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.

the theory put forward by vallortigara & rogers (v&r) to explain the versatility of directional asymmetries at the population level argues that the strength of lateralization is controlled by social learning. this shaping of behavioral asymmetries by a non-stationary pressure probably involves a marked degree of neuroplasticity. i discuss the limits of neuroplasticity along with the evolution of the corpus callosum.

We affirm the dynamical systems approach taken by Feldman and Levin, but argue that a more mathematically rigorous and standard exposition of the model according to dynamical systems theory would greatly increase readability and testability. Such an explication would also have heuristic value, suggesting new variations of the model. We present one such variant, a new solution to the redundancy problem.

Mercier and Sperber (M&S) sketch a bleak picture of logical reasoning in classic, nonargumentative tasks. I argue that recent processing data indicate that despite people's poor performance they at least seek to adhere to traditional logical norms in these tasks. This implies that classic reasoning tasks are less artificial–and logical reasoning less exceptional–than M&S's framework suggests.

correcting the relationship between tonic and burst firing modes in dopamine neurons may help normalise stimulus-reinforcement gradients and contingent behaviour in attention-deficit/hyperactivity disorder (adhd) children. but appropriate evaluations of stimuli for developing adaptive plans and controlling impulsivity will not occur without moderating the gain-like functions of serotonin. the “dynamic theory” correctly highlights the need to account for variability in adhd. the dysmaturation of pre-executive information processing is proposed as an explanation.

at the core of the article by sagvolden and colleagues there is a set of data that throws light on an aspect of the adhd phenomenon. but one asks if the authors are a measure too brave to generalise so broadly from the unusually steep reinforcement gradients reported for the human condition and an animal model to the syndrome as a whole.

The first claim in the target article was that there is as yet no transparent, causal account of the relations between consciousness and brain-and-behaviour. That claim remains firm. The second claim was that the contents of consciousness consist, psychologically, of the outputs of a comparator system; the third consisted of a description of the brain mechanisms proposed to instantiate the comparator. In order to defend these claims against criticism, it has been necessary to clarify the distinction between consciousness-as-such and the contents of consciousness, to widen the description of the neural machinery instantiating the comparator system, and to clarify the relationship between the contents of consciousness in the here-and-now and episodic memory.

The language of conscious and unconscious goals is rooted in a folk-taxonomy that is likely to inhibit progress in cognitive science. Severing the commitment to this taxonomy would allow Huang & Bargh (H&B) to consider a wider variety of representational forms with motivational force and to entertain the intriguing possibility that variations in the number of active-but-redundant representations account for variance in social behavior.

Against Mitchell et al.'s assertions, we argue that (1) the concordance between learning and awareness does not support any particular learning theory, (2) their propositional approach is at odds with examples of learned behaviours that contradict beliefs about causation, and (3) the relative virtues of the two approaches in terms of parsimony is more ambiguous than Mitchell et al. suggest.

After thirty years of the current “imagery debate,” it appears far from resolved, even though there seems to be a growing acceptance that a cortical display cannot be identified directly with the experienced mental image, nor can it account for the experimental findings on imagery, at least not without additional ad hoc assumptions. The commentaries on the target article range from the annoyed to the supportive, with a surprising number of the latter. In this response I attempt to correct some misreadings of the target article and discuss some of the ideas and evidence introduced by the commentators – much of which I found helpful, even though they do not alter my basic thesis. I also further develop the idea that the spatial character of images may come from the way they are connected to our immediate or immediately-recalled environment (by attention or by visual indexes) and towards which we may orient while we are imaging, thus leaving the alleged spatial properties of images outside the head and freeing image-representations from having to be displayed on any surface.

The problem of how certain structure–function composites of high complexity could have evolved gradually and by natural selection has been with us at least since Charles Darwin admitted how difficult it was to explain, “his” theory, the origins of “organs of extreme perfection and complication” – such as the eyes of higher animals. Human language capacity is another evolutionary achievement of extraordinary perfection and complexity. Like other skilled human activities, it involves both central (neural) and peripheral (vocal and respiratory) complexes. The reduction of these to simpler building stones to which evolutionary principles may be applied is staggeringly difficult.

Several aspects of Glover's planning–control model (PCM) appear incompatible with existing data. Moreover, there is no logical reason to suppose that separate visual representations should be required for the “planning” and “control” of actions in the first place. Although intuitively appealing, the PCM appears to lack strong empirical support.

Chow pays lip service (but not much more!) to Type I errors and thus opts for a hard (all-or-none) .05 level of significance (Superego of Neyman/Pearson theory; Gigerenzer 1993). Most working scientists disregard Type I errors and thus utilize a soft .05 level (Ego of Fisher; Gigerenzer 1993), which lets them report gradations of significance (e.g., p < .001).

Before a general cognitive model for recurrent complex visual hallucinations (RCVH) is accepted, there must be more research into the neuropsychological and cognitive characteristics of the various disorders in which they occur. Currently available data are insufficient to distinguish whether the similar phenomenology of RCVH across different disorders is in fact produced by a single or by multiple cognitive mechanisms.