Situational Panic Attacks

Woods, Scott W.

doi:10.1001/archpsyc.1987.01800160077010

Cited by 148 publications

(12 citation statements)

References 92 publications

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“…Challenge testing with yohimbine, an ~adrenergic receptor antagonist, demonstrated increases in MHPG in both patients and normals, with more severe panic patients showing the largest increases (Charney et al, 1983;Charney & Heninger, 1985a;; clonidine, an ix2 agonist, produced greater MHPG decreases in patients than normals (Chamey & Heninger, 1986a). Caffeine-induced increases in anxiety did not raise MHPG (Uhde et al, 1984a;Chamey et al, 1985), while situationally produced anxiety in panic patients did produce increases in MHPG in one study (Ko et al, 1983), but not in another (Woods et al, 1987). Norepinephrine and MHPG were minimally changed during "spontaneous" (unexpected) panic attacks, and epinephrine showed no change at all (Cameron et al, 1987); it was suggested that posture and activity levels might play a role in hormonal (and physiological) reactivity in these patients.…”

Section: Psychoendocrine Findingsmentioning

confidence: 99%

Systemic hormonal and physiological abnormalities in anxiety disorders

Cameron

Nesse

1988

Psychoneuroendocrinology

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Among the studies of systemic hormonal and physiological abnormalities associated with anxiety disorders, the most consistent and extensive findings suggest (a) peripheral adrenergic hyperactivity (including increases in norepinephrine but not epinephrine) and functional dysregulation, (b) increased incidence of mitral valve prolapse in panic patients, and (c) normal suppressibility of the hypothalamic-pituitary-adrenal cortical endocrine system with dexamethasone in panic patients. Other less-certain findings include (a) increased circulating concentrations of plasma ACTH and/or cortisol, and prolactin, in panic patients, (b) increased platelet monoamine oxidase activity in generalized anxiety and/or panic patients, (c) decreased gonadal axis activity in some anxious individuals, (d) decreased nighttime melatonin plasma concentrations in panic patients, and (e) peripheral alpha 2 and beta-adrenoreceptor down-regulation, with normal serotonin binding parameters. These findings, taken together, provide tentative support for dysfunction in adrenergic and GABAergic central nervous system mechanisms in people with anxiety disorders. Abnormal anxiety and normal stress both show evidence of adrenergic hyperactivity; however, there appear to be differences in hormonal profiles, especially the apparent lack of increase of epinephrine during panic attacks, as well as differences in the reactivity of the system, and in the "trigger" mechanisms which determine when the response occurs.

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Section: Psychoendocrine Findingsmentioning

confidence: 99%

Systemic hormonal and physiological abnormalities in anxiety disorders

Cameron

Nesse

1988

Psychoneuroendocrinology

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“…This experiment does not appear to have been done but reports of findings of separate investigations of lactate induced (Liebowitz et al 1985 a;Levin et al 1987) and situational (Woods et al 1987) panics do not suggest that there are important differences between them.…”

Section: Spontaneous and Situational Panicmentioning

confidence: 83%

Panic disorder: fact or fiction?

Gelder¹

1989

Psychol. Med.

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“…Woods and colleagues exposed 18 medication-free PD subjects with agoraphobia and paired 13 healthy subjects (most cases) to typical agoraphobic situations (e.g., parks, malls, restaurants, and bridges) and assessed subjective anxiety and physical symptoms and measured heart rate and blood pressure prior to and after exposure. They determined that PD subjects had higher anxiety, fear, and nervousness symptoms at baseline and greater physical symptoms such as palpitations, parasthesias, dyspnea (Woods et al, 1987). Post-exposure, 13 of 18 PD subjects reported having a PA while no PAs were reported in healthy subjects.…”

Section: Section 4 – Panic Attacks Triggers: Laboratory and Potentialmentioning

confidence: 99%

“…In the previously discussed studies, it is not clear if the PAs assessed were completely uPAs or in some cases ePAs, but another study provoked ePAs in agoraphobic PD subjects by exposing them to agoraphobic situations. In this previously-mentioned Woods study in 1987, they exposed healthy and agoraphobic PD subjects to typical agoraphobic situations which induced PAs in 13 out of 18 PD subjects, and no PAs in healthy subjects (Woods et al, 1987). Assessments of autonomic and endocrine responses revealed that, post-exposure, both PD and healthy subjects had an increase in heart rate, but this response was greater in PD subjects.…”

Section: Section 4 – Panic Attacks Triggers: Laboratory and Potentialmentioning

confidence: 99%

Etiology, triggers and neurochemical circuits associated with unexpected, expected, and laboratory-induced panic attacks

Johnson

Federici

Shekhar

2014

Neuroscience & Biobehavioral Reviews

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Panic disorder (PD) is a severe anxiety disorder that is characterized by recurrent panic attacks (PA), which can be unexpected (uPA, i.e., no clear identifiable trigger) or expected (ePA). Panic typically involves an abrupt feeling of catastrophic fear or distress accompanied by physiological symptoms such as palpitations, racing heart, thermal sensations, and sweating. Recurrent uPA and ePA can also lead to agoraphobia, where subjects with PD avoid situations that were associated with PA. Here we will review recent developments in our understanding of PD, which includes discussions on: symptoms and signs associated with uPA and ePAs; Diagnosis of PD and the new DSM-V; biological etiology such as heritability and gene x environment and gene x hormonal development interactions; comparisons between laboratory and naturally occurring uPAs and ePAs; neurochemical systems that are associated with clinical PAs (e.g. gene associations; targets for triggering or treating PAs), adaptive fear and panic response concepts in the context of new NIH RDoc approach; and finally strengths and weaknesses of translational animal models of adaptive and pathological panic states.

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Situational Panic Attacks

Cited by 148 publications

References 92 publications

Systemic hormonal and physiological abnormalities in anxiety disorders

Systemic hormonal and physiological abnormalities in anxiety disorders

Panic disorder: fact or fiction?

Etiology, triggers and neurochemical circuits associated with unexpected, expected, and laboratory-induced panic attacks

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