What is the primary function of consciousness in the nervous system? The answer to this question remains enigmatic, not so much because of a lack of relevant data, but because of the lack of a conceptual framework with which to interpret the data. To this end, we have developed Passive Frame Theory, an internally coherent framework that, from an action-based perspective, synthesizes empirically supported hypotheses from diverse fields of investigation. The theory proposes that the primary function of consciousness is well-circumscribed, (...) serving the 'somatic nervous system[. For this system, consciousness serves as a frame that constrains and directs skeletal muscle output, thereby yielding adaptive behavior. The mechanism by which consciousness achieves this is more counterintuitive, passive, and “low level” than the kinds of functions that theorists have previously attributed to consciousness. Passive frame theory begins to illuminate (a) what consciousness contributes to nervous function, (b) how consciousness achieves this function, and (c) the neuroanatomical substrates of conscious processes. Our untraditional, action-based perspective focuses on olfaction instead of on vision and is 'descriptive' (describing the products of nature as they evolved to be) rather than 'normative' (construing processes in terms of how they should function). Passive frame theory begins to isolate the neuroanatomical, cognitive-mechanistic, and representational (e.g., conscious contents) processes associated with consciousness. (shrink)

Müller's target article aims to summarize approaches to the question of how language elements (phonemes, morphemes, etc.) and rules are laid down in the brain. However, it suffers from being too vague about basic assumptions and empirical predictions of neurobiological models, and the empirical evidence available to test the models is not appropriately evaluated. (1) In a neuroscientific model of language, different cortical localizations of words can only be based on biological principles. These need to be made explicit. (2) Evidence (...) for and against word class differences could be evaluated more rigorously. (3) All (and only) humans are able to learn languages with complex syntactic structures; it is, therefore, not appropriate to deny innateness and universality of syntactic principles. The real question appears to be the following: Which neurobiological principles are the linguistic principles based on? (shrink)

This article argues that rapid eye movement (REM) dreaming is elaborative encoding for episodic memories. Elaborative encoding in REM can, at least partially, be understood through ancient art of memory (AAOM) principles: visualization, bizarre association, organization, narration, embodiment, and location. These principles render recent memories more distinctive through novel and meaningful association with emotionally salient, remote memories. The AAOM optimizes memory performance, suggesting that its principles may predict aspects of how episodic memory is configured in the brain. Integration and segregation (...) are fundamental organizing principles in the cerebral cortex. Episodic memory networks interconnect profusely within the cortex, creating omnidirectional “landmark” junctions. Memories may be integrated at junctions but segregated along connecting network paths that meet at junctions. Episodic junctions may be instantiated during non–rapid eye movement (NREM) sleep after hippocampal associational function during REM dreams. Hippocampal association involves relating, binding, and integrating episodic memories into a mnemonic compositional whole. This often bizarre, composite image has not been present to the senses; it is not “real” because it hyperassociates several memories. During REM sleep, on the phenomenological level, this composite image is experienced as a dream scene. A dream scene may be instantiated as omnidirectional neocortical junction and retained by the hippocampus as an index. On episodic memory retrieval, an external stimulus (or an internal representation) is matched by the hippocampus against its indices. One or more indices then reference the relevant neocortical junctions from which episodic memories can be retrieved. Episodic junctions reach a processing (rather than conscious) level during normal wake to enable retrieval. If this hypothesis is correct, the stuff of dreams is the stuff of memory. (shrink)

According to the standard view, the causal process connecting a past representation and its subsequent recall involves intermediary memory traces. Yet Bertrand Russell and Ludwig Wittgenstein held that since the physiological evidence for memory traces isn't quite conclusive, it is prudent to come up with an account of memory causation-referred to as nmemic causation—that manages without the stipulation of memory traces. Given mnemic causation, a past representation is directly causally active over a temporal distance. I argue that the stipulation of (...) memory traces is indeed indispensable for analyzing mernory causation. (shrink)

It is no secret that scientists argue. They argue about theories. But even more, they argue about the evidence for theories. Is the evidence itself trustworthy? This is a bit surprising from the perspective of traditional empiricist accounts of scientific methodology according to which the evidence for scientific theories stems from observation, especially observation with the naked eye. These accounts portray the testing of scientific theories as a matter of comparing the predictions of the theory with the data generated by (...) these observations, which are taken to provide an objective link to reality. (shrink)

There is a strong philosophical intuition that direct study of the brain can and will constrain the development of psychological theory. When this intuition is tested against case studies on the neurophysiology and psychology of perception and memory, it turns out that psychology has led the way toward knowledge of neurophysiology. An abstract argument is developed to show that psychology can and must lead the way in neuroscientific study of mental function. The opposing intuition is based on mainly weak arguments (...) about the fundamentality or objectivity of physics or physiology in relation to psychology. -/- Philosophy of Science, Vol. 67, Supplement. Proceedings of the 1998 Biennial Meetings of the Philosophy of Science Association. Part II: Symposia Papers (Sep., 2000). (shrink)

This paper describes a model of how musicians make decisions about performing notated music. The model builds on psychological theories of decision-making and was developed from empirical studies of Western art music performance that aimed to identify intuitive and deliberate processes of decision-making, a distinction consistent with dual-process theories of cognition. The model proposes that the proportion of intuitive (Type 1) and deliberate (Type 2) decision-making processes changes with increasing expertise and conceptualizes this change as movement along a continually narrowing (...) upward spiral where the primary axis signifies principal decision-making type and the vertical axis marks level of expertise. The model is intended to have implications for the development of expertise as described in two main phases. The first is movement from a primarily intuitive approach in the early stages of learning toward greater deliberation as analytical techniques are applied during practice. The second phase occurs as deliberate decisions gradually become automatic (procedural), increasing the role of intuitive processes. As a performer examines more issues or reconsiders decisions, the spiral motion toward the deliberate side and back to the intuitive is repeated indefinitely. With increasing expertise, the spiral tightens to signify greater control over decision type selection. The model draws on existing theories, particularly Evans’ (2011) Intervention Model of dual-process theories, Cognitive Continuum Theory Hammond et al. (1987), Hammond (2007), Baylor’s (2001) U-shaped model for the development of intuition by level of expertise. By theorizing how musical decision-making operates over time and with increasing expertise, this model could be used as a framework for future research in music performance studies and performance science more generally. (shrink)

This paper is a commentary on the target article by Lokendra Shastri & Venkat Ajjanagadde [S&A]: “From simple associations to systematic reasoning: A connectionist representation of rules, variables and dynamic bindings using temporal synchrony” in same issue of the journal, pp.417–451. -/- It puts S&A's temporal-synchrony binding method in a broader context, comments on notions of pointing and other ways of associating information - in both computers and connectionist systems - and mentions types of reasoning that are a challenge to (...) S&A's system (amongst many other connectionist systems, recognizing that S&A's is much more capable as regards reasoning than most other contemporary systems). (shrink)

Chomskyian claims of a genetically hard-wired and cognitively autonomous “universal grammar” are being promoted by generative linguistics as facts about language to the present day. The related doctrine of an evolutionary discontinuity in language emergence, however, is based on misconceptions about the notions of homology and preadaptation. The obvious lack of equivalence between symbolic communicative capacities in existing nonhuman primates and human language does not preclude common roots. Normal and disordered language development is strongly influenced by the genome, but there (...) is no evidence for the existence of specific genes underlying “universal grammar.” In the mature brain, stages of language processing can be distinguished and “first-pass” syntactic analyses appear to precede semantic decoding. However, this partial seriality – as well as behavioral and clinical dissociations between lexical and functional categories – can be best described, not in terms of serially activated and discrete modules, but in terms of classes of cell assemblies that differ in their distributional properties. Whereas cell assemblies involved in semantic interpretation (“content word” assemblies) are widely distributed and are generally less vulnerable to focal lesion, those involved in structural decoding (functor assemblies) are primarily distributed within the left perisylvian cortices and are selectively vulnerable to left perisylvian lesion. These distributional differences are explained in terms of the perceptuomotor components involved in the acquisition of relevant representations. The emerging “motivated” or “toposemantic” brain regional specificity can only be accommodated with “soft” and maturational versions of modularity. The failure to reproduce double dissociations in current connectionist models is due to overly simple neuroscientific assumptions, notably that of overall equipotentiality. Linguistic models should not be expected to be “implemented” in the brain, but need to be constrained by neuroscientific evidence on how biological brains function. (shrink)

One can disagree with Müller that it is neurobiologically questionable to suppose that human language is innate, specialized, and species-specific, yet agree that the precise brain mechanisms controlling language in any individual will be influenced by epigenesis and genetic variability, and that the interplay between inherited and acquired aspects of linguistic capacity deserves to be investigated.

Because Müiller fails to distinguish between two senses of the term “autonomy,” there is a danger that his results will be misinterpreted by both linguists and neuroscientists. Although he may very well have been successful in refuting one sense of autonomy, he may actually have helped to provide an explanation for the correctness of autonomy in its other sense.

We agree with Müller's epigenetic view of evolution and ontogeny and applaud his multilevel perspective. With him, we stress the importance in ontogeny of progressive specialisation rather than prewired structures. However, we argue that he slips from “speech” to “language” and that, in seeking homologies, these two levels need to be kept separate in the analysis of evolution and ontogeny.

The belief that syntax is an innate, autonomous, species-specific module is highly questionable. Syntax demonstrates the mosaic nature of evolutionary change, in that it made use of (and led to the enhancement of) numerous preexisting neurocognitive features. It is best understood as an emergent characteristic of the explosion of semantic complexity that occurred during hominid evolution.

Evidence is presented from a polyglot savant to suggest that double dissociations between linguistic and nonverbal abilities are more important than Müller's target article implies. It is also argued that the special nature of syntax makes its assimilation to other aspects of language or to nonhuman communication systems radically implausible.

Contrary to Müller's claims, and in support of modular theories, genetic factors play a substantial and significant role in language. The finding that some children with specific language impairment (SLI) have nonlinguistic impairments may reflect improper diagnosis of SLI or impairments that are secondary to linguistic impairments. Thus, such findings do not argue against the modularity thesis. The lexical/functional distinction appears to be innate and specifically linguistic and could be instantiated in either symbolic or connectionist systems.

Müller provides a valuable synthesis of neurobiological evidence on the epigenetic development of neural structures involved in language acquisition. The pluripotentiality of developing neural tissue crucially constrains linguistic/cognitive theorizing about supposedly innate neural mechanisms and contributes significantly to our understanding of experience–dependent processes involved in language acquisition. Without this understanding, any proposed explanation of language acquisition is suspect.

Segregated neural circuits that effect particular domain-specific behaviors can be differentiated from neuroanatomical structures implicated in many different aspects of behavior. The basal ganglionic components of circuits regulating nonlinguistic motor behavior, speech, and syntax all function in a similar manner. Hence, it is unlikely that special properties and evolutionary mechanisms are associated with the neural bases of human language.

The concepts of the innateness, universality, species-specificity, and autonomy of the human language capacity have had an extreme impact on the psycholinguistic debate for over thirty years. These concepts are evaluated from several neurobiological perspectives, with an emphasis on the emergence of language and its decay due to brain lesion and progressive brain disease.Evidence of perceptuomotor homologies and preadaptations for human language in nonhuman primates suggests a gradual emergence of language during hominid evolution. Regarding ontogeny, the innate component of language (...) capacity is likely to be polygenic and shared with other developmental domains. Dissociations between verbal and nonverbal development are probably rooted in the perceptuomotor specializations of neural substrates rather than the autonomy of a grammar module. Aphasiologicaldata often assumed to suggest modular linguistic subsystems can be accounted for in terms of a neurofunctional model incorporating perceptuomotor-based regional specializationsand distributivity of representations. Thus, dissociations between grammatical functors and content words are due to different conditions of acquisition and resulting differences in neural representation. Human brains are characterized by multifactorial interindividual variability, and strict universality of functional organization is biologically unrealistic.A theoretical alternative is proposed according to which (1) linguistic specialization of brain areas is due to epigenetic and probabilistic maturational events, not to genetic ”hard-wiring,” and (2) linguistic knowledge is neurally represented in distributed cell assemblies whose topography reflects the perceptuomotor modalities involved in the acquisition and use of a given item of knowledge. (shrink)

The overall goal of this target article is to demonstrate a mechanism for an embodied cognition. The particular vehicle is a much-studied, but still widely debated phenomenon seen in 7–12 month-old-infants. In Piaget's classic “A-not-B error,” infants who have successfully uncovered a toy at location “A” continue to reach to that location even after they watch the toy hidden in a nearby location “B.” Here, we question the traditional explanations of the error as an indicator of infants' concepts of objects (...) or other static mental structures. Instead, we demonstrate that the A-not-B error and its previously puzzling contextual variations can be understood by the coupled dynamics of the ordinary processes of goal-directed actions: looking, planning, reaching, and remembering. We offer a formal dynamic theory and model based on cognitive embodiment that both simulates the known A-not-B effects and offers novel predictions that match new experimental results. The demonstration supports an embodied view by casting the mental events involved in perception, planning, deciding, and remembering in the same analogic dynamic language as that used to describe bodily movement, so that they may be continuously meshed. We maintain that this mesh is a pre-eminently cognitive act of “knowing” not only in infancy but also in everyday activities throughout the life span. Key Words: cognitive development; dynamical systems theory; embodied cognition; infant development; motor control; motor planning; perception and action. (shrink)

The understanding of decision-making systems has come together in recent years to form a unified theory of decision-making in the mammalian brain as arising from multiple, interacting systems (a planning system, a habit system, and a situation-recognition system). This unified decision-making system has multiple potential access points through which it can be driven to make maladaptive choices, particularly choices that entail seeking of certain drugs or behaviors. We identify 10 key vulnerabilities in the system: (1) moving away from homeostasis, (2) (...) changing allostatic set points, (3) euphorigenic signals, (4) overvaluation in the planning system, (5) incorrect search of situation-action-outcome relationships, (6) misclassification of situations, (7) overvaluation in the habit system, (8) a mismatch in the balance of the two decision systems, (9) over-fast discounting processes, and (10) changed learning rates. These vulnerabilities provide a taxonomy of potential problems with decision-making systems. Although each vulnerability can drive an agent to return to the addictive choice, each vulnerability also implies a characteristic symptomology. Different drugs, different behaviors, and different individuals are likely to access different vulnerabilities. This has implications for an individual's susceptibility to addiction and the transition to addiction, for the potential for relapse, and for the potential for treatment. (shrink)