Werner K. Honig

Bio: Werner K. Honig is an academic researcher from Johns Hopkins University. The author has contributed to research in topics: Operant conditioning & Experimental psychology. The author has an hindex of 5, co-authored 5 publications receiving 3288 citations.

Adolescence-limited and life-course-persistent antisocial behavior: A developmental taxonomy.

Abstract: This chapter suggests that delinquency conceals two distinct categories of individuals, each with a unique natural history and etiology: A small group engages in antisocial behavior of one sort or another at every life stage, whereas a larger group is antisocial only during adolescence. According to the theory of life-course-persistent antisocial behavior, children's neuropsychological problems interact cumulatively with their criminogenic environments across development, culminating m a pathological personality. According to the theory of adolescence-limited antisocial behavior, a contemporary maturity gap encourages teens to mimic antisocial behavior in ways that are normative and adjustive. There are marked individual differences in the stability of antisocial behavior. The chapter reviews the mysterious relationship between age and antisocial behavior. Some youths who refrain from antisocial behavior may, for some reason, not sense the maturity gap and therefore lack the hypothesized motivation for experimenting with crime.

Précis of The Neuropsychology of Anxiety: An Enquiry into the Functions of the Septo-Hippocampal System..

Abstract: 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 (benzodiazepines, barbiturates, and alcohol) in animals. From such psychopharmacologi-cal experiments the concept of a “behavioural inhibition system” (BIS) 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 (SHS), the Papez circuit, the prefrontal cortex, and ascending monoaminergic and cholinergic pathways which innervate these forebrain structures. Analysis of the functions of this system (based on anatomical, physiological, and behavioural data) 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.

Emotional processing of fear : exposure to corrective information

Abstract: In this article we propose mechanisms that govern the processing of emotional information, particularly those involved in fear reduction. Emotions are viewed as represented by information structures in memory, and anxiety is thought to occur when an information structure that serves as program to escape or avoid danger is activated. Emotional processing is denned as the modification of memory structures that underlie emotions. It is argued that some form of exposure to feared situations is common to many psychotherapies for anxiety, and that confrontation with feared objects or situations is an effective treatment. Physiological activation and habituation within and across exposure sessions are cited as indicators of emotional processing, and variables that influence activation and habituation of fear responses are examined. These variables and the indicators are analyzed to yield an account of what information must be integrated for emotional processing of a fear structure. The elements of such a structure are viewed as cognitive representations of the stimulus characteristic of the fear situation, the individual's responses in it, and aspects of its meaning for the individual. Treatment failures are interpreted with respect to the interference of cognitive defenses, autonomic arousal, mood state, and erroneous ideation with reformation of targeted fear structures. Applications of the concepts advanced here to therapeutic practice and to the broader study of psychopathology are discussed.

Effects of Externally Mediated Rewards on Intrinsic Motivation.

Abstract: Two laboratory experiments and one field experiment were conducted to investigate the effects of external rewards on intrinsic motivation to perform an activity. In each experiment, subjects were performing an activity during three different periods, and observations relevant to their motivation were made. External rewards were given to the experimental subjects during the second period only, while the control subjects received no rewards. Of interest was the difference in the experimental group's motivation between Period 1 and Period 3, relative to the difference in the control's. The results indicate that (a) when money was used as an external reward, intrinsic motivation tended to decrease, whereas (b) when verbal reinforcement and positive feedback were used, intrinsic motivation tended to increase. Discrepant findings in the literature were reconciled using a new theoretical framework which employs a cognitive approach and concentrates on the nature of the external reward. If a boy who enjoys mowing lawns begins to receive payment for the task, what will happen to his intrinsic motivation for performing this activity? Or, if he enjoys gardening and his parents seek to encourage this by providing verbal reinforcement and affection when he gardens, what will happen to his intrinsic motivation for gardening? These are examples of the classical problem concerning the effects of external rewards on intrinsic motivation. One is said to be intrinsically motivated to perform an activity when he receives no apparent rewards except the activity itself. This intrinsic motivation might be either innate or learned (White, 1959). It is not the purpose of this study to deal with the specific nature of, or development of, intrinsic motivation, but rather, it assumes that at a given time a person can be intrinsically motivated to do an activity, and it then asks: What are the effects of external rewards on this motivation ? In the two examples of the boy, he is performing the activity for no apparent rewards 1 These studies were conducted at Carnegie-Mell on University. The author wishes to thank Victor H. Vroom and Daryl J. Bern for helpful suggestions about the research and about earlier drafts of the manuscript.

A model for Pavlovian learning: Variations in the effectiveness of conditioned but not of unconditioned stimuli.

Abstract: Several formal models of excitatory classical conditioning are reviewed. It is suggested that a central problem for all of them is the explanation of cases in which learning does not occur in spite of the fact that the conditioned stimulus is a signal for the reinforcer. We propose a new model that deals with this problem by specifying that certain procedures cause a conditioned stimulus (CS) to lose effectiveness; in particular, we argue that a CS will lose associability when its consequences are accurately predicted. In contrast to other current models, the effectiveness of the reinforcer remains constant throughout conditioning. The second part of the article presents a reformulation of the nature of the learning produced by inhibitory-conditioning procedures and a discussion of the way in which such learning can be accommodated within the model outlined for excitatory learning.