Recent research suggests that individuals with relatively weak global precedence (i.e., a smaller propensity to view visual stimuli in a configural manner) show a reduced face inversion effect (FIE). Coupled with such findings, a number of recent studies have demonstrated links between an advantage for feature-based processing and the presentation of traits associated with autism among the general population. The present study sought to bridge these findings by investigating whether a relationship exists between the possession of autism-associated traits (i.e., as (...) indicated by individuals’“autism quotient” [(AQ) and the size of the FIE. Participants completed an on-line study in which the AQ was measured prior to a standard face recognition task where half of the faces were inverted at test. The results confirmed that higher AQ levels were predictive of smaller FIEs. Implications for a common underlying factor relating to processing orientation are discussed. (shrink)

Recent research suggests that individuals with relatively weak global precedence (i.e., a smaller propensity to view visual stimuli in a configural manner) show a reduced face inversion effect (FIE). Coupled with such findings, a number of recent studies have demonstrated links between an advantage for feature‐based processing and the presentation of traits associated with autism among the general population. The present study sought to bridge these findings by investigating whether a relationship exists between the possession of autism‐associated traits (i.e., as (...) indicated by individuals’“autism quotient” [(AQ) and the size of the FIE. Participants completed an on‐line study in which the AQ was measured prior to a standard face recognition task where half of the faces were inverted at test. The results confirmed that higher AQ levels were predictive of smaller FIEs. Implications for a common underlying factor relating to processing orientation are discussed. (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.

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.

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.

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.

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.

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.

Recent theorizing about the nature of the cognitive impairment in autism suggests that autistic individuals display abnormally weak central coherence, the capacity to integrate information in order to make sense of one’s environment. Our article shows the relevance of computational models of coherence to the understanding of weak central coherence. Using a theory of coherence as constraint satisfaction, we show how weak coherence can be simulated ina a connectionist network that has unusually high inhibition compared to excitation. This connectionist model (...) simulates autistic behaviour on both the false belief task and the homograph task. (shrink)

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.

A mechanistic explanation is a desired outcome in many studies of perception. Such explanations require discovering the processes that contribute to the realization of a perceptual phenomenon at different levels of information processing. The present analysis aims at investigating the obstacles to develop such mechanistic explanations and their potential solutions in the context of psychopathology. Geometric-Optical Illusions (GOIs) are among perceptual phenomena that have been studied to understand psychopathology in various clinical populations. In the present analysis, the GOIs will be (...) discussed as a methodological tool in the investigation of the mechanistic approach to understanding perception in such populations. I will argue that the fact that most such studies are mainly focused on the investigation of susceptibility to GOIs can only lead to classifying such phenomena or to reporting some correlations between different aspects of such phenomena with certain brain activities, without formulating a mechanistic explanation. The investigation of the variables that mediate perceptual phenomena at earlier stages of information processing is required for the formulation of such explanations. Thus, the objective of the present analysis is twofold: 1) showing how ignoring such variables have prevented the formulation of mechanistic explanations of responses to GOIs in clinical populations, such as schizophrenia and autism, 2) analyzing the methodological aspects of an effective approach in which a top-down guidance based on phenomenological insights (the first-person data) along with the insights provided by the existing theories help overcome obstacles in developing mechanistic explanations of GOIs. (shrink)

It often seems incorrect to say that psychiatric conditions are diseases, and equally incorrect to say that they are not. This results in what would seem to be an unsatisfactory stalemate. The present essay examines the considerations that have brought us to such a stalemate in our discussions of autism. It argues that the stalemate in this particular case is a reflection of the fact that we need to find the logical space for a position that rejects both positive and (...) negative answers. It then suggests one way in which we might find such space, by applying Michael Dummett’s notion of semantic disharmony. (shrink)

Consciousness and intelligence are properties that can be misunderstood as necessarily dependent. The term artificial intelligence and the kind of problems it managed to solve in recent years has been shown as an argument to establish that machines experience some sort of consciousness. Following Russell’s analogy, if a machine can do what a conscious human being does, the likelihood that the machine is conscious increases. However, the social implications of this analogy are catastrophic. Concretely, if rights are given to entities (...) that can solve the kind of problems that a neurotypical person can, does the machine have potentially more rights than a person that has a disability? For example, the autistic syndrome disorder spectrum can make a person unable to solve the kind of problems that a machine solves. We believe the obvious answer is no, as problem-solving does not imply consciousness. Consequently, we will argue in this paper how phenomenal consciousness, at least, cannot be modeled by computational intelligence and why machines do not possess phenomenal consciousness, although they can potentially develop a higher computational intelligence than human beings. In order to do so, we try to formulate an objective measure of computational intelligence and study how it presents in human beings, animals, and machines. Analogously, we study phenomenal consciousness as a dichotomous variable and how it is distributed in humans, animals, and machines. (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.

Although enactive approaches to cognition vary in terms of their character and scope, all endorse several core claims. The first is that cognition is tied to action. The second is that cognition is composed of more than just in-the-head processes; cognitive activities are externalized via features of our embodiment and in our ecological dealings with the people and things around us. I appeal to these two enactive claims to consider a view called “direct social perception” : the idea that we (...) can sometimes perceive features of other minds directly in the character of their embodiment and environmental interactions. I argue that if DSP is true, we can probably also perceive certain features of mental disorders as well. I draw upon the developmental psychologist Daniel Stern’s notion of “forms of vitality”—largely overlooked in these debates—to develop this idea, and I use autism as a case study. I argue further that an enactive approach to DSP can clarify some ways we play a regulative role in shaping the temporal and phenomenal character of the disorder in question, and it may therefore have practical significance for both the clinical and therapeutic encounter. (shrink)

Autism, typically described as a spectrum neurodevelopmental disorder characterized by impairments in verbal ability and social reciprocity as well as obsessive or repetitious behaviours, is currently thought to markedly affect more males than females. Not surprisingly, this encourages a gendered understanding of the Autism Spectrum. Simon Baron-Cohen, a prominent authority in the field of autism research, characterizes the male brain type as biased toward systemizing. In contrast, the female brain type is understood to be biased toward empathizing. Since persons with (...) autism are characterized as hyper-systemizers and hypo-empathizers, Baron-Cohen suggests that, whether they are male or female, most possess an “extreme male brain profile.” We argue that Baron-Cohen is misled by an unpersuasive gendering of certain capacities or aptitudes in the human population. Moreover, we suggest that this may inadvertently favour boys in diagnosing children with Autism Spectrum Disorders. If this is correct, it could also have rather serious consequences for treatment and services for girls (and women) on the Autism Spectrum. (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.

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.

We propose here that a visual-motion integration deficit constitutes a crucial neuropsychological marker for at least a subgroup of ASD.

In this paper, we attempt to make a distinction between egocentrism and allocentrism in social cognition, based on the distinction that is made in visuo-spatial perception. We propose that it makes a difference to mentalizing whether the other person can be understood using an egocentric (‘‘you'') or an allocentric (‘‘he/ she/they'') stance. Within an egocentric stance, the other person is represented in relation to the self. By contrast, within an allocentric stance, the existence or mental state of the other person (...) needs to be represented as independent from the self. We suggest here that people with Asperger syndrome suffer from a disconnection between a strong naı¨ve egocentric stance and a highly abstract allocentric stance. We argue that the currently used distinction between first-person and third-person perspective-taking is orthogonal to the distinction between an egocentric and an allocentric stance and therefore cannot serve as a critical test of allocentrism. (shrink)

Pragmatic difficulties are considered a hallmark of autism spectrum conditions (ASC), but remain poorly understood. We discuss and evaluate existing hypotheses regarding the literalism of ASC individuals, that is, their tendency for literal interpretations of non‐literal communicative intentions. We present evidence that reveals a developmental stage at which neurotypical children also have a tendency for literalism and suggest an explanation for such behaviour that links it to other behavioural, rule‐following, patterns typical of that age. We discuss evidence showing that strict (...) adherence to rules is also widespread in ASC, and suggest that literalism might be linked to such rule‐following behaviour. (shrink)

Children and adults with autism do worse on tests of inferences than controls. This fact has been attributed to poor language skills, a tendency to focus on detail, and poor social understanding. This study examines whether children with autism with age-appropriate language and cognitive skills have difficulties drawing inferences from academic, expository texts. Sixteen children with autism and a control group of twenty-four children were matched on language skills, nonverbal cognitive ability, and auditory and nonverbal working memory and compared on (...) their responses to questions that require inferences. The children with autism scored significantly lower on inference questions than the controls. Although language skills explain much of the variance in inference scores, diagnostic background also made a contribution. The results are discussed in the light of theories of suppression of irrelevant information and recognition of text writers’ communicative intention. (shrink)