These are integrated and synthesised bythe editors, both acknowledged experts in the field. The scope is truly international and spans theoretical perspectives, clinical practice, and consumer views.

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)

Phillips & Silverstein argue that a range of cognitive disturbances in schizophrenia result from a deficit in cognitive coordination attributable to NMDA receptor dysfunction. We suggest that the viability of this hypothesis would be further supported by explicit implementation in a computational framework that can produce quantitative estimates of the behavior of both healthy individuals and individuals with schizophrenia.

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)

“There is a thought in me which is not mine”. This is, roughly, the complaint of patients suffering from thought insertion. This first-rank symptom of schizophrenia is particularly puzzling for it seems to challenge a very well entrenched principle to the effect that our conscious thoughts are necessarily subjective, that we necessarily have a sense of ownership for them (Cartesian principle). Despite their wide disagreement, classical accounts of the symptom save the Cartesian principle by interpreting thought insertion as a problem (...) of the sense of agency for thought rather than as a problem of subjectivity. I argue that those accounts fail and that thought insertion really is a problem of subjectivity. We can nevertheless save the Cartesian principle if we realize that the presupposition, shared by classical accounts, to the effect that inserted thoughts are unequivocally conscious, is ill-grounded. Distinguishing between reflexive awareness and phenomenal consciousness, and relying on a careful comparison between thought insertion and other pathologies of agency, I propose a novel account of the symptom which is compatible with the Cartesian principle and which allows to take the patient’s reports seriously. This account, I conclude, opens up novel perspectives on the comprehension of schizophrenia, and reveals a common confusion between two different dimensions of the mind. (shrink)

Philosophers are interested in the phenomenon of thought insertion because it challenges the common assumption that one can ascribe to oneself the thoughts that one can access first-personally. In the standard philosophical analysis of thought insertion, the subject owns the ‘inserted’ thought but lacks a sense of agency towards it. In this paper we want to provide an alternative analysis of the condition, according to which subjects typically lack both ownership and authorship of the ‘inserted’ thoughts. We argue that by (...) appealing to a failure of ownership and authorship we can describe more accurately the phenomenology of thought insertion, and distinguish it from that of non-delusional beliefs that have not been deliberated about, and of other delusions of passivity. We can also start developing a more psychologically realistic account of the relation between intentionality, rationality and self knowledge in normal and abnormal cognition. (shrink)

Dysfunctions of the neural circuits that implement social behavior are necessary but not a sufficient condition to develop schizophrenia. We propose that schizophrenia represents a disease of general connectivity that impairs not only the “social brain” networks, but also different neural circuits related with higher cognitive and perceptual functions. We discuss possible mechanisms and evolutionary considerations.

This paper examines the complex and creative strategies employed in keeping beliefs, memories, and various other mental and bodily states effectively dissociated from normal waking consciousness. First, it examines cases of hypnotic anesthesia and hypnotically induced hallucination, which illustrate: (1) our capacity for generating novel mental contents, (2) our capacity for choosing a plan of action from a wider set of options, and (3) our capacity for monitoring and responding to environmental influences threatening to undermine a dissociative state. These observations (...) are then extended to cases involving dissoci- ated memories of trauma. The strategies needed to maintain a dissociated belief or memory are strikingly similar to those involved in preventing our lies from being exposed. Moreover, these strategies are complex, and they potentially affect seemingly remote aspects of a person’s psychol- ogy. That point is illustrated by examining the dispositional nature of both memory and belief, the complex web of relations between our men- tal states and other elements of our psychology, and the interrelatedness of personality states and human capacities. [Article copies available for a.. (shrink)

It is proposed that cortical activity is normally coordinated across synaptically connected areas and that this coordination supports cognitive coherence relations. This view is consistent with the NMDA- hypoactivity hypothesis of the target article in regarding disorganization symptoms in schizophrenia as arising from disruption of normal interareal coordination. This disruption may produce abnormal contextual effects in the cortex that lead to anomalous cognitive coherence relations.

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

I compare Frith and colleagues’ influential comparator account of how the sense of agency is elicited to the multifactorial weighting model advocated by Synofzik and colleagues. I defend the comparator model from the common objection that the actual sensory consequences of action are not needed to elicit the sense of agency. I examine the comparator model’s ability to explain the performance of healthy subjects and those suffering from delusions of alien control on various self-attribution tasks. It transpires that the comparator (...) model needs case-by-case adjustment to deal with problematic data. In response to this, the multifactorial weighting model of Synofzik and colleagues is introduced. Although this model is incomplete, it is more naturally constrained by the cases that are problematic for the comparator model. However, this model may be untestable. I conclude that currently the comparator model approach has stronger support than the multifactorial weighting model approach. (shrink)

Synofzik, Vosgerau, and Newen (2008) offer a powerful explanation of the sense of agency. To argue for their model they attempt to show that one of the standard models (the comparator model) fails to explain the sense of agency and that their model offers a more general account than is aimed at by the standard model. Here I offer comment on both parts of this argument. I offer an alternative reading of some of the data they use to argue against (...) the comparator model. I argue that contrary to Synofzik, Vosgerau and Newen’s reading the case of G.L. supports rather than contradicts the comparator model. Next I suggest how the comparator model can differentiate failures of action attribution in patients suffering parietal lobe lesions and delusions of alien control. I also argue that the apparently unexpected phenomenon of ‘‘hyperassociation” is predicted by the comparator model. Finally I suggest that as it stands Synofzik, Vosgerau and Newen’s model is not well specified enough to explain deficits in the sense of agency associated with delusions of thought insertion. Thus they have not met their second argumentative burden of showing how their model is more general than the comparator model. (shrink)

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

Blackwell, 2000 Review by George Graham, Ph.D on Oct 27th 2000 Volume: 4, Number: 43.

Thomas & Karmiloff-Smith’ (T&K-S’) argument that the Residual Normality assumption is not valid for developmental disorders has implications for models of cognition in schizophrenia, a disorder that may involve a neurodevelopmental pathogenesis. A limiting factor for such theories is the lack of understanding about the nature of the cognitive system (modular components versus global processes). Moreover, it is unclear how the proposal that modularization emerges from developmental processes would change that fundamental question.

Botanical preparations used by shamans in rituals for divination, prophecy, and ecstasy contain widely different psychoactive compounds, which are incorrectly classified under a single denomination such as “hallucinogens,” “psychedelics,” or “entheogens.” Based on extensive ethnopharmacological search, I proposed a psychopharmacological classification of magic plants in 1979. This paper re-evaluates this taxonomy in the context of consciousness research. Several groups of psychodysleptic magic plants are proposed: (1) hallucinogens—psilocybin mushrooms, mescaline cacti, dimethyltryptamine snuffs, and the synthetic ergoline lysergic acid diethylamide induce strong (...) perceptual changes, affective intensification, and cognitive enhancement. Their ethnobotanical uses include long lasting divination rituals, prophecy, and sacramental practice. (2) Trance-inducers—ergoline Convolvulaceae and South American Banisteriopsis produce quietness, abstraction, lethargy, mild sensorial and cognitive changes, and salient visual imagery changes used in trance rituals and specific divination practices. (3) Cognodysleptics—marijuana (tetrahydrocannabinol) and other terpene-containing plants induce changes in thought, imagination, and affective functions and are used in short-term divination or oneiromancy. (4) Deliriants—tropane-containing Solanaceae, wild tobacco, and Amanita muscaria (muscimol) induce a delirium characterized by dim and clouded consciousness, stupor, confusion, disorientation, perception distortion, difficulties in recollection, anxiety, irritability, excitation, and behavioral disorganization employed in sorcery, purification, or exorcism rituals. The core mental effects required for a drug to be used in shamanistic rituals include light-headedness, enhanced imagery, and experience intensification. This constellation was the reason why, in his classification of psychoactive compounds, the pioneer German psychopharmacologist Louis Lewin established in 1924 a group of drugs under the appropriate name of Phantastica. (shrink)

Phillips & Silverstein (P&S, 2003) have proposed that NMDA-receptor hypofunction is the central reason for impaired cognitive coordination and abnormal gestalt-like perceptual processing in schizophrenia. We suggest that this model may also be applicable to non-pathological (or normal) aging given the compelling evidence of NMDA-receptor involvement during the aging process that results in age-related change in higher-level perceptual performance. Given that such deficits are present in other neurological disorders such as autism, an argument for a systematic assessment of perceptual functioning (...) in these conditions may be posited. (shrink)

I offer an account of thought insertion based on a certain model of self-knowledge. I propose that subjects with thought insertion do not experience being committed to some of their own beliefs. A hypothesis about self-knowledge explains why. According to it, we form beliefs about our own beliefs on the basis of our evidence for them. First, I will argue that this hypothesis explains the fact that we feel committed to those beliefs which we are aware of. Then, I will (...) point to one feature of schizophrenia that suggests that subjects with thought insertion may not be able to know their own beliefs in that way. (shrink)

We proceed to describe a model for the formation and maintenance of polythematic delusions encountered in schizophrenia, which is in adequacy with Brendan Maher's account of delusions. Polythematic delusions are considered here as the conclusions of arguments triggered by apophenia that include some very common errors of reasoning such as post hoc fallacy and confirmation bias. We describe first the structure of reasoning which leads to delusions of reference, of telepathy and of influence, by distinguishing between the primary, secondary, tertiary (...) and quaternary types of delusional arguments. These four levels of arguments correspond to a stage the nature of which is respectively instantial, inductive, interpretative at a monothematic level and interpretative at a polythematic level. We also proceed to identify accurately the fallacious steps in the corresponding reasoning. We expose then the role of apophenia in the elaboration of delusional ideas. Lastly, we describe the role played by the hallucinations in the present model. (shrink)

The paper first introduces the concept of implicit and explicit temporality, referring to time as pre-reflectively lived vs. consciously experienced. Implicit time is based on the constitutive synthesis of inner time consciousness on the one hand, and on the conative–affective dynamics of life on the other hand. Explicit time results from an interruption or negation of implicit time and unfolds itself in the dimensions of present, past and future. It is further shown that temporality, embodiment and intersubjectivity are closely connected: (...) While implicit temporality is characterised by tacit bodily functioning and by synchronisation with others, explicit temporality arises with states of desynchronisation, that is, of a retardation or acceleration of inner time in relation to external or social processes. These states often bring the body to awareness as an obstacle as well. On this basis, schizophrenia and melancholic depression are investigated as paradigm cases for a psychopathology of temporality. Major symptoms of schizophrenia such as thought disorder, thought insertion, hallucinations or passivity experiences may be regarded as manifesting a disturbance of the constitutive synthesis of time consciousness, closely connected with a weakening of the underlying pre-reflective self-awareness or ipseity. This results in a fragmentation of the intentional arc, a loss of self-coherence and the appearance of major self-disturbances. Depression, on the other hand, is mostly triggered by a desynchronisation from the social environment and further develops into an inhibition of the conative–affective dynamics of life. As will be shown, both mental illnesses bear witness of the close connection of temporality, embodiment and intersubjectivity. (shrink)

During the paradoxical dreaming sleep stage, characterized by hallucinations and delusions, as in schizophrenia, the increased subcortical release of dopamine, the presynaptic inhibition of thalamic relay nuclei, and serotonergic disinhibition are in accordance with the model for the mechanism of hallucination-induction.

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

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)

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)

Transcranial magnetic stimulation, EEG, and behavioral studies by our group implicate spurious activation of speech perception neurocircuitry in the genesis of auditory hallucinations in schizophrenia. The neurobiological basis of these abnormalities remains uncertain, however. We review our ongoing studies, which suggest that altered cortical coupling underlies speech processing in schizophrenia and is expressed via disrupted gamma resonances and impaired corollary discharge function of self-generated verbal thought.

Multidisciplinary studies indicate that auditory hallucinations may arise from speech perception neurocircuitry without disrupted theory of mind capacities. Computer simulations of excessive pruning in speech perception neural networks provide a model for these hallucinations and demonstrate that connectivity reductions just below a “psychotogenic threshold” enhance information processing. These data suggest a process whereby vulnerability to schizophrenia is maintained in the human population despite reproductive disadvantages of this illness.

N-methyl-d-aspartate receptor (NMDAR) dysfunction plays a crucial role in schizophrenia, leading to impairments in cognitive coordination. NMDAR agonists (e.g., glycine) ameliorate negative and cognitive symptoms, consistent with NMDAR models. However, not all types of cognitive coordination use NMDAR. Further, not all aspects of cognitive coordination are impaired in schizophrenia, suggesting the need for specificity in applying the cognitive coordination construct.

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

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

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)

These are set against introductory essays describing the philosophical, historical and psychological approaches, making this a uniquely inclusive overview.

Behrendt & Young (B&Y) propose a useful theoretical framework for the study of processes underlying perception and hallucinations. It focuses on gamma oscillations in thalamocortical networks and the role of the reticular thalamic nucleus in modulating these oscillations. I suggest that their theoretical model might also be applied to the investigation of temporal encoding deficits in disorders such as dyslexia. I further suggest, however, that a role for slower rhythms, such as theta, might also be considered when investigating perceptual experience.

Reinterpretation of our data concerning sleep onset, motivated by the desire to pay close attention to “intra-individual regularities,” suggests that the experience of control might be a key factor in determining the subjective sense that sleep has begun. This loss of control seems akin to what Frith and others have described as “passivity experiences,” which also occur in schizophrenia. Although clearly sleep onset is not a schizophrenic episode, this similarity might help to explain other features of sleep onset. We further (...) speculate that we could build upon the discovery of various “intra-individual regularities” to construct a model of sleep onset and other forms of sleep mentation. (shrink)

Abstract: How it is that one's own thoughts can seem to be someone else's? After noting some common missteps of other approaches to this puzzle, I develop a novel cognitive solution, drawing on and critiquing theories that understand inserted thoughts and auditory verbal hallucinations in schizophrenia as stemming from mismatches between predicted and actual sensory feedback. Considerable attention is paid to forging links between the first-person phenomenology of thought insertion and the posits (e.g. efference copy, corollary discharge) of current cognitive (...) theories. I show how deficits in the subconscious mechanisms regulating inner speech may lead to a 'fractured phenomenology' responsible for schizophrenic patients' reports of inserted thoughts and auditory verbal hallucinations. Supporting work on virtual environments is discussed, and lessons concerning the fixity of delusional belief are drawn. (shrink)

Schizophrenia patients exhibit impairments across multiple clinical, cognitive, and functional domains. A fundamental abnormality of the timing and/or efficiency of neural processes across disparate brain regions (i.e., cortico-cortical communications) may underlie many of the deficits in schizophrenia. Because gamma synchrony is temporally correlated with many cognitive processes, probing patterns of gamma activation may shed light on the functional integrity of neural circuits in schizophrenia and related disorders.

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)

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)

Kendler and Schaffner have written an exemplary case study of the rise of the dopamine hypothesis and, if not its fall, at least its stagnation and transmutation. They bring out well both the state of the science and the opportunities offered by the theory to consider some famous philosophical theories of scientific progress. So well, in fact, have they done this, that I do not have a lot to say about it. I will just mention one or two points that (...) I found interesting, and then say a little about what looks to me like an omission from the story that the two Kens recount.One point they raise is the importance of competitor theories: now, there is supposed to be an old story about a quack who was apprehended during .. (shrink)

The boundaries, the influences on, and consequences of a short-term memory (STM) capacity of 4 leads us to consider global versus local processing. We argue that in schizophrenia cognitive problems can lie partly in pre-conscious automatic selective attention and partly with the speed of processing in later controlled processes (including compound STM). The influence of automatic attentional mechanisms may be under-estimated in normal psychology and explain the loss of the magic 4 in schizophrenia.

CHAPTER 1 Neurotransmitter networks Elaine Perry and Allan Young i. Introduction This first chapter sets the scene for subsequent exploration of potential ...

A midbrain neural basis for the perceptualoscillations of binocular rivalry is suggestedon the basis of fMRI studies of rivalry andinferences from the properties of rivalry thatcannot be explained from the known propertiesof primary visual cortical (V1) neurons. Therivalry switch is proposed to activatehomologous areas of each cerebral hemispherealternately, by means of a bistable oscillatorcircuit that straddles the midline of theventral tegmentum. This bistable oscillatoroperates at the same slow rate that ischaracteristic of perceptual rivalryalternations. Whilst attempting to divert thepresent preoccupation with (...) cortical mechanismsfor rivalry, the new proposal integrates manycortical areas, in keeping with recent evidencethat binocular rivalry involves widespreadareas of the hemispheres. By linking rivalry tointerhemispheric switching mechanisms in thisway, the new proposal for the switch makes theprediction that binocular rivalry will besubject to high level influences such as moodand motivation. These predictions are beingfulfilled, with rivalry playing an increasingrole in the diagnosis and understanding if mooddisorders, schizophrenia and other psychiatricconditions. (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)

Phillips & Silverstein emphasize the gain-control properties of NMDA synapses in cognitive coordination. We endorse their view and suggest that NMDA synapses play a crucial role in biased attentional competition and (visual) working memory. Our simulations show that NMDA synapses can control the storage rate of visual objects. We discuss specific predictions of our model about cognitive effects of NMDA-antagonists and schizophrenia.

Understanding the interplay between memory and emotion is crucial for the work of researchers in many arenas--clinicians, psychologists interested in eyewitness ...

Phillips & Silverstein argue that schizophrenia is a result of a deficit of the contextual coordination of neuronal responses. The authors propose that NMDA-receptors control these modulatory effects. However, hallucinations, which are among the principle symptoms of schizophrenia, imply a flaw in the interactions between neurons that is more fundamental than just a general weakness of contextual modulation.

The most developed and the latest-to-mature mental skills represented in the creation of mono- versus polysemantic contexts are related respectively to the left and right frontal lobe. A polysemantic way of thinking is responsible for the subject's successful integration in the polydimensional world. The functional insufficiency of this right-hemispheric way of thinking displays a predisposition toward the development of mental disorders, including schizophrenia.

Numerous searches have failed to identify a single co-occurrence of total blindness and schizophrenia. Evidence that blindness causes loss of certain NMDA-receptor functions is balanced by reports of compensatory gains. Connections between visual and anterior cingulate NMDA-receptor systems may help to explain how blindness could protect against schizophrenia.

The phenomenological approach to schizophrenia has undergone something of a renaissance in Anglophone psychiatry in recent years. There has been a proliferation of works that focus on the nature of subjectivity in schizophrenia and related disorders, and that take inspiration from the work of such German and French philosophers as Husserl, Heidegger, and Merleau-Ponty, and such classical psychiatrists as Minkowski, Blankenburg, and Binswanger (Rulf 2003; Sass 2001a, 2001b). This trend includes predominantly theoretical articles, which typically incorporate clinical material as well (...) as reviews of empirical and experimental findings in psychopathology. Some very recent examples (since 2000) are studies of .. (shrink)

Behrendt & Young (B&Y) propose an explanation for schizophrenia in terms of a cortical default in the interaction between consciousness and cognition. However, schizophrenia more likely involves miscommunication between subcortical and cortical affective circuits in the brain, a default in the interaction between consciousness and emotion. The typical “affective” nature of hallucinations in schizophrenia provides compelling evidence for subcortical involvement.

Schizophrenia, like other pathological conditions of mental life, has not been systematically included in the general study of consciousness. By focusing on aspects of chronic schizophrenia, we attempt to remedy this omission. Basic components of Husserl’s phenomenology (intentionality, synthesis, constitution, epoche, and unbuilding) are explicated and then employed in an account of chronic schizophrenia. In schizophrenic experience, basic constituents of reality are lost and the subject must try to explicitly re-constitute them. “Automatic mental life” is weakened such that much of (...) the world that is normally taken-for-granted cannot continue to be so. The subject must actively re-lay the ontological foundations of reality. (shrink)

DSM-III and its revisions have provided little in the way of explicit historical or philosophical foundations. The logical empiricism embedded in its operational criteria and its external approach to validation are inadequate to account for the presumption of nosological regularities or the specific categories endorsed by the taxonomy. The nosologic operation that Jaspers referred to as the "synthesis of disease entities" is explored in connection with the central distinction in DSM-IV between mood disorders and schizophrenic disorders. This synthetic operation is (...) analyzed in terms of the paradigmatic shift from the mania-melancholia matrix of pre-modern psychiatry to the manic-depression/dementia praecox model defined by the work of Kraepelin. In the context of this analysis the self-evidence of these regularities is questioned. Keywords: DSM-III, DSM-IV, mood disorders, nosology, schizophrenic disorders CiteULike Connotea Del.icio.us What's this? (shrink)

The paper argues that a functional reduction of ordinary psychology to neuropsychology is possible by means of constructing fine-grained functional, mental sub-types that are coextensive with neuropsychological types. We establish this claim by means of considering as examples the cases of the disconnection syndrome and schizophrenia. We point out that the result is a conservative reduction, vindicating the scientific quality of the mental types of ordinary psychology by systematically linking them with neuroscience. That procedure of conservative reduction by means of (...) functional sub-types is in principle repeatable down to molecular neuroscience. (shrink)

I develop here one of the many topics raised by Sass, Parnas, and Zahavi, namely the role of phenomenology in clarifying issues not amenable to standard empirical methods. The authors of this scholarly paper mainly tackle this issue from the angle of psychopathological research in schizophrenia. I would like to build on their argument, having in mind one dimension of clinical phenomenology that has not been approached in their paper: the issue of care, that is the use of the method (...) implemented by clinical phenomenology in the therapeutic setting.I first briefly outline some methodological principles of clinical phenomenology in the context of psychopathological research that may be implemented in the context of .. (shrink)

Many of Rose's criticisms of determinism in biology have clear relevance to modern cognitive and psychiatric science; too narrow a focus on the brain as an information processing machine runs the risk of neglecting the context in which information processing takes place, and too narrow a focus on the neuroscience of psychopathology runs the risk of neglecting other levels of explanation for these phenomena. It should be emphasized, however, that animal and genetic studies of phenomena of interest to cognitive and (...) psychiatric science (e.g., Alzheimer's disorder, schizophrenia, attention deficit/hyperactivity disorder, and violence), while perhaps only providing a partial perspective, may be useful in understanding these phenomena and in leading to appropriate psychiatric interventions. (shrink)

The etiology of visual hallucinations is largely undetermined in schizophrenia. Collerton et al.'s PAD model partly concurs with what we know about neurocognition in schizophrenia, but we need to specify the types of perceptual and attentional abnormalities that are implicated in recurrent complex visual hallucinations (RCVH). Available data suggest that abnormal attentional control and top-down processing play a larger role than the ventral stream deficits.

Phillips & Silverstein's ambitious link between receptor abnormalities and the symptoms of schizophrenia involves a certain amount of fuzziness: No detailed mechanism is suggested through which the proposed abnormality would lead to psychological traits. We propose that detailed simulation of brain regions, using model neural networks, can aid in understanding the relation between biological abnormality and psychological dysfunction in schizophrenia.

It is easy to say that the analysis by Kendler and Schaffner of the status of the dopamine hypothesis of schizophrenia (DHS) is, at the very least, a scholarly read. It includes an exhaustive review of the DHS literature accompanied by a demanding critique. The authors' bar for hypothesis verification is high, and their conclusion is negative—that scientific support is insufficient to retain the hypothesis as such. They proceed to evaluate the reasons they see for both (1) the extensive testing (...) of the hypothesis extending over decades and (2) the failure of the field to falsify in a timely fashion. In a very interesting section, they review philosophical positions about how and in what context scientific advances .. (shrink)

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

This dissertation examines psychiatry from a philosophy of science perspective, focusing on issues of realism and classification. Questions addressed in the dissertation include: What evidence is there for the reality of mental disorders? Are any mental disorders natural kinds? When are disease explanations of abnormality warranted? How should mental disorders be classified? -/- In addressing issues concerning the reality of mental disorders, I draw on the accounts of realism defended by Ian Hacking and William Wimsatt, arguing that biological research on (...) mental disorders supports the inference that some mental disorders (e.g., schizophrenia, mood disorders, and anxiety disorders) are real theoretical entities, and that the evidence supporting this inference is causal and abductive. In explicating the nature of such entities, I argue that real mental disorders are natural kinds insofar as they are natural classes of abnormal behavior whose members share the same causal structure. I present this position in terms of Richard Boyd’s homeostatic cluster property theory of natural kinds, and argue that this perspective reveals limitations of Hacking’s account on the looping effects of human kinds, which suggests that the objects classified by psychiatrists are unstable entities. I subsequently argue that a subset of mental disorders (e.g., schizophrenia and Down syndrome) are mental illnesses insofar as they are disorders caused by a dysfunctional biological process that leads to harmful consequences for individuals. I present this analysis against Thomas Szasz’s argument that mental illness is a myth. -/- In addressing issues of psychiatric classification, my analysis focuses on the Diagnostic and Statistical Manual of Mental Disorders (DSM), which has been published regularly by the American Psychiatric Association since 1952, and is currently in its fourth edition. After examining the history of DSM in the twentieth century, and in particular, DSM’s shift to an atheoretical and purely descriptive system in the 1980s, I consider the relative merits of descriptive versus causal systems of classification. Drawing on Carl Hempel’s analysis of taxonomic systems in psychiatry, I argue that a causal classification system would provide a superior approach to psychiatric classification than the descriptive system currently favored by DSM. (shrink)

This paper examines Ian Hacking's analysis of the looping effects of psychiatric classifications, focusing on his recent account of interactive and indifferent kinds. After explicating Hacking's distinction between 'interactive kinds' (human kinds) and 'indifferent kinds' (natural kinds), I argue that Hacking cannot claim that there are 'interactive and indifferent kinds,' given the way that he introduces the interactive-indifferent distinction. Hacking is also ambiguous on whether his notion of interactive and indifferent kinds is supposed to offer an account of classifications or (...) objects of classification. I argue that these conceptual difficulties show that Hacking's account of interactive and indifferent kinds cannot be based on - and should be clearly separated from - his distinction between interactive kinds and indifferent kinds. In clarifying Hacking's account, I argue that interactive and indifferent kinds should be regarded as objects of classification (i.e., kinds of people) that can be identified with reference to a law-like biological regularity and are aware of how they are classified. Schizophrenia and depression are discussed as examples. I subsequently offer reasons for resisting Hacking's claim that the objects of classification in the human sciences - as a result of looping effects - are 'moving targets'. (shrink)

The volume reviews recent progress on our understanding of memory, consciousness and the brain and identifies a number of acute outstanding problems.

Machine generated contents note: -- Clinical Theory -- 1. Psychiatry on schizophrenia: clinical pictures of a sublime object -- 2. Schizophrenia: the sublime text of psychoanalysis -- Cultural Theory -- 3. Antipsychiatry: schizophrenic experience and the sublime -- 4. Anti-Oedipus and the politics of the schizophrenic sublime -- 5. Schizophrenia, modernity, postmodernity -- 6. Postmodern schizophrenia -- 7. Glamorama, postmodernity and the schizophrenic sublime -- Conclusion.

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

This volume presents essays on self-consciousness by prominent psychologists, cognitive neurologists, and philosophers.