Does the panic attack activate the hypothalamic-pituitary-adrenal axis?

Femi²,

2006

Open Life Sciences

Many studies have investigated different mechanisms of attack and defense in different species of higher brain animals including cats, rats, rodents, mice, and even in some bird species. However, detailed comparative analysis has not been carried out to understand the major similarities in the mechanisms of attack and defense across the different species of vertebrates. Although there are differences, there are also significant similarities as well, which warrant comparative assessment. By considering ethological ideas associated with the motivational defense system, we investigated the motor patterns of attack and defense in cats and rats, using the "resident-intruder" experimental paradigm. Our results reveal specific similarities and differences in the motor patterns of attack and defense in rats and cats. We discuss comparatively the mechanisms of attack and defense across different species of vertebrates, focusing on motor patterns, neuromodulating factors, brains neural substrates, and circuitry.

Section: Discussionmentioning

confidence: 99%

Comparative analysis of the mechanisms of attack and defense among higher brain animals

Femi²,

2006

Open Life Sciences

“…10 The results have shown that real-life PAs, as well as those induced by selective panicogenic agents such as lactate and carbon dioxide, do not activate the HPA axis. Agonists of the cholecystokinin receptor B, such as cholecystokinin-4 peptide and pentagastrin, increase stress hormones regardless of the occurrence of a PA and, thus, seem to activate the HPA axis directly.…”

Section: Stressmentioning

confidence: 93%

Ansiedade, pânico e o eixo hipotálamo-pituitária-adrenal

Graeff

2007

Rev. Bras. Psiquiatr.

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...

“…In fact, anxiety and panic seem to be qualitatively different: the former is an emotional state related 16 February 22, 2012|Volume 2|Issue 1| WJP|www.wjgnet.com to a potential threat, mostly activating HPA and the sympathoadrenal axes; the latter is an emotion evoked by the perception of an actual danger that causes major sympathetic activation with small effects on the HPA axis [70] . Several authors have reported no increased salivary or plasma cortisol levels during the PA [70,71] (Table 2), maybe due to a successful habituation to the repeated experiences of panic [72] . However, probably due to anticipatory anxiety, higher salivary cortisol levels have been reported at the beginning of the PA [73,74] (Table 2).…”

Section: Childhood Stressful Events Hpa Axis and Pdmentioning

confidence: 99%

Childhood stressful events, HPA axis and anxiety disorders

Faravelli

Sauro²,

Godini³

et al. 2012

WJP

143

Anxiety disorders are among the most common of all mental disorders and their pathogenesis is a major topic in psychiatry, both for prevention and treatment. Early stressful life events and alterations of hypothalamic pituitary adrenal (HPA) axis function seem to have a significant role in the onset of anxiety. Existing data appear to support the mediating effect of the HPA axis between childhood traumata and posttraumatic stress disorder. Findings on the HPA axis activity at baseline and after stimuli in panic disordered patients are inconclusive, even if stressful life events may have a triggering function in the development of this disorder. Data on the relationship between stress, HPA axis functioning and obsessive-compulsive disorder (OCD) are scarce and discordant, but an increased activity of the HPA axis is reported in OCD patients. Moreover, normal basal cortisol levels and hyperresponsiveness of the adrenal cortex during a psychosocial stressor are observed in social phobics. Finally, abnormal HPA axis activity has also been observed in generalized anxiety disordered patients. While several hypothesis have attempted to explain these findings over time, currently the most widely accepted theory is that early stressful life events may provoke alterations of the stress response and thus of the HPA axis, that can endure during adulthood, predisposing individuals to develop psychopathology. All theories are reviewed and the authors conclude that childhood life events and HPA abnormalities may be specifically and transnosographically related to all anxiety disorders, as well as, more broadly, to all psychiatric disorders.