TL;DR: In this article, the authors reviewed 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.
Abstract: 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.
TL;DR: Theories of Anxiety and Cognition and theoretical Framework: A Framework for Investigating Attentional Processes and Comprehension and Memory.
Abstract: Theorists are increasingly arguing that it is fruitful to approach anxiety from the cognitive perspective, and the empirical evidence supports that contention. The cognitive perspective is also adopted in this book, but the approach represents a development and extension of earlier ones. For example, most previous theories and research have been based on anxiety either in clinical or in normal groups. In contrast, one of the central themes of this book is that there are great advantages to be gained from a joint consideration of clinical and normal anxiety.Another theme of this book is that it is of major importance to establish whether or not there is a cognitive vulnerability factor which is associated with at least some forms of clinical anxiety. It is argued (with supporting evidence) that there is a latent cognitive vulnerability factor for generalized anxiety disorder which manifests itself under stressful conditions. This vulnerability factor is characterized by hypervigilance, and is found predominantly in normals high in the personality dimension of trait anxiety.The scope of the book extends to the effects of anxiety on performance and to the phenomenon of worry, which is regarded as the cognitive component of anxiety. In both cases, a new theoretical framework is presented.
TL;DR: How pathological anxiety may develop from adaptive fear states is addressed, and hyperexcitability of fear circuits that include the amygdala and extended amygdala is expressed as hypervigilance and increased behavioral responsivity to fearful stimuli.
Abstract: In this article the authors address how pathological anxiety may develop from adaptive fear states. Fear responses (e.g., freezing, startle, heart rate and blood pressure changes, and increased vigilance) are functionally adaptive behavioral and perceptual responses elicited during danger to facilitate appropriate defensive responses that can reduce danger or injury (e.g., escape and avoidance). Fear is a central motive state of action tendencies subserved by fear circuits, with the amygdala playing a central role. Pathological anxiety is conceptualized as an exaggerated fear state in which hyperexcitability of fear circuits that include the amygdala and extended amygdala (i.e., bed nucleus of the stria terminalis) is expressed as hypervigilance and increased behavioral responsivity to fearful stimuli. Reduced thresholds for activation and hyperexcitability in fear circuits develop through sensitization- or kindling-like processes that involve neuropeptides, hormones, and other proteins. Hyperexcitability in fear circuits is expressed as pathological anxiety that is manifested in the various anxiety disorders.
TL;DR: Pictures of human emotional expressions elicit robust differences in amygdala activation levels in borderline patients, compared with normal control subjects, and can be used as probes to study the neuropathophysiologic basis of borderline personality disorder.
TL;DR: Evidence for a distinction between fear and anxiety in animal and human experimental models using the startle reflex as an operational measure of aversive states is reviewed and experimental models of anxiety, not fear, in humans are described.
Abstract: Rationale Preclinical data indicates that threat stimuli elicit two classes of defensive behaviors, those that are associated with imminent danger and are characterized by flight or fight (fear), and those that are associated with temporally uncertain danger and are characterized by sustained apprehension and hypervigilance (anxiety). Objective The objectives of the study are to (1) review evidence for a distinction between fear and anxiety in animal and human experimental models using the startle reflex as an operational measure of aversive states, (2) describe experimental models of anxiety, as opposed to fear, in humans, (3) examine the relevance of these models to clinical anxiety. Results The distinction between phasic fear to imminent threat and sustained anxiety to temporally uncertain danger is suggested by psychopharmacological and behavioral evidence from ethological studies and can be traced back to distinct neuroanatomical systems, the amygdala and the bed nucleus of the stria terminalis. Experimental models of anxiety, not fear, are relevant to non-phobic anxiety disorders. Conclusions Progress in our understanding of normal and abnormal anxiety is critically dependent on our ability to model sustainedaversivestates to temporallyuncertain threat.