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.

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.

Reductive, naturalistic psychosemantic theories do not have a good track record when it comes to accommodating the representation of kinds. In this paper, I will suggest a particular teleosemantic strategy to solve this problem, grounded in the neurocomputational details of the cerebral cortex. It is a strategy with some parallels to one that Ruth Millikan has suggested, but to which insufficient attention has been paid. This lack of attention is perhaps due to a lack of appreciation for the severity of (...) the problem, so I begin by explaining why the situation is indeed a dire one. One of the main tasks for a naturalistic psychosemantic theory is to describe how the extensions of mental representations are determined. (Such a theory may also attempt to account for other aspects of the “meaning” of mental representations, if there are any.) Some mental representations, e.g. the concept of water, denote kinds (I shall be assuming this is non-negotiable). How is this possible? Unfortunately, I haven’t the space to canvass all the theories out there and show that each one fails to accommodate the representation of kinds, but I will point out the major types of problems that arise for the kinds of theories that, judging by the literature, are considered viable contenders.1 In general, the theories either attempt and fail to account for the representation of kinds, or they fall back on something like an intention to refer to a kind – not exactly the most auspicious move for a reductive theory. There are a number of problems that prevent non-teleosemantic theories from explaining how it is possible to represent kinds. A concept of a kind K must.. (shrink)

I present an account of mental representation based upon the ‘SINBAD’ theory of the cerebral cortex. If the SINBAD theory is correct, then networks of pyramidal cells in the cerebral cortex are appropriately described as representing, or more specifically, as modelling the world. I propose that SINBAD representation reveals the nature of the kind of mental representation found in human and animal minds, since the cortex is heavily implicated in these kinds of minds. Finally, I show how SINBAD neurosemantics can (...) provide accounts of misrepresentation, equivocal representation, twin cases, and Frege cases. (shrink)

We present a theoretical view of the cellular foundations for network-level processes involved in producing our conscious experience. Inputs to apical synapses in layer 1 of a large subset of neocortical cells are summed at an integration zone near the top of their apical trunk. These inputs come from diverse sources and provide a context within which the transmission of information abstracted from sensory input to their basal and perisomatic synapses can be amplified when relevant. We argue that apical amplification (...) enables conscious perceptual experience and makes it more flexible, and thus more adaptive, by being sensitive to context. Apical amplification provides a possible mechanism for recurrent processing theory that avoids strong loops. It makes the broadcasting hypothesized by global neuronal workspace theories feasible while preserving the distinct contributions of the individual cells receiving the broadcast. It also provides mechanisms that contribute to the holistic aspects of integrated information theory. As apical amplification is highly dependent on cholinergic, aminergic, and other neuromodulators, it relates the specific contents of conscious experience to global mental states and to fluctuations in arousal when awake. We conclude that apical dendrites provide a cellular mechanism for the context-sensitive selective amplification that is a cardinal prerequisite of conscious perception. (shrink)

Kampis proposes the study of chaotic itinerancy, pointing out its significance in domains of cognitive science and philosophy. He has discovered in the concept of chaotic itinerancy the possibility for a new dynamical approach that elucidates mental states with a physical basis. This approach may therefore provide the means to go beyond the connectionist approach. In accordance with his theory, I here highlight three issues regarding chaotic itinerancy: transitory dynamics, diversity, and self-modifying system.

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 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.

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.

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.

The central idea is that the cerebral cortex is a model building machine, where regularities in the world serve as templates for the models it builds. First it is shown how this idea can be naturalized, and how the representational contents of our internal models depend upon the evolutionarily endowed design principles of our model building machine. Current neuroscience suggests a powerful form that these design principles may take, allowing our brains to uncover deep structures of the world hidden behind (...) surface sensory stimulation, the individuals, kinds, and properties that form the objects of human perception and thought. It is then shown how this account solves various problems that arose for previous attempts at naturalizing intentionality, and also how it supports rather than undermines folk psychology. As in the parable of the blind men and the elephant, the seemingly unrelated pieces of earlier theories (information, causation, isomorphism, success, and teleology) emerge as different aspects of the evolved model-building mechanism that explains the intentional features of our kind of mind. (shrink)

The ability to predict is the most importantability of the brain. Somehow, the cortex isable to extract regularities from theenvironment and use those regularities as abasis for prediction. This is a most remarkableskill, considering that behaviourallysignificant environmental regularities are noteasy to discern: they operate not only betweenpairs of simple environmental conditions, astraditional associationism has assumed, butamong complex functions of conditions that areorders of complexity removed from raw sensoryinputs. We propose that the brain's basicmechanism for discovering such complexregularities is implemented in (...) the dendritictrees of individual pyramidal cells in thecerebral cortex. Pyramidal cells have 5–8principal dendrites, each of which is capableof learning nonlinear input-to-outputtransfer functions. We propose that eachdendrite is trained, in learning its transferfunction, by all the other principal dendritesof the same cell. These dendrites teach eachother to respond to their separate inputs with matching outputs. Exposed to differentbut related information about the sensoryenvironment, principal dendrites of the samecell tune to functions over environmentalconditions that, while different, are correlated . As a result, the cell as awhole tunes to the source of the regularitiesdiscovered by the cooperating dendrites,creating a new representation. When organizedinto feed-forward/feedback layers, pyramidalcells can build their discoveries on thediscoveries of other cells, graduallyuncovering nature's hidden order. Theresulting associative network is powerfulenough to meet a troubling traditionalobjection to associationism: that it is toosimple an architecture to implement rationalprocesses. (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.

Unsupervised statistical learning is the standard setting for the development of the only advanced visual system that is both highly sophisticated and versatile, and extensively studied: that of monkeys and humans. In this extended abstract, we invoke philosophical observations, computational arguments, behavioral data and neurobiological findings to explain why computer vision researchers should care about (1) unsupervised learning, (2) statistical inference, and (3) the visual brain. We then outline a neuromorphic approach to structural primitive learning motivated by these considerations, survey (...) a range of neurobiological findings and behavioral data consistent with it, and conclude by mentioning some of the more challenging directions for future research. (shrink)

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.

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.

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.

If one formulates Helmholtz's ideas about perception in terms of modern-day theories one arrives at a model of perceptual inference and learning that can explain a remarkable range of neurobiological facts. Using constructs from statistical physics it can be shown that the problems of inferring what cause our sensory inputs and learning causal regularities in the sensorium can be resolved using exactly the same principles. Furthermore, inference and learning can proceed in a biologically plausible fashion. The ensuing scheme rests on (...) Empirical Bayes and hierarchical models of how sensory information is generated. The use of hierarchical models enables the brain to construct prior expectations in a dynamic and context-sensitive fashion. This scheme provides a principled way to understand many aspects of the brain's organisation and responses. In this paper, we suggest that these perceptual processes are just one emergent property of systems that conform to a free-energy principle. The free-energy considered here represents a bound on the surprise inherent in any exchange with the environment, under expectations encoded by its state or configuration. A system can minimise free-energy by changing its configuration to change the way it samples the environment, or to change its expectations. These changes correspond to action and perception, respectively, and lead to an adaptive exchange with the environment that is characteristic of biological systems. This treatment implies that the system's state and structure encode an implicit and probabilistic model of the environment. We will look at models entailed by the brain and how minimisation of free-energy can explain its dynamics and structure. (shrink)

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.

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.

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.

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.

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.

The target article sketched and explored a mechanism (action-oriented predictive processing) most plausibly associated with core forms of cortical processing. In assessing the attractions and pitfalls of the proposal we should keep that element distinct from larger, though interlocking, issues concerning the nature of adaptive organization in general.

The computational program for theoretical neuroscience initiated by Marr and Poggio (1977) calls for a study of biological information processing on several distinct levels of abstraction. At each of these levels — computational (defining the problems and considering possible solutions), algorithmic (specifying the sequence of operations leading to a solution) and implementational — significant progress has been made in the understanding of cognition. In the past three decades, computational principles have been discovered that are common to a wide range of (...) functions in perception (vision, hearing, olfaction) and action (motor control). More recently, these principles have been applied to the analysis of cognitive tasks that require dealing with structured information, such as visual scene understanding and analogical reasoning. Insofar as language relies on cognition-general principles and mechanisms, it should be possible to capitalize on the recent advances in the computational study of cognition by extending its methods to linguistics. (shrink)

A critical discussion is provided of three central assumptions underlying Nunez's approach to modeling cortical activity. A plea is made for neurophysiologically realistic models involving nonlinearities, multiple time scales, and stochasticity.

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)

Life is preserved and enhanced by coordinated selectivity in local neural circuits. Narrow receptive-field selectivity is necessary to avoid the curse-of-dimensionality, but local activities can be made coherent and relevant by guiding learning and processing using broad coordinating contextual gain-controlling interactions. Better understanding of the functions and mechanisms of those interactions is therefore crucial to the issues Clark examines.

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.

In attempts to formulate a computational understanding of brain function, one of the fundamental concerns is the data structure by which the brain represents information. For many decades, a conceptual framework has dominated the thinking of both brain modelers and neurobiologists. That framework is referred to here as "classical neural networks." It is well supported by experimental data, although it may be incomplete. A characterization of this framework will be offered in the next section. Difficulties in modeling important functional aspects (...) of the brain on the basis of classical neural networks alone have led to the recognition that another, general mechanism must be invoked to explain brain function. That mechanism I call " binding." Binding by neural signal synchrony had been mentioned several times in the liter ature before it was fully formulated as a general phenomenon. Although experimental evidence for neural syn chrony was soon found, the idea was largely ignored for many years. Only recently has it become a topic of animated discussion. In what follows, I will summarize the nature and the roots of the idea of binding, especially of temporal binding, and will discuss some of the objec tions raised against it. (shrink)

We propose that a top priority of the cerebral cortex must be the discovery and explicit representation of the environmental variables that contribute as major factors to environmental regularities. Any neural representation in which such variables are represented only implicitly (thus requiring extra computing to use them) will make the regularities more complex and therefore more difficult, if not impossible, to learn. The task of discovering such important environmental variables is not an easy one, since their existence is only indirectly (...) suggested by the sensory input patterns the cortex receives – these variables are “hidden.” We present a candidate computational strategy for (1) discovering regularity-simplifying environmental variables, (2) learning the regularities, and (3) using regularities in perceptual and decision-making tasks. The SINBAD computational model discovers useful environmental variables through a search for different, but nevertheless highly correlated functions of any kind over non-overlapping subsets of the known variables, this being indicative of some important environmental variable that is responsible for the correlation. We suggest that such a search is performed in the neocortex by the dendritic trees of individual pyramidal cells. According to the SINBAD model, the basic function of each pyramidal cell is (1) to discover and represent one of the regularity-simplifying environmental variables, and (2) to learn to infer the state of its variable from the states of other variables, represented by other pyramidal cells. A network of such cells – each cell just attending to representation of its variable – can function as a sophisticated and useful inferential model of the outside world. (shrink)

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.

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.

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.

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 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.

According to one productive and influential approach to cognition, categorization, object recognition, and higher level cognitive processes operate on a set of fixed features, which are the output of lower level perceptual processes. In many situations, however, it is the higher level cognitive process being executed that influences the lower level features that are created. Rather than viewing the repertoire of features as being fixed by low-level processes, we present a theory in which people create features to subserve the representation (...) and categorization of objects. Two types of category learning should be distinguished. Fixed space category learning occurs when new categorizations are representable with the available feature set. Flexible space category learning occurs when new categorizations cannot be represented with the features available. Whether fixed or flexible, learning depends on the featural contrasts and similarities between the new category to be represented and the individual's existing concepts. Fixed feature approaches face one of two problems with tasks that call for new features: If the fixed features are fairly high level and directly useful for categorization, then they will not be flexible enough to represent all objects that might be relevant for a new task. If the fixed features are small, subsymbolic fragments (such as pixels), then regularities at the level of the functional features required to accomplish categorizations will not be captured by these primitives. We present evidence of flexible perceptual changes arising from category learning and theoretical arguments for the importance of this flexibility. We describe conditions that promote feature creation and argue against interpreting them in terms of fixed features. Finally, we discuss the implications of functional features for object categorization, conceptual development, chunking, constructive induction, and formal models of dimensionality reduction. Key Words: concept learning; conceptual development; features; perceptual learning; stimulus encoding. (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.

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.

For scene analysis, it is important to ask the question of how synchronized population codes – the basic representation employed in the target article – are generated. Recent computational advances have resolved the critical challenges of rapid synchronization with local coupling and rapid desynchronization. The synchronized codes make real contributions to tackling the problem of scene analysis.

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.

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.

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.

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).