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)

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 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 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)

When the University of Chicago opened its four-year medical program in 1929, the medical departments were established on the same footing as other biological departments. One of the first priorities was to build a department of psychiatry based on an interdisciplinary and holistic research program with important social implications. This plan was soon frustrated by structural factors and conflicts of interest both internal and external to the university. The story illuminates crucial dilemmas of neuropsychiatry in the interwar years and suggests (...) some of the limits to the pursuit of biology at the University of Chicago. (shrink)

Neuropsychiatry integrates neuroscience and clinical pathophysiology of the human brain-mind interface. Kalisch et al. provide an important advance with a clear, quantitative, unified neuropsychiatric model of resilience, a crucial adaptive response to adversity. They highlight positive appraisal style, describing underlying neural circuitry and mechanisms. This provides a foundation for the development of biomarkers and targeted therapeutics across the range of neuropsychiatric disorders.

Animal models have long been used to investigate human mental disorders, including depression, anxiety, and schizophrenia. This practice is usually justified in terms of the benefits (to humans) outweighing the costs (to the animals). I argue on utility maximization grounds that we should phase out animal models in neuropsychiatric research. Our leading theories of how human minds and behavior evolved invoke sociocultural factors whose relation to nonhuman minds, societies, and behavior has not been homologized. Thus it is not at all (...) clear that we are gaining the epistemic or clinical benefits we want from this animal-based research. (shrink)

BackgroundCurrent policies regulating the use of animals for scientific purposes are based on balancing between potential gain of knowledge and suffering of animals used in experimentation. The balancing process is complicated, on the one hand by plurality of views on our duties towards animals, and on the other hand by more recent discussions on uncertainty in the probability of reaching the final aim of the research and problems of translational failure.MethodsThe study combines ethical analysis based on a literature review with (...) neuropsychiatry-related preclinical research as a case study.ResultsBased on the analysis and the case study we show that neuropsychiatry-related preclinical research is an especially interesting case from an ethical perspective. The 3R principles are used to minimize the negative consequences for the animals used in research. However, neuropsychiatric research is characterized by specific challenges in assessing the probability of success of reaching the final aim, due to our limited mechanistic knowledge of human neuropsychiatric illness. Consequently, the translational value of the currently used animal models may be difficult to prove, which undermines the validity of these models and complicated the ethical assessment.ConclusionsWe conclude that a combined approach that deals with both science and the ethical dimensions is necessary to address the problems of validity and translation in neuropsychiatry-related preclinical research. We suggest this approach to comprise first, improved experimental methods, e.g. by using systematic reviews, second, a more patients-based approach that leads to models that reflect interindividual variation better, and third, more interdisciplinary cooperation. (shrink)

In lieu of an abstract, here is a brief excerpt of the content:Commentary on “Free Will in the Light of Neuropsychiatry”Benjamin Libet (bio)Is Free Will Incompatible with Neuroscience?Sean Spence sets forth some interesting approaches to the issue of free will. His concepts are provocative and his marshalling of related quotations is informative.However, I shall argue with some of his crucial assumptions, in a way that affects the validity of some of Spence’s major conclusions. The latter are that “conscious experience is (...) always temporally postneural activity and thus... ‘caused’ not causal. Our ‘control’ is a sense which may be lost.... Our sense of agency is apparently illusory.”I have, of course, no quarrel with the view that even a fully voluntary act is initiated unconsciously (non-consciously). That condition was in fact demonstrated experimentally by us (Libet et al. 1983) when we found that cerebral neural activity (“readiness potential”) precedes the subject’s awareness of his/her intention or wish to act by at least 350 msec. This applied to fully self-initiated acts that occurred without “pre-planning” by the subject of when to move. (Incidentally, those finding have been replicated by others—see Keller and Heckhansen, 1990 with commentary thereon by Libet 1992, and Wong et al. 1988).However, we also found that conscious intention did precede that actual motor act by about 200 msec. That left open the potentiality for the conscious function to control the outcome of the process that was initiated in the brain unconsciously (see Libet 1985). We have all had the experience of consciously suppressing or vetoing the performance of an urge or intention to act. The 200 msec interval provides sufficient time in which the voluntary process could be stopped, before final activation of the motor area about 50 msec before the act. We were able to show that subjects could veto an act in the 100–200 msec interval before the expected time for the action.Spence dismisses this free will potentiality in the control or veto of a voluntary process. He says: “It is flawed because the ‘decision’ (in consciousness) to act or not to act is itself the ‘result’ of preceding neural activity.” This argument is based on my own evidence that a period of up to 500 msec of cerebral activity is required to produce a conscious sensory experience (Libet 1993, for review).But conscious control of a process is not the same as becoming aware of the volitional intent (Libet 1985, 563–564). Control implies the imposing of a change, in this case after the appearance of the awareness of intention to act. Conscious control may not necessarily require the same neural “time-on” feature that precedes the appearance of awareness per se. There is presently [End Page 95] no directly applicable evidence against the appearance of a conscious control function without prior neural processes specific to its initiation.In short, one cannot cavalierly dismiss the possibility of a conscious free will function on the basis of a belief that such a control function must be itself initiated unconsciously by prior specific neural processes. The argument that conscious free will control is simply a useful delusion must still be regarded as a philosophical belief, not a scientifically demonstrated proposition.Spence goes on to suggest that “Consciousness is necessary for purposeful (intentional) action but it is not the initiator.” But if Spence is consistent in his view that all conscious functions are preceded by specific neural activities that initiate the function, then his putative role for consciousness would have been itself initiated unconsciously. How, then, would consciousness be “performing (purposeful, intentional) actions with subtlety and invention” if it is simply an after-effect of the responsible cerebral process? It would appear that Spence is postulating an active role for consciousness in directing the course of neural activities carrying out purposeful, intentional actions. That is the kind of potentiality I was suggesting must be kept open, but one that Spence dismissed elsewhere as “flawed.”On a technical point: The Grey Walter experiment is cited as evidence for postulated effects of timing, in the “illusion” of self-initiation of an act. However, that experimental result was simply due to the fact that the motor cortex initiates the command... (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)

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)

In the last few decades, philosophy of science has increasingly focused on multilevel models and causal mechanistic explanations to account for complex biological phenomena. On the one hand, biological and biomedical works make extensive use of mechanistic concepts; on the other hand, philosophers have analyzed an increasing range of examples taken from different domains in the life sciences to test—support or criticize—the adequacy of mechanistic accounts. The article highlights some challenges in the elaboration of mechanistic explanations with a focus on (...) cancer research and neuropsychiatry. It jointly considers fields, which are usually dealt with separately, and keeps a close eye on scientific practice. The article has a twofold aim. First, it shows that identification of the explananda is a key issue when looking at dynamic processes and their implications in medical research and clinical practice. Second, it discusses the relevance of organizational accounts of mechanisms, and questions whether thorough self-sustaining mechanistic explanations can actually be provided when addressing cancer and psychiatric diseases. While acknowledging the merits of the wide ongoing debate on mechanistic models, the article challenges the mechanistic approach to explanation by discussing, in particular, explanatory and conceptual terms in the light of stances from medical cases. (shrink)

If the notion of free will is to be retained by philosophers, psychiatrists and psychologists, then it will be a free will which is essentially non-conscious. The purpose of this paper is to demonstrate that a conscious free will (in the sense of consciousness initiating action) is incompatible with the evidence of neuroscience, and the phenomenology described in the literature of normal creativity, psychotic passivity, and the neurological syndrome of the alien limb or hand. In particular the work of Libet (...) and others who have directly stimulated the brain and measured activity from its surface leads to the conclusion that subjective states (be they sensory or intentional) are preceded by predictive neural activity. Subjective phenomenology is temporally distinct from the initiation of “voluntary” action. In addition it will be argued that free will is more than a belief and that it comprises a perceptual sensorimotor component. Free will is conceptualized as a three component phenomenon consisting of a perceptual, non-linguistic experience of freedom, an experiential belief which is linguistic, and related to a specified action in time, and an abstract belief which is linguistic but remote from any particular action and akin to philosophical discourse (the abstract belief or otherwise, in free will). A theoretical explanation of some of the pathological phenomenology of possession of action is offered in terms of temporal considerations. The direction of action within mental/virtual space is hypothesized to be a function of the temporal sequence of its initiation and awareness of the latter “reaching” consciousness. It is suggested that perturbation of this temporal sequence may lead to the misattribution of host-as-alien-initiated action. Work of this kind, which is beyond subjective introspection, is necessary if we are to develop adequate models to use in conjunction with modern investigation techniques. (shrink)

In lieu of an abstract, here is a brief excerpt of the content:Commentary on “Free Will in the Light of Neuropsychiatry”G. Lynn Stephens (bio)A necessary condition of our having free will is that we initiate some of our actions by our own will or decision. Spence argues that, in light of certain empirical findings, we can accept that willing causes action, only if we acknowledge that willing is a non-conscious phenomenon. “If the notion of free will is retained... it will (...) be a free will which is essentially non-conscious.... [A] conscious free will (in the sense of consciousness initiating action) is incompatible with the evidence....” I shall argue that Spence’s conclusion depends upon a highly questionable understanding of what it is for a decision to be conscious.The evidence to which Spence refers above comes from experimental studies by Libet. This work suggests that, at least for simple motor performances, we become aware of willing the action only after the act has been initiated. This raises the possibility that our subjective experience of willing an action generally follows rather than precedes initiation of the relevant act and, hence, does not cause that action.What does all this entail concerning the causal efficacy of willing or deciding? Spence carefully refrains from drawing the conclusion that decisions never cause actions. Rather he concludes that “conscious decisions do not cause acts.... “Our decision or freedom is illusory (if by these terms we mean conscious phenomena).” We can continue to maintain that our decisions sometimes initiate actions, but only provided that we regard our decisions as non-conscious.In order to evaluate the claim that conscious decisions do not cause actions, we need to distinguish two questions: (1) Does my decision, of which I am conscious, cause me to do A? and (2) Does my being conscious of my decision cause me to do A?We might answer (1) in the affirmative, but (2) in the negative. That is, it might be true that my decision to do A caused me to do A and that I was conscious of that decision, but false that my being conscious of my decision caused me to do A. Indeed, we might suppose that, although my decision caused me to do A, I did not become conscious of that decision until after I had done A. How could this be? Suppose that my subjective experience of deciding to do A results from an (internal) perceptual process and that this process takes time. In that case it is possible that, having decided to do A, it requires more time for me to become conscious of that decision than is required for the decision to initiate my doing A. By the time I become aware of my decision, I have already done what I decided to do.The evidence Spence offers is incompatible with the hypothesis that the subjective experience of [End Page 97] my decision to do A causes me to do A, but quite compatible with the hypothesis that my decision to do A, of which I was conscious, caused me to do A. When he expresses his point by saying, “decisions to act arise prior to our consciousness of them,” or “The role of consciousness in volition is not that of initiator,” he is drawing the conclusion warranted by his evidence.However, he goes beyond his evidence when he says, “Thus our decision or freedom is illusory (if by these terms we mean conscious phenomena),” or “Conscious decision do not cause acts.” To justify these conclusions he needs to argue that something counts as a conscious decision only if we become conscious of it at precisely the instant at which it occurs. (Compare: Something counts as an event that we see, only if we begin to see it precisely at the instant at which it occurs.) Absent some defense of this view, a defense provided nowhere in Spence’s paper, we may continue to maintain that conscious decisions do cause actions.Related ArticlesFeature Article: Free Will in the Light of NeuropsychiatryCommentary: Commentary by FrithCommentary: Commentary by LibetCommentary: Commentary by StephensResponse: Response to the CommentariesG. Lynn Stephens G. Lynn Stephens, Ph.D., Department of Philosophy, University of Alabama... (shrink)

In everyday language as well as scientific language, there are but few terms and concepts with such a comprehensive negative meaning and connotation as the term "disease." Disease is a universal evil. Nobody wants disease and everybody would agree that disease should be defeated and eradicated. But what if disease strikes one's own body and mind? What if the imperative of disease eradication targets properties of the body, which is me? This is the reality for many patients with psychiatric diagnoses (...) and their families. This is the reality of psychiatry. Psychiatry is a clinical discipline in the borderland between natural sciences and humanities. Psychiatric concepts of mental health and disease affect the self-image and self-worth of patients and their families in a very pervasive manner. Therefore, it is important to reflect on what we mean with psychiatric diagnoses, how we define it and how we delineate phenomena we would regard as unusual but healthy from those we would consider reflecting a disease. In this paper, the different meanings of the concept of normality will be presented. I will briefly discuss if or not there is a generally accepted concept of what a disease is. Then I will address the definition of what a psychiatric disorder is. Based on the example of autism, I will finally illustrate that phenomenologically identical medical syndromes can be regarded as well as a norm variant, as a psychological disorder, and as a psychiatric disease. This comprehensive perspective on the diverse phenomena of body and mental functioning illustrates that many if not most of the present psychiatric diagnoses cannot be considered as names of diseases, but as umbrella terms for a wide range of differently caused mental phenomena. (shrink)

A recurring problem in psychiatry is the meaningfulness, or otherwise, of its domain. Critics of psychiatry accuse the discipline of misconstruing mental phenomena and behavior, including the verbal sort, as meaningless symptoms, in keeping with other medical specialisms. A myoclonic jerk is taken by the neurologist to mean nothing beyond signaling pathology of the nervous system. But this approach, critics argue, strips psychiatric phenomena of their meaning. Accordingly, Louis Sass has described a tendency, "particularly among organic psychiatrists… to ignore the (...) psychological interpretation or empathic understanding of mental symptoms". Neuropsychiatric symptoms such as visual hallucinations... (shrink)

Bioethics needs an elaborated concept of autonomy based on empirical knowledge about the prerequisites of the capacity of autonomy. Whereas Beauchamp and Childress, and many other bioethicists have discussed social influences on the capacity of autonomy in depth, neurobiological influences have received less attention. A comprehensive concept of autonomy should consider both social and biological factors that can diminish the capacity of autonomy. This article focuses on neurobiological influences that can reduce the capacity of autonomy. The thesis of this article (...) is that the integration of neuropsychiatric knowledge into the concept of autonomy is essential for evaluating demands for harmful medical treatments which might be caused by a brain disease, and deciding on involuntary treatments of patients who suffer from substantial lack of autonomy due to neuropsychiatric disorders. Diametrically opposed to such a comprehensive concept of the capacity of autonomy is the concept of ‘liberty of illness’. In Germany, this concept is supported not only by anti-psychiatric groups but also by the Federal Constitutional Court. Several real cases demonstrate how the brain can be ‘hijacked’ by parasites, antibodies or technical devices. Applying the concept of ‘liberty of illness’ to persons whose decision-making capacity is severely affected by neuropsychiatric disorders is cynical. These patients neither chose their disease nor would refuse effective treatment if their will was not disturbed by the disease. Respect for autonomy should be understood as the positive obligation to save, support or restore the biological prerequisites of the capacity for autonomous decision-making. (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)

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)

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)

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)

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)

This book relates work in neuroscience, psychology and psychiatry to questions about what a person is and the nature of a persons unity across a lifetime. The neuropsychiatry is now dated. The philosophy has three themes still perhaps of interest. The first is a response to Derek Parfits powerful and influential work on personal identity, which, like many other people, I discussed with him as he worked it out. I accept his view that there is no ego that owns the (...) stream of our experiences, and the unity of a person over time is constructed out of continuities in our mental life. But I argue against Parfits view that personal unity thereby becomes less deep or less morally important. The second theme is an emphasis on the importance of self-creation and an attempt to work out how far it is possible. The third theme is about the way self-creation is linked to recognition by other people, and the importance of this for understanding the role of tribalism in human life. "This book is about what it is to be a person, to think of oneself as an "I". It is about the ways people think of themselves, and how they use these ideas in shaping their own distinctive characteristics. It is about how far we create ourslves." "When a way of life does not fit with what you think you are really like, you can feel like a plant away from the light, distorted by having to twist and grope towards the sun. This analogy suggests that we might have a genetic programme to unfold, in the way plants do. But no doubt it is too simple to think that "the real me" is genetically laid down. These strong affinities we have for some kinds of life, and the sense of drowning that others give us, are likely to have been created by the interaction of our genetic make-up with thigs we have come across and responded to... We care a bit like trees would be, if they were conscious and could partly choose their direction of growth. Perhaps oaks could not become beeches, and stunted trees could not become giants, but they could influence the angle and direction of their branches. Trees thinking about determinism and free will might find it impossible to assess their own contribution to their final shape.". (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)

Long-standing psychiatric practice confirms the pervasive use of pharmacological therapies for treating severe mental disorders. In many circumstances, drugs constitute the best allies of psychotherapeutic interventions. A robust scientific literature is oriented on finding the best strategies to improve therapeutic efficacy through different modes and timing of combined interventions. Nevertheless, we are far from triumphal therapeutic success. Despite the advances made by neuropsychiatry, this medical discipline remains lacking in terms of diagnostic and prognostic capabilities when compared to other branches of (...) medicine. An ethical principle remains as the guidance of therapeutic interventions: improving the quality of life for patients. Unfortunately, psychotropic drugs and psychotherapies do not always result in an efficient remission of symptoms. In this paper I corroborate the idea that therapists should provide drug-resistant patients with every effective and available treatment, even if some of such interventions could be invasive, like Electroconvulsive Therapy (ECT). ECT carries upon its shoulders a long and dramatic history that should be better investigated to provide new insights. In fact, ECT has attracted renewed interest in recent years. This is due to the fact that antidepressant drugs in younger patients show often scarce effectiveness and unpleasant side-effects. Moreover, I show that, thanks to modern advances, ECT may work as a successful form of treatment for specific and rare cases, such as severe depression (with suicide attempts) and catatonia. (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)

This book discusses consciousness from the perspectives of neuroscience, neuropsychiatry and philosophy. The author argues that the central issue in brain studies is to explain the unity, continuity, and adherence of experience, whether it is sensory or mental awareness, phenomenal- or self-consciousness. The fascinating discussion that this book presents is: How do the brain and the self create the conspiracy of experience where the physicality of the brain is lost in the subjectivity of the self?

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.

Progress in neuroscience will allow us to reveal the neuronal correlates of psychological processes involved in ethically relevant notions such as informed consent. Informed consent involves decision making, the psychological and neural processes of which have been investigated extensively in neuroscience. The neuroscience of decision making may be able to contribute to an ethics of informed consent by providing empirical and thus descriptive criteria. Since, however, descriptive criteria must be distinguished from normative criteria, the neuroscience of decision making cannot replace (...) the ethics of informed consent. Instead, the neuroscience of decision making could complement the current ethics, resulting in what can be called neuroethics of informed consent. It is concluded that current progress in the neurosciences could complement and change the way in which we approach ethical problems in neuropsychiatry. (shrink)

In lieu of an abstract, here is a brief excerpt of the content:Commentary on “Wilhelm Griesinger”Aaron L. Mishara (bio)Arens situates Wilhelm Griesinger in a historical context with which we are no longer familiar. In doing so, she has performed an important task for contemporary clinicians, philosophers, and historians. We find ourselves working and thinking (both in everyday clinical practice and in the construction of our models of mental disorder) with the same categories that Griesinger struggled to sort out and redefine; (...) we often do so, however, without awareness of their history or lack of permanence. Ackerknecht writes that all the dominant trends in modern psychiatry can be traced back to Griesinger; he states that Griesinger is the “founder of neuropsychiatry,” a “merging of the two disciplines” neurology and psychiatry. Griesinger presents us with a “systematic synthesis of the anatomical, physiological, psychological and clinical points of view” (Ackerknecht 1959, 63). Somewhat contrarily, Karl Jaspers, in his General Psychopathology, groups Griesinger with the great observers and describers of clinical experience rather than among the systematic analyzers (Jaspers 1963, 849–50). Although Griesinger is best known for his identification of mental disorders as a subset of brain diseases, Karl Bonhoeffer, a successor to Griesinger as director of the Charité Clinic in Berlin, cautions that Griesinger “continued to see in psychological causes the most frequent and abundant source of mental disorders” (Bonhoeffer 1911, 53). Kales, Kales, and Vela-Bueno, however, write, “Griesinger was representative of a clinical movement that minimized the value of psychological concepts in the understanding of mental diseases” (Kales, Kales, and Vela-Bueno 1990, 15). Precisely because of his importance, contention surrounds his legacy.If Griesinger is the pioneer of empirical approaches in biological neuropsychiatry (as Ackerknecht and others claim), he is also precursor to philosophical criticisms of their limits. It is not so easy to lump Griesinger to one side of the oppositions with which we think today: Griesinger’s scientific psychiatry (formed on the basis of the newly emergent empirical physiology) was meant to steer between the Scylla of the previously reigning overspeculative romantic medicine and the Charybdis of the antitheoretical and “positivistic” materialism of Magendie. As Arens suggests, even during the same generation of university psychiatry which Griesinger was critical in forming, he was posthumously denounced as belonging to the Hegelian idealists; later, he was proclaimed to be an empiricist. Griesinger’s work contained both idealism and empiricism in a fragile synthesis that soon broke asunder.Hermeneutic theory points out that we inevitably interpret an author, in this case, Griesinger, in terms of the prejudices of our own present context of understanding and our current problems of application to clinical practice (Gadamer 1993). On the one hand, we benefit from the advantage of seeing all that follows Griesinger’s work and are able to “understand the author [End Page 165] better than he understood himself.” We are able to see what he only anticipates but is still not able to explicitly articulate as the unpredicted effects of his work. On the other hand, our interpretations are encumbered by the sedimentations of the views of his successors: his work lies buried under the subsequent interpretations and vicissitudes of a reception with its own agendas, contexts of interpretation, and realms of application. It would be easier if we could simply assign him to one side of our current debates concerning mind/body, individual/culture, and explanation/understanding rather than seeing that our present quandaries in understanding, classifying, and treating mental disorder result precisely from a reading of Griesinger that is not careful enough. It is here that Arens can help us develop our present views further by reviewing their past.Although Griesinger is heralded as the pioneer of an empirical physiological approach which employs a natural scientific concept of mechanism (Ackerknecht, O. Marx, Verwey), Arens situates him in the tradition of Kant and German idealism. It is perhaps this solution of being both philosophical and empirical which seems hard for us, today, to understand. We have come to view these directions as contradictory, to be necessarily in a mutually exclusive relationship. (But that is rather the expression of the present impasse and not the way that Griesinger originally approached these problems.) Arens ambitiously retraces the genealogy of Griesinger’s model... (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)