longer a matter for philosophical speculation; how the mind links with the brain can be studied experimentally. The strength of this belief is demonstrated by a stream of popular science books purporting to show how consciousness emerges from the brain. In contrast, Sean Spence presents a rigorous, modest and wholly admirable discussion of the physiological underpinnings of free will. It is of particular importance that he brings to (...) our attention various phenomena associated with psychotic illnesses. It is generally agreed that schizophrenia has a biological basis. Yet the characteristic symptoms reflect disorders of self-awareness, especially in the experience of free will (delusions of control). It follows that studies of the physiological basis of psychotic symptoms (e.g. Silbersweig et al. 1995) must also increase our understanding of the physiological basis of free will. The test for any discussion of the mind-brain problem from a scientific stance is that it suggests new possibilities for experimental studies. I think a number of the points raised in this essay provide clear starting points for the development of such experiments. (shrink)

We evaluate a growing trend towards anti-representationalism in cognitive science in the context of recent research into the development and maintenance of anorexia nervosa in cognitive neuropsychiatry. We argue two things: first, that this research relies on an explanatorily robust concept of representation—the concept of a long-term body schema; second, that this body representation underlies our most basic environmental interactions and affordance perception—the psychological phenomena supposed to be most hospitable to a non-representationalist treatment.

A Kuhnian reformulation of the recent debate in psychiatric nosography suggested that the current psychiatric classification system (the DSM) is in crisis and that a sort of paradigm shift is awaited (Aragona, 2009). Among possible revolutionary alternatives, the proposed fi ve-axes etiopathogenetic taxonomy (Charney et al., 2002) emphasizes the primacy of the genotype over the phenomenological level as the relevant basis for psychiatric nosography. Such a position is along the lines of the micro-reductionist perspective of E. Kandel (1998, 1999), which (...) sees mental disorders reducible to explanations at a fundamental epistemic level of genes and neurotransmitters. This form of micro-reductionism has been criticized as a form of genetic-molecular fundamentalism (e.g. Murphy, 2006) and a multi-level approach, in the form of the burgeoning Cognitive Neuropsychiatry, was proposed. This article focuses on multi-level mechanistic explanations, coming from Cognitive Science, as a possible alternative etiopathogenetic basis for psychiatric classification. The idea of a mechanistic approach to psychiatric taxonomy is here defended on the basis of a better conception of levels and causality. Nevertheless some critical remarks of Mechanism as a psychiatric general view are also offered. (shrink)

Cognitive neuropsychiatry (CN) is the explanation of psychiatric disorder by the methods of cognitive neuropsychology. Within CN there are, broadly speaking, two approaches to delusion. The first uses a one-stage model, in which delusions are explained as rationalizations of anomalous experiences via reasoning strategies that are not, in themselves, abnormal. Two-stage models invoke additional hypotheses about abnormalities of reasoning. In this paper, I examine what appears to be a very strong argument, developed within CN, in favor of (...) a twostage explanation of the difference in content between the Capgras and Cotard delusions. That explanation treats them as alternative rationalizations of essentially the same phenomenology. I show, however, that once we distinguish the phenomenology (and the neuroetiology), a one-stage model is adequate. In the final section I make some more general remarks on the oneand two-stage models. (shrink)

Since Darwin, the idea of psychological continuity between humans and other animals has dominated theory and research in investigating the minds of other species. Indeed, the field of comparative psychology was founded on two assumptions. First, it was assumed that introspection could provide humans with reliable knowledge about the causal connection between specific mental states and specific behaviors. Second, it was assumed that in those cases in which other species exhibited behaviors similar to our own, similar psychological causes were at (...) work. In this paper. we show how this argument by analogy is flowed with respect to the case of second-order mental states. As a test case, we focus on the question of how other species conceive of visual attention, and in particular whether chimpanzees interpret seeing as a mentalistic event involving internal states of perception, attention, and belief. We conclude that chimpanzees do not reason about seeing in this manner, and indeed, there is considerable reason to suppose that they do not harbor representations of mental states in general. We propose a reinterpretation model in which the majority of the rich social behaviors that humans and other primates share in common emerged long before the human lineage evolved the psychological means of interpreting those behaviors in mentalistic terms. Although humans, chimpanzees, and most other species may be said to possess mental states, humans alone may have evolved a cognitive specialization for reasoning about such states. (shrink)

Cognitive neuropsychiatry (CN) is the explanation of psychiatric disorder by the methods of cognitive neuropsychology. Within CN there are, broadly speaking, two approaches to delusion. The first uses a one-stage model, in which delusions are explained as rationalizations of anomalous experiences via reasoning strategies that are not, in themselves, abnormal. Two-stage models invoke additional hypotheses about abnormalities of reasoning. In this paper, I examine what appears to be a very strong argument, developed within CN, in favor of (...) a two-stage explanation of the difference in content between the Capgras and Cotard delusions. That explanation treats them as alternative rationalizations of essentially the same phenomenology. I show, however, that once we distinguish the phenomenology (and the neuroetiology), a one-stage model is adequate. In the final section I make some more general remarks on the one- and two-stage models. (shrink)

An elegant theory in cognitive neuropsychiatry explains the Capgras and Cotard delusions as resulting from the same type of anomalous phenomenal experience explained in different ways by different sufferers. ‘Although the Capgras and Cotard delusions are phenomenally distinct, we thus think that they represent patients’ attempts to make sense of fundamentally similar experiences’ (Young and Leafhead, 1996, p. 168). On the theory proposed by Young and Leafhead, the anomalous experience results from damage to an information processing subsystem which (...) associates an affect of ‘familiarity’ with overt recognition of faces, and, sometimes, scenes and objects. When the normal affect of familiarity is absent the subject experiences an unusual feeling of derealization or depersonalization. The Cotard and Capgras patients adopt different, delusional, explanations of this unusual qualitative state, for reasons to do with ‘attributional style’. It is part of this attribution hypothesis that delusional subjects, like normal people, interpret perceptual phenomena in the light of a set of background beliefs whose structure is a product of social/contextual influences and individual psychological dispositions. That structure predisposes people to reason in certain ways, to discount or reinterpret evidence and to favour certain hypoth-. (shrink)

Detailed studies of people who have experienced the Capgras delusion (the delusion that certain other people, usually close relatives, have been replaced by impostors) have led to advances in constructing an account which can deal with the basic symptomatology, testing alternative possibilities, generating and testing non‐trivial predictions, and broadening the scope of the basic account to encompass other delusions. This paper outlines these developments. It uses them to explore implications for understanding the formation and maintenance of beliefs, and to discuss (...) basic principles of what has come to be known as cognitive neuropsychiatry. (shrink)

Young and colleagues . Betwixt life and death: case studies of the Cotard delusion. In P. W. Halligan & J. C. Marshall , Method in madness: Case studies in cognitive neuropsychiatry. Mahway, NJ: Lawrence Erlbaum Associates.) have suggested that cases of the Cotard delusion result when a particular perceptual anomaly occurs in the context of an internalising attributional style. This hypothesis has not previously been tested directly. We report here an investigation of attributional style in a 24-year-old woman (...) with Cotard delusion . LU’s attributional style was assessed using the Internal, Personal and Situational Attributions Questionnaire . A new measure of causal locus: the internal, personal and situational attributions questionnaire. Personality and Individual Differences, 20, 261–264.). LU showed a significantly greater proportion of internalising attributions than the control group, both overall and for negative events specifically. The results obtained thus support an association of Cotard delusion with an internalising attributional style, and are therefore consistent with the account of Young and colleagues. The potential brain basis of Cotard delusion is discussed. (shrink)

In lieu of an abstract, here is a brief excerpt of the content:Philosophy, Psychiatry, & Psychology 9.1 (2002) 55-59 [Access article in PDF] One Stage Is Not Enough Andrew W. Young and Karel W. de Pauw Keywords: delusions, Cotard delusion, Capgras delusion, cognitive neuropsychiatry. WE WELCOME THE OPPORTUNITY to offer our reflections on Philip Gerrans' interesting paper. Our opinion is that on fundamental issues we agree quite a bit—but there are clear differences when it comes to details.The most (...) basic issue concerns the nature of the enterprise. Like Gerrans, we think that it is possible to create testable accounts of the formation and maintenance of what would otherwise seem bizarre and inexplicable delusions, and that these accounts should be grounded in theoretical models of factors that underpin our everyday perception and reasoning. This general approach certainly forms part of what has been called cognitive neuropsychiatry. However, we disagree with Gerrans in that we see cognitive neuropsychiatry as an attempt to draw on the underlying logic of cognitive neuropsychology, rather than (as Gerrans implies) its current methods. The underlying logic of cognitive neuropsychological approaches has been to try to understand the effects of brain injury in terms of disruption of different components of theoretical models of normal abilities. In this approach, a model of normal performance is tested by its ability to account for the effects of brain injury. Where the model of normal performance also provides a convincing account of brain injury it is retained, and when it fails to account for effects of brain injury, it is revised or abandoned. In cognitive neuropsychiatry, the key theoretical move has been to argue that an adequate model of normal performance should be able to account for any disordered pattern (Ellis and Young 1990). The same logic of seeking to explain disordered performance by reference to models of normal function is then attempted, but for disorders that would usually fall within the province of psychiatry.In our opinion, however, cognitive neuropsychiatry will not simply involve importing the methods of cognitive neuropsychology into the new domain; they will need to be developed and adapted to fit the new agenda (Young 2000).In cognitive neuropsychology, progress has often come from the careful investigation of people with stable, selective deficits of fundamental cognitive functions involved in sensory analysis, memory, and verbal or motor output. In contrast, delusional beliefs can be relatively unstable; often they are only held for a few weeks or even days. When the delusions change, patients may modify or abandon them as suddenly as they seemed to form them, or they may give them up much more slowly and reluctantly. At the very least, this creates difficulties in the timing of investigations and in interpreting the relation of deficits and symptoms, which may be recorded on separate dates. These methodological problems [End Page 55] are exacerbated by the fact that deficits linked to complex abnormal experiences such as delusions may be multifaceted and diffuse, even when the delusions themselves have a specific content or theme. Such complications do not invalidate cognitive neuropsychiatry, but they do mean it will need to develop its own methods for dealing with them and making appropriate inferences.One of the key complexities that has surfaced already involves the idea that delusional beliefs might reflect the interaction of two or more contributory factors. Gerrans discusses a particular variant of this idea, which had been suggested by Young and Leafhead (1996) as an approach to understanding the Cotard delusion: The Cotard delusion represents a depressed person's attempt to account for abnormal perceptual experiences. It follows that the delusion is based on an unfortunate interaction between different contributory factors. One set of factors creates the abnormal perceptual experiences, which are characterised by lack of emotional responses and feelings of emptiness, depersonalisation and derealisation. The other factors result in a misinterpretation of these perceptual changes, in which the patients' depressed moods lead them correctly to attribute the changes to themselves, but to exaggerate their consequences. (Young and Leafhead, 1996, 166) Gerrans describes this as a two-stage account, but argues that a one-stage account based only on abnormal perceptual... (shrink)

Delusions are explanations of anomalous experiences. A theory of delusion requires an explanation of both the anomalous experience _and _the apparently irrational explanation generated by the delusional subject. Hence, we require a model of rational belief formation against which the belief formation of delusional subjects can be evaluated. _Method. _I first describe such a model, distinguishing procedural from pragmatic rationality. Procedural rationality is the use of rules or procedures, deductive or inductive, that produce an inferentially coherent set of propositions. Pragmatic (...) rationality is the use of procedural rationality _in context_. I then apply the distinction to the explanation of the Capgras and the Cotard delusions. I then argue that delusions are failures of pragmatic rationality. I examine the nature of these failures employing the distinction between performance and competence familiar from Chomskian linguistics. _Results. _This approach to the irrationality of delusions reconciles accounts in which the explanation of the anomalous experience exhausts the explanation of delusion, accounts that appeal to further deficits within the reasoning processes of delusional subjects, and accounts that argue that delusions are not beliefs at all. (Respectively, one-stage, two-stage, and expressive accounts.) _Conclusion. _In paradigm cases that concern cognitive neuropsychiatry the irrationality of delusional subjects should be thought of as a performance deficit in pragmatic rationality. (shrink)

In this paper I consider a theory developed within cognitive neuropsychiatry to explain two delusions of misidentification, the Capgras and the Cotard delusions. These delusions are classified together with others in which the subject misidentifies persons, places or objects, including parts of her own body. Strictly speaking, the Cotard may not, at the level of content, be a delusion of misidentification, but I have described it as such because the theory I discuss treats it as sharing a causal (...) and a conceptual structure with the Capgras delusion. That theory, associated particularly with the work of Andy Young, raises a Wittgensteinian echo in its claim that, at the subpersonal, information-processing, level, perceptual recognition of familiar faces and scenes is laden with affect. Where affect is absent or distorted as a result of neurological damage the subject “feels” strange in the presence of familiar scenes or people. Thus Young and Leafhead in their discussion of the Cotard delusion: “What the patients often give as evidence of their nonexistence or death is that they don’t have proper feeling.”. (shrink)

In this paper I consider a theory developed within cognitive neuropsychiatry to explain two delusions of misidentification, the Capgras and the Cotard delusions. These delusions are classified together with others in which the subject misidentifies persons, places or objects, including parts of her own body. Strictly speaking, the Cotard may not, at the level of content, be a delusion of misidentification, but I have described it as such because the theory I discuss treats it as sharing a causal (...) and a conceptual structure with the Capgras delusion. That theory, associated particularly with the work of Andy Young, raises a Wittgensteinian echo in its claim that, at the subpersonal, information-processing, level, perceptual recognition of familiar faces and scenes is laden with affect. Where affect is absent or distorted as a result of neurological damage the subject “feels” strange in the presence of familiar scenes or people. Thus Young and Leafhead in their discussion of the Cotard delusion: “What the patients often give as evidence of their nonexistence or death is that they don’t have proper feeling.”. (shrink)

Kanaan and McGuire elegantly describe three challenges facing the use of fMRI to uncover cognitive mechanisms. They shows how these challenges ramify in the case of identifying the mechanisms responsible for psychiatric disorders. In this commentary, I would like to raise another difficulty for fMRI that also appears to ramify in similar cases. This is that there are good reasons for doubting one of the assumptions on which many fMRI studies are based: that neural mechanisms are always and everywhere (...) sufficient for cognition. I suggest that in the case of the mechanisms underlying psychiatric disorders, this assumption should be doubted. I do not dispute that a malfunctioning neural mechanism is likely to be a necessary component of a psychiatric disorder—as Kanaan and McGuire say, the experimental evidence from cognitive neuropsychiatry gives us excellent reasons to think that this is so. My question is whether a story only in terms of these neural mechanisms is sufficient to explain the mechanism of a psychiatric disorder. Is the reduction, projected by cognitive neuropsychiatry, of psychiatric disorders to disorders in neural functioning even in principle possible? Drawing on recent concerns about the location of mental states, I argue that such a reduction is likely to fail. Even if the considerable problems raised by Kanaan and McGuire for fMRI could be addressed, we have no reason to think that the mechanisms involved in psychiatric disorders are entirely neural, and that fMRI, or even a perfect science-fiction brain-scanner, would be capable of uncovering them. Psychiatric disorders, like numerous other cognitive processes, are liable to cross the brain–world boundary in such a promiscuous way as to be resistant to neural reduction. (shrink)

The enhancement debate in neuroscience and biomedical ethics tends to focus on the augmentation of certain capacities or functions: memory, learning, attention, and the like. Typically, the point of contention is whether these augmentative enhancements should be considered permissible for individuals with no particular “medical” disadvantage along any of the dimensions of interest. Less frequently addressed in the literature, however, is the fact that sometimes the _diminishment_ of a capacity or function, under the right set of circumstances, could plausibly contribute (...) to an individual's overall well-being: more is not always better, and sometimes less is more. Such cases may be especially likely, we suggest, when trade-offs in our modern environment have shifted since the environment of evolutionary adaptation. In this article, we introduce the notion of “diminishment as enhancement” and go on to defend a _welfarist_ conception of enhancement. We show how this conception resolves a number of definitional ambiguities in the enhancement literature, and we suggest that it can provide a useful framework for thinking about the use of emerging neurotechnologies to promote human flourishing. (shrink)

The brain scanner is a piece of philosophical fiction made fact. It was among the most common creations of thought experiments, along with the brain-vat and the mindless robot. With the imaginary scanner, readings were taken of each other's brain activity, thereby learning everything about other minds, or very little, depending on the outcome of the thought experiment. The scanners that are now in use—those that allow us to do functional magnetic resonance imaging (fMRI), for example—are a little different to (...) those imagined, perhaps, but they have very much arrived. They are in daily use in hundreds of laboratories, and for the past 15 years or so have been grabbing headlines the world over with breakthrough .. (shrink)

F. Brencio (2023), Embodied Attention. A phenomenological hypothesis, in D. Stoyanov (Ed.), Contemporary Neuropsychiatry: Implications from Cognitive Neuroscience, Cambridge Scholars Publishing, Cambridge, pp. 26-42.

This book investigates the relationship between our present and future selves. It focuses specifically on diachronic self-regarding decisions: choices involving our earlier and later selves, in which the earlier self makes a decision for the later self. The author connects the scientific understanding of the neurobehavioral processes at the core of individuals' perceptions of their future selves with the philosophical reflection on individuals' moral relationship with their future selves. She delineates a descriptive theory of the perception of the future self (...) that is based on empirical evidence and that systematizes and integrates the current theoretical literature. She then argues for the morality of prudence and interprets diachronic self-regarding decisions as decisions between two agents-the earlier and later selves-that belong to the realm of intergenerational ethics, which regulates the relationship between contemporary people and future generations. Finally, the author provides a moral theory of prudence based on respect for one's agency. This theory identifies what the present and the future selves owe to one another in diachronic self-regarding decisions. Moral Choices for Our Future Selves will be of interest to researchers and students working in ethics, moral psychology, philosophy of mind, and cognitive science. (shrink)

Neuroethics studies the ethical, social, and legal issues raised by actual or expected advances in neuroscience. The relevant fields in neuroscience include, but are not limited to, neuroimaging, cognitive neuroscience, neuropsychopharmacology, neurogenetics, and neuropsychiatry. For many, neuroethics is best understood as a subcategory of bioethics, and although not all agree, for the purposes of the present collection of articles, this definition is assumed. Although bioethics as a field of study started in the early 1970s as a normative enterprise, (...) mainly practiced by philosophers and theologians, it has since become truly inter- and multidisciplinary, comprising also law, sociology, psychology, gender studies, disability studies, anthropology, history, and many other approaches. What we particularly wanted to do in this issue, however, was to find the most pertinent questions of neuroethics from the viewpoint of philosophy, and the call for papers was drafted accordingly.Tuija Takala, Ph.D., is Academy Research Fellow at the Academy of Finland and Adjunct Professor of Social and Moral Philosophy at the University of Helsinki, Finland. She is president-elect of the European Society for Philosophy of Medicine and Health Care and holds a number of international editorial positions. Her current research interests lie in the conceptual, methodological, and theoretical aspects of philosophical bioethics.FootnotesThe editorial work for this special issue was supported by my project Neuroscience and Norms: Ethical and Legal Aspects of Norms in Neuroimaging / Ethical Concepts and Norms funded by the Academy of Finland. (shrink)

Embodied and phenomenological approaches to neuropsychiatry have proven to be promising for assessing social cognition and its impairments. Second-person neuroscience has demonstrated that the dynamics of social interaction make a difference when it comes to how people understand each other. This article presents the Perceptual Crossing Experiment (PCE) as a paradigm for studying real-time dyadic embodied interactions in the context of schizophrenia. We draw on the phenomenological concept of interbodily resonance (IR) and show how the PCE can be used (...) to accurately model and assess IR. We then turn to disembodied interaction in schizophrenia and finally propose the PCE as a translational tool for systematically assessing the hindered IR that individuals with schizophrenia suffer from. We offer an experimental approach to phenomenology which could be informative for the development of more embodied interventions aiming to remedy the profoundly disrupted social life that patients with schizophrenia live with. (shrink)

_The first part called the Preamble tackles: (a) the issues of silence and speech, and life and disease; (b) whether we need to know some or all of the truth, and how are exact science and philosophical reason related; (c) the phenomenon of Why, How, and What; (d) how are mind and brain related; (e) what is robust eclecticism, empirical/scientific enquiry, replicability/refutability, and the role of diagnosis and medical model in psychiatry; (f) bioethics and the four principles of beneficence, non-malfeasance, (...) autonomy, and justice; (g) the four concepts of disease, illness, sickness, and disorder; how confusion is confounded by these concepts but clarity is imperative if we want to make sense out of them; and how psychiatry is an interim medical discipline. The second part called The Issues deals with: (a) the concepts of nature and nurture; the biological and the psychosocial; and psychiatric disease and brain pathophysiology; (b) biology, Freud and the reinvention of psychiatry; (c) critics of psychiatry, mind-body problem and paradigm shifts in psychiatry; (d) the biological, the psychoanalytic, the psychosocial and the cognitive; (e) the issues of clarity, reductionism, and integration; (f) what are the fool-proof criteria, which are false leads, and what is the need for questioning assumptions in psychiatry. The third part is called Psychiatric Disorder, Psychiatric Ethics, and Psychiatry Connected Disciplines. It includes topics like (a) psychiatric disorder, mental health, and mental phenomena; (b) issues in psychiatric ethics; (c) social psychiatry, liaison psychiatry, psychosomatic medicine, forensic psychiatry, and neuropsychiatry. The fourth part is called Antipsychiatry, Blunting Creativity, etc. It includes topics like (a) antipsychiatry revisited; (b) basic arguments of antipsychiatry, Szasz, etc.; (c) psychiatric classification and value judgment; (d) conformity, labeling, and blunting creativity. The fifth part is called The Role of Philosophy, Religion, and Spirituality in Psychiatry. It includes topics like (a) relevance of philosophy to psychiatry; (b) psychiatry, religion, spirituality, and culture; (c) ancient Indian concepts and contemporary psychiatry; (d) Indian holism and Western reductionism; (e) science, humanism, and the nomothetic-idiographic orientation. The last part, called Final Goal, talks of the need for a grand unified theory. The whole discussion is put in the form of refutable points._. (shrink)

Dans cet article, nous nous proposons d?établir une analyse comparative entre l?approche de la notion de schéma corporel dans la Phénoménologie de la perception 1 et dans les Cours de Sorbonne , réalisés entre 1949 et 1952, et dédiés, surtout, à la psychologie de l?enfant. Dans la Phénoménologie de la perception , Merleau-Ponty critique le caractère associationiste qui a marqué l?émergence de la notion de schéma corporel dans la neuropsychiatrie au passage du xix e au xx e siècle. Pour le (...) philosophe, le sens vraiment fructueux de ce dispositif repose dans son caractère intentionnel. Merleau-Ponty opère une désubstantialisation de la notion concernée. De représentation ou de no­yau cognitif organisateur de notre expérience corporelle, elle passe à fonction pré-cognitive, expression de la perméabilité des parties de notre corps les unes en relation aux autres, et, également, de la perméabilité du corps au monde et à autrui. Après la Phénoménologie de la perception , cette perméa­bilité sera pensée de plus en plus dans les termes d?une « proximité vertigi­neuse » entre nous et les objets, entre nous et autrui. Le passage, que réalise Merleau-Ponty, de l?idée d?incarnation à la conception de chair commence à être conçu dans la période entre 1945 et 1952, et se nourrit de discussions concernant la corporéité à l?intérieur, principalement, de la psychologie de l?enfant et de la psychanalyse, ainsi. (shrink)

Corlett (2019) raises two groups of challenges against the two-factor theory of delusions: One focuses on weighing “the evidence for … the two-factor theory”; the other aims to question “the logic of the two-factor theory” (p. 166). McKay (2019) has robustly defended the two-factor theory against the first group. But the second group, which Corlett believes is in many aspects independent of the first group and Darby (2019, p. 180) takes as “[t]he most important challenge to the two-factor theory raised (...) by Dr. Corlett”, has by large remained. Here I offer my two cents in response to the second group. More specifically, I argue that Corlett’s challenges to the logic of the two-factor theory, concerning modularity, double dissociation and cognitive penetration, seem to be based on some misunderstandings of the two-factor theory. (shrink)

Introduction: Neuropsychiatry has generally been regarded as a hybrid discipline that lies in the borderland between the disciplines of psychiatry and neurology. There is much debate on its current and future identity and status as a discipline. Materials and Methods: Taking a historical perspective, the future of neuropsychiatry is placed within the context of recent developments in clinical neuroscience. Results: The authors argue that with the maturation of the discipline, it must define its own identity that is not (...) dependent entirely upon the parent disciplines. The requirements for this are the claiming of neuropsychiatric territory, a strong training agenda, an emphasis on treatments that are uniquely neuropsychiatric, and a bold embrace of new developments in clinical neuroscience. Conclusion: The exponential growth in neuroscientific knowledge places neuropsychiatry in an excellent position to carve out a strong identity. It is imperative that the leaders of the discipline seize the moment. (shrink)

If our experiences are cognitively penetrable, they can be influenced by our antecedent expectations, beliefs, or other cognitive states. Theorists such as Churchland, Fodor, Macpherson, and Siegel have debated whether and how our cognitive states might influence our perceptual experiences, as well as how any such influences might affect the ability of our experiences to justify our beliefs about the external world. This article surveys views about the nature of cognitive penetration, the epistemological consequences of denying (...) class='Hi'>cognitive penetration, and the epistemological consequences of affirming cognitive penetration. (shrink)

Cognitive penetration of perception, broadly understood, is the influence that the cognitive system has on a perceptual system. The paper shows a form of cognitive penetration in the visual system which I call ‘architectural’. Architectural cognitive penetration is the process whereby the behaviour or the structure of the perceptual system is influenced by the cognitive system, which consequently may have an impact on the content of the perceptual experience. I scrutinize a study in perceptual learning (...) that provides empirical evidence that cognitive influences in the visual system produce neural reorganization in the primary visual cortex. The type of cognitive penetration can be synchronic and diachronic. (shrink)