Physiological, biochemical and subjective parameters in anxiety patients with panic disorder during stress exposure as compared with healthy controls

Hoehn, Thomas; Braune, S; Scheibe, G.; Albus, Margot

doi:10.1007/bf02900305

Cited by 46 publications

(22 citation statements)

References 79 publications

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“…There are numerous reports of increased physiological arousal or subjective anxiety in anxious patients during conditions of distal threat, for example, during the period that precedes a future psychological or chemical challenges (Alpers et al 2003;Braune et al 1994;Charney et al 1984;Coplan et al 1998;Hoehn et al 1997;Parente et al 2005). Similarly, mere participation in an experiment involving the future delivery of aversive stimuli can generate substantial anticipatory anxiety that can be measured with the startle reflex (Bocker et al 2004;Grillon and Ameli 1998).…”

Section: Clinical Anxietymentioning

confidence: 99%

Models and mechanisms of anxiety: evidence from startle studies

2007

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Rationale-Preclinical data indicates that threat stimuli elicit two classes of defensive behaviors, those that are associated with imminent danger and are characterized by avoidance or fight (fear), and those that are associated with temporally uncertain danger and are characterized by sustained apprehension and hypervigilance (anxiety).Objective-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 nonphobic anxiety disorders.Conclusions-Progress in our understanding of normal and abnormal anxiety is critically dependent on our ability to model sustained aversive states to temporally uncertain threat.

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Section: Clinical Anxietymentioning

confidence: 99%

Models and mechanisms of anxiety: evidence from startle studies

2007

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“…This matches findings of Petrowski et al [8], who reported a blunted cortisol reactivity to the TSST with concurrent normal cortisol awakening responses in PD patients compared to HC participants. The similar baseline cortisol levels between PD patients and HC subjects have already been reported elsewhere [29]. Interestingly, baseline cortisol values (–10 min, 0 min) of CIPD patients were slightly higher than those of HC participants (and higher than PD patients), although this difference did not reach statistical significance (Fig.…”

Section: Discussionmentioning

confidence: 56%

Comparison of Cortisol Stress Response in Patients with Panic Disorder, Cannabis-Induced Panic Disorder, and Healthy Controls

Petrowski

Conrad

2019

Psychopathology

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Background/Aims: Little research effort has so far been dedicated to the analysis of the hypothalamic-pituitary-adrenal axis of aetiologically differing subgroups of patients with panic disorder (PD). The current study aimed at a deeper understanding of the cortisol stress response in cannabis-induced PD (CIPD) patients. Methods: Matched groups of 7 PD patients (mean age ± SD: 32.95 ± 9.04 years), 7 CIPD patients (31.94 ± 8.40 years), and 7 healthy controls (HC) (31.13 ± 8.57 years) were included in the study. The Trier Social Stress Test (TSST) was used for stress induction. Salivary cortisol samples were collected and panic- and depression-related questionnaires were applied. Results: A stress response to the TSST was found in 28.6% of PD patients, in 51.1% of CIPD patients, and in 100% of HC subjects. Statistical analyses revealed a cortisol hyporesponsiveness in PD and CIPD patients. While cortisol values of PD patients and HC participants differed significantly, CIPD patients’ cortisol courses balanced between those of PD patients and HC subjects. Conclusions: Current findings show a distinctive pattern of the stress-induced cortisol reaction in CIPD patients, which is markedly different from the hormonal response in PD patients as well as HC subjects. Previous findings of cortisol hyporesponsiveness in PD patients compared to HC subjects were confirmed.

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“…Leyton et al [15] observed greater increases in plasma levels of cortisol in patients compared to controls in response to a psychological stressor. The main problem of other studies using mental stress paradigms was that the stress challenge used did not induce a rise in cortisol levels [16,17,18]. As there was no stress-induced rise in cortisol release in the control groups, a similar pattern of cortisol concentrations observed in patients with panic disorder does not necessarily mean that the stress response is not altered in panic disorder.…”

Section: Introductionmentioning

confidence: 84%

“…Plasma noradrenaline and adrenaline concentrations were found to be either unchanged or elevated in patients at rest [16,19]. In general, plasma catecholamine responses to mental or combined laboratory stress situations did not differ substantially between patients with panic disorder and healthy subjects [19,20,21].…”

Section: Introductionmentioning

confidence: 99%

Attenuated Neuroendocrine Response to Hypoglycemic Stress in Patients with Panic Disorder

Ježová¹,

Vigaŝ

Hlavacova³

et al. 2010

Neuroendocrinology

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Background/Aims: There is a lack of information on the effects of metabolic stress exposure on hormone release in patients with panic disorder. The aim of this study was to test the hypothesis that neuroendocrine activation during hypoglycemic stress is altered in panic disorder patients compared to healthy subjects. Methods: Hormone responses to an intravenous bolus of insulin (0.1 IU/kg) were evaluated in both fully remitted, medication-free panic disorder patients and healthy controls (n = 9/group). Blood samples for determination of cortisol, growth hormone, prolactin, adrenaline and noradrenaline concentrations were obtained at rest and over a 90-min period after insulin injection. Results: In patients with panic disorder, basal prestress hormone levels were comparable to those in healthy subjects with the exception of plasma adrenaline, which was higher in panic disorder patients compared to controls. The degree of hypoglycemia induced by insulin administration was similar in patients and healthy subjects. Hypoglycemia-induced increases in growth hormone, prolactin and cortisol concentrations were significantly attenuated in panic disorder patients compared to healthy individuals. No differences between patients and controls were observed in adrenalin release induced by hypoglycemia. Conclusions: The present data demonstrate that somatotropic, lactotropic and corticotropic activation during hypoglycemic stress is blunted in patients with panic disorder. It is suggested that in contrast to the effects of relatively mild stress conditions used in other studies published in the literature, intensive stressors inducing a broad spectrum of hormonal changes fail to provoke an adequate neuroendocrine response in patients with panic disorder.

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Physiological, biochemical and subjective parameters in anxiety patients with panic disorder during stress exposure as compared with healthy controls

Cited by 46 publications

References 79 publications

Models and mechanisms of anxiety: evidence from startle studies

Models and mechanisms of anxiety: evidence from startle studies

Comparison of Cortisol Stress Response in Patients with Panic Disorder, Cannabis-Induced Panic Disorder, and Healthy Controls

Attenuated Neuroendocrine Response to Hypoglycemic Stress in Patients with Panic Disorder

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