The nature of the cognition-motor interface has been brought to prominence by Butterfill & Sinigaglia, who argue that the representations employed by the cognitive and motor systems should not be able to interact with each other. Here I argue that recent empirical evidence concerning the interface contradicts several of the assumptions incorporated in Butterfill & Sinigaglia’s account, and I seek to develop a theoretical picture that will allow us to explain the structure of the interface presented by this evidence. The (...) central idea is that neural plasticity incorporates metarepresentational rules for constructing representational systems and linking them. The structure of the cognition-motor interface is constructed flexibly during development and skill learning based on information processing demands. (shrink)

In this paper, I make a case for the modularity of the motor system. I start where many do in discussions of modularity, by considering the extent to which the motor system is cognitively penetrable, i.e., the extent to which its processing and outputs are causally influenced, in a semantically coherent way, by states of central cognition. I present some empirical findings from a range of sensorimotor adaptation studies that strongly suggest that there are limits to such influence under certain (...) conditions. These results cry out for an explanation. In the remainder of the paper, I provide one: The motor system is cognitively penetrable, but nonetheless modular along broadly Fodorian lines, insofar as it is informationally encapsulated. This means that its access is limited to its own proprietary database in computing its function from input to output, which does not include the information stored in central cognition. I then offer a model of action control, from distal intention to action outcomes, that further helps to illustrate this picture and can accommodate the target empirical findings. (shrink)

The lack of consensus on how to characterize humans’ capacity for belief reasoning has been brought into sharp focus by recent research. Children fail critical tests of belief reasoning before 3 to 4 years (Wellman, Cross, & Watson, 2001; Wimmer & Perner, 1983), yet infants apparently pass false belief tasks at 13 or 15 months (Onishi & Baillargeon, 2005; Surian, Caldi, & Sperber, 2007). Non-human animals also fail critical tests of belief reasoning but can show very complex social behaviour (e.g., (...) Call & Tomasello, 2005). Fluent social interaction in adult humans implies efficient processing of beliefs, yet direct tests suggest that belief reasoning is cognitively demanding, even for adults (e.g., Apperly, Samson & Humphreys, 2005). We interpret these findings by drawing an analogy with the domain of number cognition, where similarly contrasting results have been observed. We propose that the success of infants and non-human animals on some belief reasoning tasks may be best explained by a cognitively efficient but inflexible capacity for tracking belief-like states. In humans this capacity persists in parallel with later-developing, more flexible but more cognitively demanding theory of mind abilities. (shrink)

Cognitive Science is a promising field of research that deals with one of the most fundamental questions ever: how do beings know? However, despite the long and extensive tradition of the field it has not yet become an area of knowledge with scientific identity. This is primarily due to three reasons: the lack of boundaries in defining the object of study, i.e. cognition, the lack of a precise, robust and consistent scientific methodology and results, and the inner problems derived from (...) its interdisciplinary nature. This paper presents a background review, a theoretical frame and a humble reflection on these topics in order to arouse the internal debate among readers once more. (shrink)

The neurosciences are generating new findings regarding genetic and neurobiological aspects of the pathophysiology of mental disorders. Especially, certain genetic risk factors like neuregulin-1 seem to predispose individuals to a psychotic phenotype beyond the limits of traditional classificatory boundaries between organic psychoses in Alzheimer’s disease, bipolar affective disorder and schizophrenia. Little, however, is known about how such genetic risk factors actually confer an increased risk for psychosis in an individual patient. A gap between neuroscientific findings and psychopathological phenomena exists. The (...) main hypothesis how this gap may be bridged is that mental disorders arise as a consequence of dysfunctions of normal mental functions. Modularity may provide a useful conceptual framework in that temporally and/or spatially stable neural circuits subserve certain physiological functions of the human brain, which become the target of pathophysiological effectors. The idea of a modular construction of the human brain is based on neurobiological evidence regarding the columnar architecture of the cerebral cortex, which provides certain elementary analytical functions. Modular dysfunctions may be assessed with methods of experimental psychopathology, in which subsystems of brain functions are tested with standardized experimental psychological techniques (functional psychopathology). The main questions here are how to define a module, and whether the classical neuroscientific definitions can be used to characterize higher integrative functions of the human brain. (shrink)