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.

We welcome network theory as a tool for modelling the multi-directional interactions that characterise disease. However, we feel that Cramer et al. have neglected one important aspect: how diseases change over developmental time. We discuss principles such as fan in, fan out, bottlenecks, and common pathways, and argue that modelling these developmental aspects can be vital, particularly in deriving properly targeted treatments.

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.

In the multidisciplinary field of developmental cognitive neuroscience, statistical associations between levels of description play an increasingly important role. One example of such associations is the observation of correlations between relatively common gene variants and individual differences in behavior. It is perhaps surprising that such associations can be detected despite the remoteness of these levels of description, and the fact that behavior is the outcome of an extended developmental process involving interaction of the whole organism with a variable environment. Given (...) that they have been detected, how do such associations inform cognitive-level theories? To investigate this question, we employed a multiscale computational model of development, using a sample domain drawn from the field of language acquisition. The model comprised an artificial neural network model of past-tense acquisition trained using the backpropagation learning algorithm, extended to incorporate population modeling and genetic algorithms. It included five levels of description—four internal: genetic, network, neurocomputation, behavior; and one external: environment. Since the mechanistic assumptions of the model were known and its operation was relatively transparent, we could evaluate whether cross-level associations gave an accurate picture of causal processes. We established that associations could be detected between artificial genes and behavioral variation, even under polygenic assumptions of a many-to-one relationship between genes and neurocomputational parameters, and when an experience-dependent developmental process interceded between the action of genes and the emergence of behavior. We evaluated these associations with respect to their specificity, to their developmental stability, and to their replicability, as well as considering issues of missing heritability and gene–environment interactions. We argue that gene–behavior associations can inform cognitive theory with respect to effect size, specificity, and timing. The model demonstrates a means by which researchers can undertake multiscale modeling with respect to cognition and develop highly specific and complex hypotheses across multiple levels of description. (shrink)

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.

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.

Neuroconstructivism: How the Brain Constructs Cognition proposes a unifying framework for the study of cognitive development that brings together (1) constructivism (which views development as the progressive elaboration of increasingly complex structures), (2) cognitive neuroscience (which aims to understand the neural mechanisms underlying behavior), and (3) computational modeling (which proposes formal and explicit specifications of information processing). The guiding principle of our approach is context dependence, within and (in contrast to Marr [1982]) between levels of organization. We propose that three (...) mechanisms guide the emergence of representations: competition, cooperation, and chronotopy; which themselves allow for two central processes: proactivity and progressive specialization. We suggest that the main outcome of development is partial representations, distributed across distinct functional circuits. This framework is derived by examining development at the level of single neurons, brain systems, and whole organisms. We use the terms encellment, embrainment, and embodiment to describe the higher-level contextual influences that act at each of these levels of organization. To illustrate these mechanisms in operation we provide case studies in early visual perception, infant habituation, phonological development, and object representations in infancy. Three further case studies are concerned with interactions between levels of explanation: social development, atypical development and within that, developmental dyslexia. We conclude that cognitive development arises from a dynamic, contextual change in embodied neural structures leading to partial representations across multiple brain regions and timescales, in response to proactively specified physical and social environment. (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.

Evolutionary psychologists argue that selective pressures in our ancestral environment yield a highly specialized set of modular cognitive capacities. However, recent papers in developmental psychology and neuroscience claim that evolutionary accounts of modularity are incompatible with the flexibility and plasticity of the developing brain. Instead, they propose cortical and neuronal brain structures are fixed through interactions with our developmental environment. Buller and Gray Hardcastle contend that evolutionary accounts of cognitive development are unacceptably rigid in light of evidence of cortical plasticity. (...) The developing structure of the brain is both too random and too sensitive to external stimuli to be the product of a fixed genetic mechanism. They also claim that the complexity of the human brain cannot be explained in terms of our meager genetic endowment. There simply are not enough genes to program the intricate neuronal structures that are essential to cognition. I argue that neither of these arguments are persuasive. Small numbers of genes can function to determine diverse phenotypical outcomes through evolutionarily selected developmental systems. Similarly, theories of modularity do not rule out the possibility that innate cognitive systems exploit environmental regularities to guide the developing structure of the brain. Consequently, the anti-adaptionist consequences of these positions should be rejected. (shrink)

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.

has a more specific role to play in the development of Of course, the conclusion to draw is not that innateness innate cognitive structure. In particular, a common claim claims are trivially false or that they cannot be character-.

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.

Language evolution resulted from changes in our biology, behavior, and culture. One source of these changes might be human self-domestication. Williams syndrome (WS) is a clinical condition with a clearly defined genetic basis and resulting in a distinctive behavioral and cognitive profile, including enhanced sociability. In this paper we show evidence that the WS phenotype can be satisfactorily construed as a hyper-domesticated human phenotype, plausibly resulting from the effect of the WS hemydeletion on selected candidates for domestication and neural crest (...) function. Specifically, we show that genes involved in animal domestication and neural crest development and function are significantly dysregulated in the blood of subjects with WS. We also discuss the consequences of this link between domestication and WS for our current understanding of language evolution. (shrink)

This paper is an attempt at exploring the possibility of reconciling the two interpretations of biolinguistics which have been recently projected by Koster(Biolinguistics 3(1):61–92, 2009). The two interpretations—trivial and nontrivial—can be roughly construed as non-internalist and internalist conceptions of biolinguistics respectively. The internalist approach boils down to a conception of language where language as a mental grammar in the form of I-language grows and functions like a biological organ. On the other hand, under such a construal consistent with Koster’s (Biolinguistics (...) 3(1):61-92, 2009), the non-internalist version does not necessarily have to be externalist in nature; rather it is a matter of mutual reinforcement of biology and culture under the rubric of a co-evolutionary dynamics. Here it will be argued that the apparent dichotomy between these two conceptions of biolinguistics can perhaps be resolved if we have a richer synthesis that accounts for both internalism and non-internalism. (shrink)

The broad issue in this paper is the relationship between cognitive psychology and neuroscience. That issue arises particularly sharply for cognitive neurospsychology, some of whose practitioners claim a methodological autonomy for their discipline. They hold that behavioural data from neuropsychological impairments are sufficient to justify assumptions about the underlying modular structure of human cognitive architecture, as well as to make inferences about its various components. But this claim to methodological autonomy can be challenged on both philosophical and empirical grounds. A (...) priori considerations about (cognitive) multiple realisability challenge the thesis on philosophical grounds, and neuroscientific findings from developmental disorders substantiate that challenge empirically. The conclusion is that behavioural evidence alone is inadequate for scientific progress since appearances of modularity can be thoroughly deceptive, obscuring both the dynamic processes of neural development and the endstate network architecture of real cognitive systems. (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.

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.

The development of analogical reasoning has traditionally been understood in terms of theories of adult competence. This approach emphasizes structured representations and structure mapping. In contrast, we argue that by taking a developmental perspective, analogical reasoning can be viewed as the product of a substantially different cognitive ability – relational priming. To illustrate this, we present a computational (here connectionist) account where analogy arises gradually as a by-product of pattern completion in a recurrent network. Initial exposure to a situation primes (...) a relation that can then be applied to a novel situation to make an analogy. Relations are represented as transformations between states. The network exhibits behaviors consistent with a broad range of key phenomena from the developmental literature, lending support to the appropriateness of this approach (using low-level cognitive mechanisms) for investigating a domain that has normally been the preserve of high-level models. Furthermore, we present an additional simulation that integrates the relational priming mechanism with deliberative controlled use of inhibition to demonstrate how the framework can be extended to complex analogical reasoning, such as the data from explicit mapping studies in the literature on adults. This account highlights how taking a developmental perspective constrains the theory construction and cognitive modeling processes in a way that differs substantially from that based purely on adult studies, and illustrates how a putative complex cognitive skill can emerge out of a simple mechanism. (shrink)

This study presents the evaluation of a computer-based learning program for children with developmental dyscalculia and focuses on factors affecting individual responsiveness. The adaptive training program Calcularis 2.0 has been developed according to current neuro-cognitive theory of numerical cognition. It aims to automatize number representations, supports the formation and access to the mental number line and trains arithmetic operations as well as arithmetic fact knowledge in expanding number ranges. Sixty-seven children with developmental dyscalculia from second to fifth grade (mean age (...) 8.96 years) were randomly assigned to one of two groups (Calcularis group, waiting control group). Training duration comprised a minimum of 42 training sessions à 20 minutes within a maximum period of 13 weeks. Compared to the waiting control group, children of the Calcularis group demonstrated a higher benefit in arithmetic operations and number line estimation. These improvements were shown to be stable after a 3-months post training interval. In addition, this study examines which predictors accounted for training improvements. Results indicate that this self-directed training was especially beneficial for children with low math anxiety scores and without an additional reading and/or spelling disorder. In conclusion, Calcularis 2.0 supports children with developmental dyscalculia to improve their arithmetical abilities and their mental number line representation. However, it is relevant to further adapt the setting to the individual circumstances. (shrink)

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.

What was the role of music in the evolutionary history of human beings? We address this question from the point of view that musicality can be defined as a cognitive trait. Although it has been argued that we will never know how cognitive traits evolved (Lewontin, 1998), we argue that we may know the evolution of music by investigating the fundamental cognitive mechanisms of musicality, for example, relative pitch, tonal encoding of pitch, and beat induction. In addition, we show that (...) a nomological network of evidence (Schmitt & Pilcher, 2004) can be built around the hypothesis that musicality is a cognitive adaptation. Within this network, different modes of evidence are gathered to support a specific evolutionary hypothesis. We show that the combination of psychological, medical, physiological, genetic, phylogenetic, hunter–gatherer, and cross-cultural evidence indicates that musicality is a cognitive adaptation. (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.

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.

Evolutionary Psychology is based on the idea that the mind is a set of special purpose thinking devices or modules whose domain-specific structure is an adaptation to ancestral environments. The modular view of the mind is an uncontroversial description of the periphery of the mind, the input-output sensorimotor and affective subsystems. The novelty of EP is the claim that higher order cognitive processes also exhibit a modular structure. Autism is a primary case study here, interpreted as a developmental failure of (...) a module devoted to social intelligence or Theory of Mind. In this article I reappraise the arguments for innate modularity of TOM and argue that they fail. TOM ability is a consequence of domain general development scaffolded by early, innately specified, sensorimotor abilities. The alleged Modularity of TOM results from interpreting the outcome of developmental failures characteristic of autism at too high a level of cognitive abstraction. (shrink)

Nativists about syntactic processing have argued that linguisticprocessing, understood as the implementation of a rule-basedcomputational architecture, is spared in Williams syndrome, (WMS)subjects – and hence that it provides evidence for a geneticallyspecified language module. This argument is bolstered by treatingSpecific Language Impairments (SLI) and WMS as a developmental doubledissociation which identifies a syntax module. Neuroconstructivists haveargued that the cognitive deficits of a developmental disorder cannot beadequately distinguished using the standard gross behavioural tests ofneuropsychology and that the linguistic abilities of the (...) WMS subject canbe equally well explained by a constructivist strategy of neurallearning in the individual, with linguisitic functions implemented in anassociationist architecture. The neuroconstructivist interpretation ofWMS undermines the hypothesis of a double dissociation between SLI andWMS, leaving unresolved the question of nativism about syntax. Theapparent linguistic virtuosity of WMS subjects is an artefact ofenhanced phonological processing, a fact which is easier to demonstratevia the associationist computational model embraced byneuroconstructivism. (shrink)