This systematic investigation of computation and mental phenomena by a noted psychologist and computer scientist argues that cognition is a form of computation, that the semantic contents of mental states are encoded in the same general way as computer representations are encoded. It is a rich and sustained investigation of the assumptions underlying the directions cognitive science research is taking. 1 The Explanatory Vocabulary of Cognition 2 The Explanatory Role of Representations 3 The Relevance of Computation 4 The Psychological Reality (...) of Programs: Strong Equivalence 5 Constraining Functional Architecture 6 The Bridge from Physical to Symbolic: Transduction 7 Functional Architecture and Analogue Processes 8 Mental Imagery and Functional Architecture 9 Epilogue: What is Cognitive Science the Science of? (shrink)

This interdisciplinary book considers the relationship between language and thought from a philosophical perspective, drawing both on the philosophical study of language and the purely formal study of grammar, and arguing that the two should align. The claim is that grammar provides homo sapiens with the ability to think in certain grammatical ways and that this in turn explains the vast cognitive powers of human beings. Evidence is considered from biology, the evolution of language, language disorders, and linguistic phenomena.

In these essays the minimalist approach to linguistic theory is formulated and progressively developed.

For the past two decades, it has widely been assumed by linguists that there is a single computational operation, Merge, which is unique to language, distinguishing it from other cognitive domains. The intention of this paper is to progress the discussion of language evolution in two ways: (i) survey what the ethological record reveals about the uniqueness of the human computational system, and (ii) explore how syntactic theories account for what ethology may determine to be human-specific. It is shown that (...) the operation Label, not Merge, constitutes the evolutionary novelty which distinguishes human language from non-human computational systems; a proposal lending weight to a Weak Continuity Hypothesis and leading to the formation of what is termed Computational Ethology. Some directions for future ethological research are suggested. (shrink)

Autism and psychosis manifest private speech disruptions analogous to their diametrical opposition along the autism-psychosis continuum. Autism has naturally suppressed private speech with predictable structural deficits when it does surface; psychosis has overt but ineffectual private speech with similar structural deficits. These private speech oppositions are best understood in the context of the control processes of cognitive-computational architectures.

Autistic-spectrum conditions and psychotic-spectrum conditions (mainly schizophrenia, bipolar disorder, and major depression) represent two major suites of disorders of human cognition, affect, and behavior that involve altered development and function of the social brain. We describe evidence that a large set of phenotypic traits exhibit diametrically opposite phenotypes in autistic-spectrum versus psychotic-spectrum conditions, with a focus on schizophrenia. This suite of traits is inter-correlated, in that autism involves a general pattern of constrained overgrowth, whereas schizophrenia involves undergrowth. These disorders also (...) exhibit diametric patterns for traits related to social brain development, including aspects of gaze, agency, social cognition, local versus global processing, language, and behavior. Social cognition is thus underdeveloped in autistic-spectrum conditions and hyper-developed on the psychotic spectrum.;>We propose and evaluate a novel hypothesis that may help to explain these diametric phenotypes: that the development of these two sets of conditions is mediated in part by alterations of genomic imprinting. Evidence regarding the genetic, physiological, neurological, and psychological underpinnings of psychotic-spectrum conditions supports the hypothesis that the etiologies of these conditions involve biases towards increased relative effects from imprinted genes with maternal expression, which engender a general pattern of undergrowth. By contrast, autistic-spectrum conditions appear to involve increased relative bias towards effects of paternally expressed genes, which mediate overgrowth. This hypothesis provides a simple yet comprehensive theory, grounded in evolutionary biology and genetics, for understanding the causes and phenotypes of autistic-spectrum and psychotic-spectrum conditions. (shrink)