Mechanisms that contribute to perceptual processing dysfunction in schizophrenia were examined by Phillips & Silverstein, and formulated as involving disruptions in both local and higher-level coordination of signals. We agree that dysfunction in the coordination of cognitive functions (disconnection) is also indicated for many of the linguistic processing deficits documented for schizophrenia. We suggest, however, that it may be necessary to add a timing mechanism to the theoretical account.

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.

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.

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.

The target article presents a model for schizophrenia extending four levels of abstraction: molecules, cells, cognition, and syndrome. An important notion in the model is that of coordination, applicable to both the level of cells and of cognition. The molecular level provides an “implementation” of the coordination at the cellular level, which in turn underlies the coordination at the cognitive level, giving rise to the clinical symptoms.

This article will explore the representation of certain mental and somatic phenomena in Beckett’s trilogy of novels Molloy, Malone Dies and The Unnamable, exploring how his understanding of schizophrenia and psychosis informs his representation of the relationship between mind and body. It will also examine recent phenomenological and philosophical accounts of schizophrenia that see the condition as a disorder of selfhood and concentrate in it on the disruption to ipseity, a fundamental and pre-reflective awareness of self that leads to a (...) loss of ‘grip’ on concepts and percepts. Beckett’s writing might, it is argued, make such disruptions more tangible and intelligible. The article will also consider John Campbell’s argument that immunity of the first person to error—Sydney Shoemaker’s foundational philosophical idea that we cannot misspeak the first person pronoun—is revoked in states of psychosis, and relate such states to the moments in Beckett’s writing where this immunity is challenged, and quasi-psychotic experiences represented. (shrink)

This commentary compares clinical aspects of ketamine with the amphetamine model of schizophrenia. Hallucinations and loss of insight, associated with amphetamine, seem more schizophrenia-like. Flat affect encountered with ketamine is closer to the clinical presentation in schizophrenia. We argue that flat affect is not a sign of schizophrenia, but rather, a risk factor for chronic schizophrenia.

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

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

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.

Although interesting, the hypotheses proposed by Phillips & Silverstein lack unifying structure both in specific mechanisms and in cited evidence. They provide little to support the notion that low-level sensory processing and high-level cognitive coordination share dynamic grouping by synchrony as a common processing mechanism. We suggest that more realistic large-scale modeling at multiple levels is needed to address these issues.

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

In chronic schizophrenic patients with both positive and negative symptoms (see Table 1), interhemispheric connections at the high frequency beta2-rhythm are absent during cognitive tasks, in contrast to normal controls, who have many interhemispheric connections at this frequency in the same situation. Connectivity is a fundamental brain feature, evidently greatly promoted by the NMDA system. It is a more reliable measure of brain function than the spectral power of this rhythm.

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)

Impairments in cognitive coordination in schizophrenia are supported by phenomenological data that suggest deficits in the processing of visual context. Although the target article is sympathetic to such a phenomenological perspective, we argue that the relevance of phenomenological data for a wider understanding of consciousness in schizophrenia is not sufficiently addressed by the authors.

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.

After a brief perusal of the various meanings of phenomenology in psychopathology, the contributions to schizophrenia of phenomenological psychology in the European sense are reviewed. The last twenty years are deemed fruitful and productive. Following the central themes and motives of this literature allows us to come to a different and perhaps wider understanding of schizophrenia than that proposed currently by mainstream psychiatry. These diverse investigations converge in seeing as the core of schizophrenia the disorders related to inter-subjectivity and ipseity (...) , in turn related to what Bleuler had once called Autism. Finally, a critical discussion of the limitations and the strengths of the phenomenological approach is offered. (shrink)

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.

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.

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

This commentary highlights methods for using scalp EEG to make inferences about contextual field interactions, which, in view of the target article, may be specially relevant to the study of schizophrenia. Although scalp EEG has limited spatial resolution, prior knowledge combined with experimental manipulations may be used to strengthen inferences about underlying brain processes. Both spatial and temporal context are discussed within the framework of nonlinear interactions. Finally, results from a visual contour integration EEG pilot study are summarized in view (...) of a hypothesis that relates receptive field and contextual field processing to evoked and induced activity, respectively. (shrink)

Although context-processing deficits may be core features of schizophrenia, context remains a poorly defined concept. To test Phillips & Silverstein's model, we need to operationalize context more precisely. We offer several useful ways of framing context and discuss enhancing or facilitating schizophrenic patients' performance under different contextual situations. Furthermore, creativity may be a byproduct of cognitive uncoordination.

Context, connection, and coordination (CCC) describe well where the problems that apply to thought-disordered patients with schizophrenia lie. But they may be part of the experience of those with other symptom constellations. Switching is an important mechanism to allow context to be applied appropriately to changing circumstances. In some cases, NMDA-voltage modulations may be central, but gain and shift are also functions that monoaminergic systems express in CCC.

This commentary challenges the authors to use their computational modeling techniques to support one of their central claims: that schizophrenic deficits in bottom-up (Gestalt-type tasks) and top-down (cognitive control tasks) context processing tasks arise from the same dysfunction. Further clarification about the limits of cognitive coordination would also strengthen the hypothesis.

Schizophrenics exhibit a deficit in theory of mind (ToM), but an intact theory of biology (ToB). One explanation is that ToM relies on an independent module that is selectively damaged. Phillips & Silverstein's analyses suggest an alternative: ToM requires the type of coordination that is impaired in schizophrenia, whereas ToB is spared because this type of coordination is not involved.

Neurophysiological investigations of the past two decades have consistently demonstrated a deficit in sensory gating associated with schizophrenia. Phillips & Silverstein interpret this impairment as being consistent with cognitive coordination dysfunction. However, the physiological mechanisms that underlie sensory gating have not been shown to involve gamma-band oscillations or NMDA-receptors, both of which are critical neural elements in the cognitive coordination model.

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 propose that the primary cause of schizophrenia is a pathological extension of synaptic pruning involving local connectivity that unfolds ordinarily during adolescence. Computer simulations suggest that this pathology provides reasonable accounts of a range of symptoms in schizophrenia, and is consistent with recent postmortem and genetic studies. NMDA-receptors play a regulatory role in maintaining and/or eliminating cortical synapses, and therefore may play a pathophysiological role.

This commentary addresses: (a) the problems of definition which have been prominent in the use of the term context in schizophrenia research; (b) potentially useful distinctions and links with other theories of schizophrenic cognition; and (c) possible pathways to schizophrenic symptoms. It is suggested that at least two major aspects of the operation of context may be distinguished and that both may be impaired in schizophrenia.

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).

The Phillips & Silverstein model of NMDA-mediated coordination deficits provides a useful heuristic for the study of schizophrenic cognition. However, the model does not specifically account for the development of schizophrenia-spectrum disorders. The P&S model is compared to Meehl's seminal model of schizotaxia, schizotypy, and schizophrenia, as well as the model of schizophrenic cognitive dysfunction posited by McCarley and colleagues.

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

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)

I can be aware of myself, and thereby come to know things about myself, in a variety of different ways. But is there some special way in which I—and only I—can learn about myself? Can I become aware of myself by introspecting? Do I somehow show up in my own conscious experiences? David Hume and most contemporary philosophers say no. They deny that the self shows up in experience. However, in this paper I appeal to research on schizophrenia—on thought insertion, (...) in particular—to argue that Hume and his follows are wrong: The self does, in fact, show up in experience. (shrink)

Subjectivity is that feature of consciousness whereby there is something it is like for a subject to undergo an experience. One persistent challenge in the study of consciousness is to explain how subjectivity relates to, or arises from, purely physical brain processes. But, in order to address this challenge, it seems we must have a clear explanation of what subjectivity is in the first place. This has proven challenging in its own right. For the nature of subjectivity itself seems to (...) resist straightforward characterization. In this paper, I won't address how subjectivity relates to the physical. Instead, I'll address subjectivity itself. I'll do this by introducing and defending a model of subjectivity based on self-acquaintance. My model does not purport to reduce, eliminate, or naturalize subjectivity, but it does make subjectivity more tractable, less paradoxical, and perhaps less dubious to those averse to obscurity. (shrink)

My discussion will focus on what is arguable the main claim of Being No One: That no such things as selves exist in the world and that nobody ever was or had a self. In discussing to what extent Metzinger can be said to argue convincingly for this claim, I will also comment on his methodological use of pathology and briefly make some remarks vis-à-vis his understanding and criticism of phenomenology.