Well-being : the foundations of hedonic psychology

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.

https://www.cambridge.org/core/services/aop-cambridge-core/content/view/S0140525X00013066

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

In an attempt to explain how and why some individuals with musculoskeletal pain develop a chronic pain syndrome, Lethem et al. (Lethem J, Slade PD, Troup JDG, Bentley G. Outline of fear-avoidance model of exaggerated pain perceptions. Behav Res Ther 1983; 21: 401-408).ntroduced a so-called 'fear-avoidance' model. The central concept of their model is fear of pain. 'Confrontation' and 'avoidance' are postulated as the two extreme responses to this fear, of which the former leads to the reduction of fear over time. The latter, however, leads to the maintenance or exacerbation of fear, possibly generating a phobic state. In the last decade, an increasing number of investigations have corroborated and refined the fear-avoidance model. The aim of this paper is to review the existing evidence for the mediating role of pain-related fear, and its immediate and long-term consequences in the initiation and maintenance of chronic pain disability. We first highlight possible precursors of pain-related fear including the role negative appraisal of internal and external stimuli, negative affectivity and anxiety sensitivity may play. Subsequently, a number of fear-related processes will be discussed including escape and avoidance behaviors resulting in poor behavioral performance, hypervigilance to internal and external illness information, muscular reactivity, and physical disuse in terms of deconditioning and guarded movement. We also review the available assessment methods for the quantification of pain-related fear and avoidance. Finally, we discuss the implications of the recent findings for the prevention and treatment of chronic musculoskeletal pain. Although there are still a number of unresolved issues which merit future research attention, pain-related fear and avoidance appear to be an essential feature of the development of a chronic problem for a substantial number of patients with musculoskeletal pain.

/pdf/fear-avoidance-and-its-consequences-in-chronic-25jwj42o35.pdf

Fear-avoidance and its consequences in chronic musculoskeletal pain: a state of the art

&NA; In an attempt to explain how and why some individuals with musculoskeletal pain develop a chronic pain syndrome, Lethem et al.(Lethem J, Slade PD, Troup JDG, Bentley G. Outline of fear‐avoidance model of exaggerated pain perceptions. Behav Res Ther 1983; 21: 401‐408).ntroduced a so‐called ‘fear‐avoidance’ model. The central concept of their model is fear of pain. ‘Confrontation’ and ‘avoidance’ are postulated as the two extreme responses to this fear, of which the former leads to the reduction of fear over time. The latter, however, leads to the maintenance or exacerbation of fear, possibly generating a phobic state. In the last decade, an increasing number of investigations have corroborated and refined the fear‐avoidance model. The aim of this paper is to review the existing evidence for the mediating role of pain‐related fear, and its immediate and long‐term consequences in the initiation and maintenance of chronic pain disability. We first highlight possible precursors of pain‐related fear including the role negative appraisal of internal and external stimuli, negative affectivity and anxiety sensitivity may play. Subsequently, a number of fear‐related processes will be discussed including escape and avoidance behaviors resulting in poor behavioral performance, hypervigilance to internal and external illness information, muscular reactivity, and physical disuse in terms of deconditioning and guarded movement. We also review the available assessment methods for the quantification of pain‐related fear and avoidance. Finally, we discuss the implications of the recent findings for the prevention and treatment of chronic musculoskeletal pain. Although there are still a number of unresolved issues which merit future research attention, pain‐related fear and avoidance appear to be an essential feature of the development of a chronic problem for a substantial number of patients with musculoskeletal pain.

Fear-avoidance and its consequences in chronic musculoskeletal pain: a state of the art.

Objective: This article presents a new formulation of the relationship between stress and the processes leading to disease. It emphasizes the hidden cost of chronic stress to the body over long time periods, which act as a predisposing factor for the effects of acute, stressful life events. It also presents a model showing how individual differences in the susceptibility to stress are tied to individual behavioral responses to environmental challenges that are coupled to physiologic and pathophysiologic responses. Data Sources: Published original articles from human and animal studies and selected reviews. Literature was surveyed using MEDLINE. Data Extraction: Independent extraction and cross-referencing by us. Data Synthesis: Stress is frequently seen as a significant contributor to disease, and clinical evidence is mounting for specific effects of stress on immune and cardiovascular systems. Yet, until recently, aspects of stress that precipitate disease have been obscure. The concept of homeostasis has failed to help us understand the hidden toll of chronic stress on the body. Rather than maintaining constancy, the physiologic systems within the body fluctuate to meet demands from external forces, a state termed allostasis . In this article, we extend the concept of allostasis over the dimension of time and we define allostatic load as the cost of chronic exposure to fluctuating or heightened neural or neuroendocrine response resulting from repeated or chronic environmental challenge that an individual reacts to as being particularly stressful. Conclusions: This new formulation emphasizes the cascading relationships, beginning early in life, between environmental factors and genetic predispositions that lead to large individual differences in susceptibility to stress and, in some cases, to disease. There are now empirical studies based on this formulation, as well as new insights into mechanisms involving specific changes in neural, neuroendocrine, and immune systems. The practical implications of this formulation for clinical practice and further research are discussed. (Arch Intern Med. 1993;153:2093-2101)

https://jamanetwork.com/journals/INTEMED/articlepdf/617820/archinte_153_18_004.pdf

Stress and the Individual: Mechanisms Leading to Disease

Predicting the Abuse Liability of Drugs with Animal Drug Self-Administration Procedures: Psychomotor Stimulants and Hallucinogens

Ulcers in executive monkeys.

&NA; In studies involving biochemical measurement of plasma 17‐OH‐CS, norepinephrine, and epinephrine levels during conditioned emotional disturbances in monkeys, elevations in 17‐OH‐CS and norepinephrine levels were observed in a variety of experimental situations. The regulation of epinephrine secretion, however, appeared to have a more selective basis. In relatively stereotyped, predictable situations such as avoidance and CER, patterns of 17‐OH‐CS and norepinephrine elevation, with little or no change in plasma epinephrine levels, were observed. In first experience situations and rather complicated, multiple‐schedule conditioning procedures, a pattern of marked 17‐OH‐CS, norepinephrine, and epinephrine elevations were observed. These experiments suggest that several interacting elements may be necessary for marked epinephrine release during anticipatory responses. An effort has been made to identify some of these elements in terms of both environmental and biological factors that appear to be common to those situations in which marked epinephrine elevations were observed. It is suggested that the element of uncertainty or unpredictability, in combination with such factors as the threat of a noxious stimulus and the anticipation of coping activity, may be a particularly critical factor in the determination of epinephrine release during emotional disturbances.

Concurrent plasma epinephrine, norepinephrine and 17-hydroxycorticosteroid levels during conditioned emotional disturbances in monkeys.

/pdf/avoidance-behavior-and-the-development-of-gastroduodenal-5e6ytb6wj6.pdf

Avoidance behavior and the development of gastroduodenal ulcers.

Cocaine, diethylpropion, chlorphentermine, and fenfluramine were compared on a drug-maintained progressive-ratio procedure in baboons. Intravenous infusions of drug were contingent on completion of a fixed-ratio response requirement (fixed number of lever-press responses) with a 3-h time-out period following each infusion. Prior to testing each dose of drug, stable self-infusion performance was first established with 0.4 mg/kg cocaine when the fixed-ratio requirement was 160. Subsequently, a test dose of drug was substituted for the standard dose of cocaine. If the dose of drug maintained a criterion level of self-infusion performance (six or more infusions per day for 2 days), the ratio requirement was systematically increased every day until the ‘breaking point’ at which the self-infusion performance fell below a criterion level (one or zero infusionsper day). Fenfluramine did not maintain criterion self-infusion performance at any dose tested (0.02–5.0 mg/kg). The dose ranges of the other drugs that maintained maximum breaking points were 1.0–5.6 mg/kg for chlorphentermine, 1.0–3.0 mg/kg for diethylpropion, and 0.1–0.4 mg/kg for cocaine. Within-animal comparison of the maximum breaking points indicated that cocaine maintained the highest breaking points, followed in order by diethylpropion, chlorphentermine, and fenfluramine. The rank ordering of these drugs with the breaking point measure corresponds well with both the results of other animal experiments on measurement of reinforcing efficacy of these drugs and with the clinical information about the human subjective effects and abuse of these drugs.

Joseph V. Brady

Papers

Predicting the Abuse Liability of Drugs with Animal Drug Self-Administration Procedures: Psychomotor Stimulants and Hallucinogens

Ulcers in executive monkeys.

Concurrent plasma epinephrine, norepinephrine and 17-hydroxycorticosteroid levels during conditioned emotional disturbances in monkeys.

Avoidance behavior and the development of gastroduodenal ulcers.

Progressive-ratio performance maintained by drug infusions: comparison of cocaine, diethylpropion, chlorphentermine, and fenfluramine.