CO2 challenge induced HPA axis activation in panic

Duinen, Marlies A. van; Schruers, Koen; Maes, Michaël; Griez, Eric

doi:10.1017/s1461145706007358

Cited by 57 publications

(33 citation statements)

References 44 publications

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“…This suggestion is supported by our previous observation of blunted plasma and salivary cortisol responses to an intensive psychosocial stress paradigm in subjects with high trait anxiety [32,33]. Actually, a relatively low activation of the HPA axis with respect to concomitant changes in subjective anxiety has been repeatedly observed in patients with panic disorder, particularly in response to panicogenic agents [11]. …”

Section: Discussionsupporting

confidence: 59%

“…There are a number of reports showing that panicogenic stimuli, such as sodium lactate, carbon dioxide or caffeine, failed to induce increased cortisol release [7]. Other studies, however, demonstrated an activation of the HPA axis following exposure to carbon dioxide in healthy volunteers [8,9,10] as well as in patients with panic disorder [11]. As to the spontaneously occurring panic attacks, again no changes [12,13] or an increase [14] in cortisol release have been reported.…”

Section: Introductionmentioning

confidence: 99%

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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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Section: Discussionsupporting

confidence: 59%

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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“…As a result, it has been suggested that the HPA axis becomes progressively subsensitized in PD patients after repeated exposure to PAs. 15 Another possibility is the uncoupling of the HPA axis and the noradrenergic system in PD. 16 It is well known that the sympathoadrenal axis is markedly activated during the PA.…”

Section: Stressmentioning

confidence: 99%

Ansiedade, pânico e o eixo hipotálamo-pituitária-adrenal

Graeff

2007

Rev. Bras. Psiquiatr.

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A b s t r a c t Objective: This article focuses on the differential activation of the hypothalamic-pituitary-adrenal axis in generalized anxiety disorder and panic disorder. Method: The results of recently reported reviews of the literature are summarized and discussed. Results: The results of experimental studies that assayed adrenocorticotropic hormone, cortisol and prolactin show that real-life panic attacks, as well as those induced by selective panicogenic agents such as lactate and carbon dioxide, do not activate the hypothalamic-pituitary-adrenal axis. Agonists of the cholecystokinin receptor B such as the cholecystokinin-4 peptide and pentagastrin increase stress hormones regardless of the occurrence of a panic attack and, thus, seem to activate the hypothalamicpituitary-adrenal axis directly. The benzodiazepine antagonist flumazenil does not increase stress hormones, but this agent does not reliably induce panic attacks. Pharmacological agents that increase anxiety in both normal people and panic patients (caffeine, yohimbine, serotonergic agonists) raise stress hormone levels. Conclusions: In addition to the differences in symptomatology and pharmacological response, generalized anxiety disorder and panic disorder affect stress hormones in distinct ways. While anticipatory anxiety and generalized anxiety disorder activate both the hypothalamic-pituitary-adrenal and the sympathoadrenal axes, panic attack causes major sympathetic activation, but has little effect on the hypothalamic-pituitaryadrenal axis.Descriptors: Stress; Hormones; Anxiety disorders; Hypothalamus; Pituitary-adrenal system Resumo Objetivo: Este artigo discute a ativação diferencial do eixo hipotálamo-pituitária-adrenal no transtorno de ansiedade generalizada e no transtorno de pânico. Método: Resultados de recentes revisões da literatura são resumidos e discutidos. Resultados: Os resultados de estudos experimentais que dosaram o hormônio adrenocorticotrópico, o cortisol e a prolactina mostram que ataques de pânico espontâneos, bem como os provocados por agentes panicogênicos seletivos -como lactato de sódio e dióxido de carbono -, não ativam o eixo hipotálamo-pituitária-adrenal. Agonistas do receptor de colecistocinina do tipo B, como o peptídeo colecistocinina-4 e pentagastrina, elevam os hormônios de estresse, independentemente da ocorrência de um ataque de pânico, parecendo ativar diretamente o eixo hipotálamo-pituitária-adrenal. O antagonista benzodiazepínico flumazenil não eleva o nível dos hormônios de estresse; porém, este agente farmacológico não induz ataques de pânico de modo consistente. Agentes farmacológicos que aumentam a ansiedade em pacientes de pânico (cafeína, ioimbina, agonistas serotonérgicos), assim como em pessoas saudáveis, elevam o nível dos hormônios de estresse. Conclusões: Além das diferenças na sintomatologia e na resposta farmacológica, o transtorno de ansiedade generalizada e o transtorno de pânico afetam os hormônios de estresse de modo distinto. Enquanto a ansiedade antecipatória e o transtorno de ansied...

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“…Specifically, sodium lactate infusions and CO2 inhalation regularly produce panic attacks in patients with panic disorder (Liebowitz et al, 1984b), Gorman et al, 1984, Papp et al 1993). However, while normal controls or patients with other anxiety disorders rarely show such reactivity (i.e., progress to a full-blown panic attack) (Klein 1993), higher concentrations of inhaled CO2 are highly aversive and can produce respiratory panic symptomatology in a dose-dependent fashion (Griez et al, 2007;Esquivel et al, 2010;Leibold et al, 2013).…”

Section: Panic and Comorbid Conditionsmentioning

confidence: 99%

Lifelong Opioidergic Vulnerability Through Early Life Separation: A Recent Extension of the False Suffocation Alarm Theory of Panic Disorder

Preter¹

2016

Panic Disorder

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We briefly reference previous material on Klein's suffocation false alarm theory (SFA) of panic disorder (Klein, 1993) and its amplification in 2008 (Preter andKlein, 2008). We then discuss a recent finding showing a fundamental difference in opioidergic reactivity to a naloxone challenge in psychiatrically and medically healthy adults, based on the presence or absence of childhood separation/parental loss.In 1993, Klein published the original SFA theory of panic disorder (Klein, 1993), attempting to integrate the multiplicity of apparently unrelated clinical and laboratory observations. We posited "that a physiologic misinterpretation by a suffocation monitor misfires an evolved suffocation alarm system. This produces sudden respiratory distress followed swiftly by a brief hyperventilation, panic, and the urge to flee. Carbon dioxide hypersensitivity is seen as due to the deranged suffocation alarm monitor. If other indicators of potential suffocation provoke panic, this theoretical extension is supported." In the original paper, we tested "the theory by examining Ondine's curse as the physiologic and pharmacologic converse of panic disorder, splitting panic in terms of symptomatology and challenge studies, reevaluating the role of hyperventilation, and reinterpreting the contagiousness of sighing and yawning, as well as mass hysteria." (Klein, 1993) Original SFA focused on relating the observed lactate and carbon dioxide hypersensitivity in panic disorder to a putative dysfunction in a hypothesized suffocation alarm. At the time, the underlying pathophysiology that might connect the apparent disparate "phenomena of panic during relaxation and sleep, late luteal phase dysphoric disorder, pregnancy, childbirth, pulmonary disease, separation anxiety, and treatment", was unknown.

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CO2 challenge induced HPA axis activation in panic

Cited by 57 publications

References 44 publications

Attenuated Neuroendocrine Response to Hypoglycemic Stress in Patients with Panic Disorder

Attenuated Neuroendocrine Response to Hypoglycemic Stress in Patients with Panic Disorder

Ansiedade, pânico e o eixo hipotálamo-pituitária-adrenal

Lifelong Opioidergic Vulnerability Through Early Life Separation: A Recent Extension of the False Suffocation Alarm Theory of Panic Disorder

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