To understand the endogenous components of the event-related brain potential (ERP), we must use data about the components' antecedent conditions to form hypotheses about the information-processing function of the underlying brain activity. These hypotheses, in turn, generate testable predictions about the consequences of the component. We review the application of this approach to the analysis of the P300 component. The amplitude of the P300 is controlled multiplicatively by the subjective probability and the task relevance of the eliciting events, whereas its (...) latency depends on the duration of stimulus evaluation. These and other factors suggest that the P300 is a manifestation of activity occurring whenever one's model of the environment must be revised. Tests of three predictions based on this “context updating” model are reviewed. Verleger's critique is based on a misconstrual of the model as well as a partial and misleading reading of the relevant literature. (shrink)

P3 is the most prominent of the electrical potentials of the human electroencephalogram that are sensitive to psychological variables. According to the most influential current hypothesis about its psychological significance [E. Donchin's], the “context updating” hypothesis, P3 reflects the updating of working memory. This hypothesis cannot account for relevant portions of the available evidence and it entails some basic contradictions. A more general formulation of this hypothesis is that P3 reflects the updating of expectancies. This version implies that P3-evoking stimuli (...) are initially unexpected but later become expected. This contradiction cannot be resolved within this formulation. The alternative “context closure” hypothesis retains the concept of “strategic information processing” emphasized by the context updating hypothesis. P3s are evoked by events that are awaited when subjects deal with repetitive, highly structured tasks; P3s arise from subjects' combining successive stimuli into larger units. The tasks in which P3s are elicited can accordingly be classified in terms of their respective formal sequences of stimuli. P3 may be a physiological indicator of excess activation being released from perceptual control areas. (shrink)

Among the many peculiarities of schizophrenics perhaps the most obvious is their tendency to say odd things. Indeed, for most clinicians, the hallmark of schizophrenia is “thought disorder”. Decades of clinical observations, experimental research, and linguistic analyses have produced many hypotheses about what, precisely, is wrong with schizophrenic speech and language. These hypotheses range from assertions that schizophrenics have peculiar word association hierarchies to the notion that schizophrenics are suffering from an intermittent form of aphasia. In this article, several popular (...) hypotheses are critically assessed. Work in the area turns out to be flawed by errors in experimental method, faulty observations, tautological reasoning, and theoretical models that ignore the complexities of both speech and language. This does not mean that schizophrenics are indistinguishable from nonschizophrenics. They are clearly deviant in many situations. Their problem, however, appears to be in processing information and in selective attention, not in language itself. (shrink)

All recent memory theories of hippocampal function have incorporated the idea that the hippocampus is required to process items only of some qualitatively specifiahle kind, and is not required to process items of some complementary set. In contrast, it is now proposed that the hippocampus is needed to process stimuli of all kinds, but only when there is a need to associate those stimuli with other events that are temporally discontiguous. In order to form or use temporally discontiguous associations, it (...) is essential to maintain some memory of the first component until the second component has occurred. When the temporal gap to he spanned is small, and the number of items to be temporarily retained is low, a limited-capacity, short-term store is sufficient to allow associations to be formed. Such a store is presumed to operate in parallel with the hippocampus in normal animals. Hippocampal damage disrupts a much higher-capacity store that has a slower decay rate, and so leaves animals with only a very limited ability to form temporally discontiguous associations. Hippocampal damage, however, is not held to affect the long-term storage of associations of any kind, if they can be formed. Analyses of both new and existing data are presented to show that by classifying tasks in terms of the need to use a temporary memory store to retain temporally discontiguous information one can cut right across existing classifications as well as achieve a better fit to the data. The hippocampus thus seems best described as a high-capacity, intermediate-term memory store. (shrink)

How is it that many schizophrenics identify certain instances of verbal imagery as hallucinatory? Most investigators have assumed that alterations in sensory features of imagery explain this. This approach, however, has not yielded a definitive picture of the nature of verbal hallucinations. An alternative perspective suggests itself if one allows the possibility that the nonself quality of hallucinations is inferred on the basis of the experience of unintendedness that accompanies imagery production. Information-processing models of “intentional” cognitive processes call for abstract (...) planning representations that are linked to goals and beliefs. Unintended actions - and imagery - can reflect planning disruptions whereby cognitive products do not cohere with concurrent goals. A model of schizophrenic speech disorganization is presented that postulates a disturbance of discourse planning. Insofar as verbal imagery can be viewed as inwardly directed speech, a consequence of such planning disturbances could be the production of unintended imagery. This link between the outward disorganization of schizophrenic speech and unintended verbal imagery is statistically supported by comparing the speech behavior of hallucinating and nonhallucinating schizophrenics. Studies of “borderline” hallucinations during normal, “goal-less” relaxation and drowsiness suggest that experiential unintendedness leads to a nonpathological variant of hallucinatory otherness that is correctable upon emerging from such passive cognitive states. This contrasts with the schizophrenic case, where nonconcordance with cognitive goals reinforces the unintendedness of verbal images and sustains the conviction of an external source. This model compares favorably with earlier models of verbal hallucinations and provides further evidence for a language production disorder in many schizophrenics.Short Abstract: How is it that many schizophrenics identify certain instances of verbal imagery as hallucinatory? This paper proposes that the critical feature identifying hallucinations is the experience of unintendedness. This experience is nonpathological during passive conscious states but pathological if occurring during goal-directed cognitive processing. A model of schizophrenic speech disorganization is presented that postulates a disturbance of discourse planning that specifies communicative intentions. These alterations could generate unintended verbal imagery as well. Statistical data are offered to support the model, and relevant empirical studies are reviewed. (shrink)

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)

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