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.

The conceptual framework of behaviorism is reconstructed in a logical scheme rather than along chronological lines. The resulting reconstruction is faithful to the history of behaviorism and yet meets the contemporary challenges arising from cognitive science, psycholinguistics, and philosophy. In this reconstruction, the fundamental premise is that psychology is to be a natural science, and the major corollaries are that psychology is to be objective and empirical. To a great extent, the reconstruction of behaviorism is an elaboration of behaviorist views of what it is for a science to be objective and empirical. The reconstruction examines and evaluates behaviorist positions on observation and the rejection of introspection, the behavioral data language, theory construction, stimulus-response psychology, the organization of behavior, complex processes, agency, and the interpretation of mentalistic language. The resulting reconstruction shows behaviorism to be a pragmatic psychological version of positivism based on a behavioral epistemology.

Animal research suggests that central serotonergic neurons are involved in behavioral suppression, particularly anxiety-related inhibition. The hypothesis linking decreased serotonin transmission to reduced anxiety as the mechanism in the anxiolytic activity of benzodiazepines conflicts with most clinical observations. Serotonin antagonists show no marked capacity to alleviate anxiety. On the other hand, clinical signs of reduced serotonergic transmission (low 5-HIAA levels in the cerebrospinal fluid) are frequently associated with aggressiveness, suicide attempts, and increased anxiety. The target article attempts to reconcile such human and animal findings by investigating whether anxiety reduction or increased impulsivity is more Likely to account for animal behavioral changes associated with decreased serotonergic transmission. The effects of manipulating central serotonin in experimental anxiety paradigms in animals (punishment, extinction, novelty) are reviewed and compared with the effects of antianxiety drugs. Anxiety seems neither necessary nor sufficient to induce control by serotonergic neurons on behavior. Further evidence suggests that behavioral effects of anxiolytics thought to be mediated by decreases in anxiety are not caused by the ability of these drugs to reduce serotonin transmission. Blockade of serotonin transmission, especially at the level of the substantia nigra, results in a shift of behavior toward facilitation of responding. This behavioral shift is particularly marked when there is competition between acting and restraining response tendencies and when obstacles prevent the immediate attainment of an anticipated reward. It is proposed that serotonergic neurons are involved not only in behavioral arousal but also in enabling the organism to arrange or tolerate delay before acting. Decreases in serotonin transmission seem to be associated with the increased performance of behaviors that are usually suppressed, though not necessarily because of the alleviation of anxiety, which might contribute to the suppression.