From normal fear to pathological anxiety.

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.

Rorschach Performance Assessment System (R-PAS) and vulnerability to stress: A preliminary study on electrodermal activity during stress

“…In fact, high levels of stress hormones increase the risk for phenomena such as hypertension, insulin resistance, hypercholesterolemia, and hyperlipidemia (e.g., Brindley andRolland, 1989, Rosmond et al, 1995), which in turn are primary risk factors for various life-threatening metabolic and cardiovascular conditions. High levels of stress hormones also tend to affect the activity of neurotransmitters important to brain structures such as the amygdala and the hippocampus, increasing the likelihood to develop psychological problems such as anxiety, sleep disorders, or selective cognitive impairments (Arnsten, 1998;Lupien and Meaney 1998;De Kloet et al, 1998;McEwen et al, 1999;Nemeroff, 1996;Rosen and Schulkin, 1998). As such, individuals who are vulnerable to stress and distress are generally show exaggerated sympathetic reactions to stress (Meaney, 2001).…”

Symptom Presentation and Symptom Meaning Among Traumatized Cambodian Refugees: Relevance to a Somatically Focused Cognitive-Behavior Therapy

“…Multiple studies indicate that anxiety sensitivity should be categorized by its origin (for a review, see , 2006: (a) catastrophic cognitions-caused anxiety sensitivity, (b) trauma associations-caused anxiety sensitivity, (c) metaphor-caused anxiety sensitivity, (d) direct conditioning-caused anxiety sensitivity (i.e., fear becoming directly conditioned to anxiety symptoms [Barlow, 2002]), (e) sensitization-caused anxiety sensitivity (i.e., repeatedly experiencing a symptom-e.g., dizziness during repeated malaria attacks-causing it to be more easily triggered, that is, results in neural sensitization [Rosen & Schulkin, 1998]), and (f) other-caused anxiety sensitivity (i.e., reactivity resulting from other causes, as in a biologically inherited reactivity to anxiety symptoms). (At present, there is no method by which direct conditioning-caused anxiety sensitivity, sensitization-caused anxiety sensitivity, or other-caused anxiety sensitivity can be assessed; they are purely hypothetical constructs.)…”

Induction and Expression of Fear Sensitization Caused by Acute Traumatic Stress

“…Inappropriate fear responses in humans can result in the development of anxiety disorders (Rosen and Schulkin, 1998), including PTSD. PTSD develops in some individuals who experience a traumatic event and affects 4-7% of the United States population.…”

“…Repeated activation modifies the HPA axis negative feedback system and makes the stress response become more easily triggered. Sensitization results in a lowered activation threshold for subsequent stimuli, facilitating higher responding to neutral stimuli now perceived as threatening (Rosen and Schulkin, 1998;Hagemen et al, 2001). Moreover, re-experiencing aspects of the traumatic event sensitizes fear systems leading to exaggerated reactions, as observed in PTSD patients (Post et al, 1997;Hagemen et al, 2001).…”