A model of the neuropsychology of anxiety is proposed. The model is based in the first instance upon an analysis of the behavioural effects of the antianxiety drugs in animals. From such psychopharmacologi-cal experiments the concept of a “behavioural inhibition system” has been developed. This system responds to novel stimuli or to those associated with punishment or nonreward by inhibiting ongoing behaviour and increasing arousal and attention to the environment. It is activity in the BIS that constitutes anxiety and that (...) is reduced by antianxiety drugs. The effects of the antianxiety drugs in the brain also suggest hypotheses concerning the neural substrate of anxiety. Although the benzodiazepines and barbiturates facilitate the effects of γ-aminobutyrate, this is insufficient to explain their highly specific behavioural effects. Because of similarities between the behavioural effects of certain lesions and those of the antianxiety drugs, it is proposed that these drugs reduce anxiety by impairing the functioning of a widespread neural system including the septo-hippocampal system, the Papez circuit, the prefrontal cortex, and ascending monoaminergic and cholinergic pathways which innervate these forebrain structures. Analysis of the functions of this system suggests that it acts as a comparator: it compares predicted to actual sensory events and activates the outputs of the BIS when there is a mismatch or when the predicted event is aversive. Suggestions are made as to the functions of particular pathways within this overall brain system. The resulting theory is applied to the symptoms and treatment of anxiety in man, its relations to depression, and the personality of individuals who are susceptible to anxiety or depression. (shrink)

This important new book analyses these core issues and reviews the evidence from both introspection and experiment.

How does conscious experience arise out of the functioning of the human brain? How is it related to the behaviour that it accompanies? How does the perceived world relate to the real world? Between them, these three questions constitute what is commonly known as the Hard Problem of consciousness. Despite vast knowledge of the relationship between brain and behaviour, and rapid advances in our knowledge of how brain activity correlates with conscious experience, the answers to all three questions remain controversial, (...) even mysterious. This important book analyses these core issues and reviews the evidence from both introspection and experiment. To many its conclusions will be surprising and even unsettling: * The entire perceived world is constructed by the brain. The relationship between the world we perceive and the underlying physical reality is not as close as we might think * Much of our behaviour is accomplished with little or no participation from conscious experience. * Our conscious experience of our behaviour lags the behaviour itself by around a fifth of a second - we become aware of what we do only after we have done it. * The lag in conscious experience applies also to the decision to act - we only become aware of our decisions after they have been formed. * The self is as much a creation of the brain as is the rest of the perceived world. Written by a leading scientist, this accessible and compelling analysis of how conscious experience relates to brain and behaviour will have major implications for our understanding of human nature. (shrink)

Drawing on previous models of anxiety, intermediate memory, the positive symptoms of schizophrenia, and goal-directed behaviour, a neuropsychological hypothesis is proposed for the generation of the contents of consciousness. It is suggested that these correspond to the outputs of a comparator that, on a moment-by-moment basis, compares the current state of the organism's perceptual world with a predicted state. An outline is given of the information-processing functions of the comparator system and of the neural systems which mediate them. The hypothesis (...) appears to be able to account for a number of key features of the contents of consciousness. However, it is argued that neitherthis nor any existing comparable hypothesis is yet able to explain why the brain should generate conscious experience of any kind at all. (shrink)

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. (shrink)

[opening paragraph]: Imagine you are a scientist from Mars observing Gary Kasparov playing a tournament with a chess computer. Would you have any reason to postulate consciousness in one player, but not the other? What is consciousness? How does the body produce it, and what is it for? Most people do not realize that there is a problem here because our conscious experience is the thing we know best. We are all familiar with the colours, smells and scenes around us, (...) the pains and itches we feel and the thoughts that are in our heads. Our world consists of conscious experiences. By `conscious experience' I mean anything that you have an awareness of, absolutely anything. I do not mean anything recondite like your capacity to reflect upon your own experiences, something which one might suppose that only we as human beings have and animals do not. I mean the absolute basics, like feeling pain. (shrink)

As well as data indicating relationships (emphasised in the target article) (1) between dopaminergic transmission in the nucleus accumbens and positive incentive motivation, and (2) between dopaminergic transmission and extraversion, other data (not accounted for by the hypotheses developed in the target article) indicate relationships (3) between accumbens dopaminergic transmission and cognitive, especially perceptual, processes that are disrupted in schizophrenia, and (4) between dopaminergic transmission and psychoticism. The tension between relationships 1 + 2 and 3 + 4 is discussed and (...) a tentative resolution proposed. (shrink)

What makes conscious experiences necessary for in- formation processing or behaviour (no one knows)? Would it be easier first to divide consciousness into different levels (probably not)? Is consciousness tied to information processing or brain states (no one knows)? Would the target article's comparator be improved by adding a continuously adjusting feedback (probably not)?

The use of neural transplantation to alleviate cognitive deficits is still in its infancy. We have an inadequate understanding of the deficits induced by different types of brain damage and their homologies in animal models against which to assess graft-induced recovery, and of the ways in which graft growth and function are influenced by factors within the host brain and the environment in which the host is operating. Further, use of fetal tissue may only be a transitory phase in the (...) search for appropriate donor sources. Nevertheless, findings from our laboratory and elsewhere have made a prima facie case for successful cognitive reconstruction by graft methods. (shrink)

Cognitive deficits were produced in rats by different methods of damaging the brain: chronic ingestion of alcohol, causing widespread damage to diffuse cholinergic and aminergic projection systems; lesions (by local injection of the excitotoxins, ibotenate, quisqualate, and AMPA) of the nuclei of origin of the forebrain cholinergic projection system (FCPS), which innervates the neocortex and hippocampal formation; transient cerebral ischaemia, producing focal damage especially in the CA1 pyramidal cells of the dorsal hippocampus; and lesions (by local injection of the neurotoxin, (...) colchicine) of the granule cells of the dentate gyrus. Following chronic alcohol or lesions of the FCPS, transplants of cholinergically rich fetal brain tissue into the terminal areas (neocortex and/or hippocampus) restored performance almost to control levels, with a time course consistent with growth of the transplants and integration with host tissue; transplants of cholinergically poor fetal tissue (hippocampus) were without effect, as were transplants of cholinergically rich tissue into the region containing the nuclei of origin of the FCPS. Grafts of primary cells enriched in glia and cultured neuroblastoma cells into the terminal areas of the FCPS were equally effective, suggesting that there are multiple mechanisms by which neural transplants can restore cognitive function following diffuse cholinergic damage. In contrast, after ischaemia- or neurotoxin-induced damage to CA1 or dentate granule cells respectively, cholinergically rich fetal transplants into the damaged hippocampal formation were ineffective in restoring performance. After ischaemic damage, however, performance was restored by suspension grafts of CA1 cells but not by transplants containing CA3 pyramidal cells or granule cells; and after colchicine damage it was restored by solid grafts containing granule but not CA1 pyramidal cells. Furthermore, electrophysiological evidence has demonstrated functional, graft type-specific host-graft functional neuronal connectivity. Thus, restoration of cognitive function by neural transplants is possible after damage to either diffuse (cholinergic) or point-to-point (intrahippocampal) forebrain systems, but the transplant must be appropriate to the damage to be repaired. Because the different types of brain damage studied provide analogues of human alcoholic dementia, Alzheimer's disease, and heart attack, these results are encouraging with regard to the eventual application of neural transplant surgery to the treatment of cognitive deficits in humans. (shrink)