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The aim of this study was to verify if the fall of plasma concentrations of steroid hormones in the first 12 h postpartum would be associated with changes in the same period in the emotional state of healthy women. Subjective and hormonal data were collected from 14 women (28.5 ± 7.1 years old) at zero (only hormones), 1, 2, 6 and 12 h after delivery. Subjective measures were taken using the Visual Analogue Mood Scale (VAMS), which consists of four factors (anxiety, sedation, discomfort, and cognitive impairment). Cortisol was measured by radioimmunoassay and estradiol and progesterone by chemiluminescence immunoassay. Women reported a significant increase in anxiety (relative increase: 43.8%±77.6) and discomfort (125.9%±218.5) within the 12 h postpartum. There were also significant decreases in the plasma concentration of estradiol (relative decrease: 96.5%±3.1), progesterone (78.1%±8.7) and cortisol (71.7%±18.0). The relative decrease in estradiol concentrations was significantly correlated with the relative increase in anxiety. No significant associations between progesterone and cortisol concentrations and subjective measures were observed. Changes of estradiol but not of progesterone and cortisol concentrations were associated with changes in the reported emotional state of healthy women in the immediate postpartum period. The role of this association as a predictor of mood disorders in the postpartum period should be explored in further studies.

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BACKGROUND: This study aimed to investigate associations between indicators of hypothalamic-pituitary-adrenal axis (HPA) functioning and metabolite levels in the anterior cingulate gyrus (ACG) of women with postpartum depression (PPD). METHODS: The sample (mean age = 28.5 ±â€¯4.6 years) consisted of 20 women with PPD and 19 postpartum euthymic (PPE) women. Brain metabolites were quantified by proton magnetic resonance spectroscopy (1H-MRS). Salivary cortisol samples were collected upon awakening and 30 min and 12 h later, at 20.6 ±â€¯6.6 (PPD) and 23.0 ±â€¯7.4 (PPE) weeks after childbirth. RESULTS: There were no significant differences between groups in respect to metabolite levels in the ACG. Compared with PPE, PPD women had less diurnal variation (DVr%). In the PPD group, positive correlations were found between DVr% and myo-inositol (mI/Cr) levels, and between cortisol awakening response (CARi%) and glutamate + glutamine (Glx/Cr) levels. The correlation between CARi% and Glx/Cr remained significant even after controlling for the interval, in weeks, from birth and MR spectroscopy and to hormonal data collection, and the use of contraceptives. LIMITATIONS: The limitations of the study include the small sample size and the use of oral contraceptives by around half of the sample. CONCLUSIONS: In the remote postpartum period (mean 21.8 ±â€¯6.9 weeks) and in the presence of depressive episodes, the decreased responsiveness of the HPA axis after awakening and a smaller decrease in cortisol levels over the day were associated with lower levels of metabolites in the ACG. These results may contribute to the development of biological models to explain the etiology of PPD.

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INTRODUCTION: A large body of literature suggests the role of the hypothalamic-pituitary-adrenal (HPA) axis in postpartum depression (PPD). Nonetheless, these studies present discrepant methodology and results; thus, this hypothesis deserves further exploration. Areas covered: This review included studies investigating the HPA axis in PPD or postpartum blues published until November 2016. In total, 48 studies met the inclusion criteria. The HPA axis was mostly investigated in the immediate postpartum period (62.5%), and the majority of studies collected samples in the morning (43.8%), with one measure in a single day (43.8%), and blood was the fluid more often collected (58.4%). Seven out of 21 studies evaluating postpartum blues, and 15 out of 28 studies evaluating PPD detected abnormalities in the HPA axis functioning. Expert commentary: We found a significant heterogeneity in the methodology adopted by studies and consequently, in the results. Despite that, the majority of studies reported HPA changes in women with PPD during the remote period. Notably, reactivity tests pointed to attenuated HPA axis response. Ideally, future investigations should use validated reactivity tests, include larger sample sizes, consider many measures of cortisol throughout the day, and more than one day of collection. We also recommend that studies continue to use validated scales for mood assessment.

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BACKGROUND: The present study aimed to evaluate the relationship between the functioning of the hypothalamic-pituitary-adrenal (HPA) axis and major depressive episodes in the remote postpartum period. METHODS: The sample (mean age, 28.0±5.3 years) consisted of 37 depressed postpartum women (DPP), 42 euthymic postpartum women (EPP) and 25 non-postpartum healthy women (HC). Salivary cortisol samples were collected immediately after awakening and 30min, 3 and 12h later, at approximately the sixth month postpartum (mean, 169.6±60.3 days). RESULTS: Differences in cortisol levels were observed at awakening (DPPEPP=HC). The relative increment in the cortisol awakening response (CARi%) was significantly higher in HC (113.5±94.3) than in EPP (63.1±69.8) and DPP (32.2±49.6). The relative reduction in diurnal variation (DVr%) was lower in DPP (56.5±41.8) than in EPP (75.6±22.4) and HC (75.1±13.0). LIMITATIONS: The main limitation was cortisol collection on a single day and without measurement at midnight. CONCLUSIONS: Our findings suggest that the remote postpartum period involves attenuation of HPA axis reactivity; this dysregulation is more pronounced in the presence of DPP, which is associated with a reduction in cortisol diurnal variation. Abnormalities in the neuroendocrine system related to stress processing, present even several months after delivery, can represent vulnerability to mental disorders. Thus, improvements in the mental health care of postpartum women are needed.

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Public speaking is widely used as a model of experimental fear and anxiety. This review aimed to evaluate the effects of pharmacological challenges on public speaking responses and their implications for the understanding of the neurobiology of normal and pathological anxiety, specifically panic disorder. We also describe methodological features of experimental paradigms using public speaking as an inducer of fear and stress. Public speaking is a potent stressor that can provoke significant subjective and physiological responses. However, variations in the manners in which public speaking is modelled can lead to different responses that need to be considered when interpreting the results. Results from pharmacological studies with healthy volunteers submitted to simulated public speaking tests have similarities with the pharmacological responses of panic patients observed in clinical practice and panic patients differ from controls in the response to the public speaking test. These data are compatible with the Deakin and Graeff hypothesis that serotonin inhibits fear, as accessed by public speaking tasks, and that this inhibition is likely related to the actions of serotonin in the dorsal periaqueductal grey matter.

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This study measured the effects of the preferential 5-HT1D/1B receptor agonist sumatriptan in healthy volunteers who performed the Simulated Public Speaking Test (SPST), which recruits the neural network involved in panic disorder and social anxiety disorder. In a double-blind, randomised experiment, 36 males received placebo (12), 50 mg (12) or 100 mg (12) of sumatriptan 2 h before the SPST. Subjective, physiological and hormonal measures were taken before, during and after the test. The dose of 100 mg of sumatriptan increased speech-induced fear more than either a 50mg dose of the drug or placebo. The largest dose of sumatriptan also enhanced vigilance more than placebo, without any change in blood pressure, heart rate or electrical skin conductance. Sumatriptan decreased plasma levels of prolactin. A significant but moderate increase in plasma cortisol after SPST occurred, independent of treatment. Because sumatriptan decreases 5-HT release into the extracellular space, the potentiation of SPST-induced fear caused by the drug supports the hypothesis that 5-HT attenuates this emotional state. As acute administration of antidepressants has also been shown to enhance speaking fear and increase plasma prolactin, in contrast to sumatriptan, the 5-HT regulation of stress-hormone release is likely to be different from that of emotion.

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Realizou-se levantamento bibliográfico no indexadorMEDLINE, através das palavras-chave "cortisol" e "panic", sem limite de tempo, restringindo-se a sereshumanos e à localização das palavras-chave no título e no resumo. Foram excluídos artigos de revisão e relatos de caso, estudos sobre alterações ocorridas entre dois ataques, e os que tratavam de outras doenças psiquiátricas ou de sujeitos sadios, quando não comparados com pacientes de pânico. Os resultados mostraram que ataques de pânico naturais ou provocados pelos agentes panicogênicos seletivos, lactato de sódio e dióxido de carbono, não ativam o eixo hipotálamo-pituitária-adrenal (HPA). Agonistas do receptor de colecistocinina B elevam os hormônios de estresse, quer haja ataque de pânico ou não, parecendo ativar diretamente o eixo HPA. O antagonista benzodiazepínico flumazenil não eleva o nível dos hormônios de estresse, porém não induz ataques de pânico de modo consistente. Agentes farmacológicos que produzem ansiedade em pacientes de pânico e em voluntários saudáveis elevam o nível dos hormônios de estresse, entre estes o antagonista a2-adrenérgico ioimbina, os agentes serotonérgicos 1-(m-clorofenil) piperazina (mCPP) e fenfluramina, bem como o agente psicostimulante cafeína. Portanto, o ataque de pânico não parece ativar o eixo HPA, ao contrário da ansiedade antecipatória.

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A bibliographic search has been performed in MEDLINE using cortisol and panic as key-words, occurring in the title and/or in the abstract. Human studies were selected, with no time limit. The following publications were excluded: review articles, case reports, panic attacks in disorders other than panic disorder, and studies on changes that occurred in-between panic attacks. The results showed 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 (HPA) axis. Agonists of the colecystokinin receptor B, such as the colecystokinin-4 peptide and pentagastrin, increase stress hormones regardless of the occurrence of a panic attack and thus, seem to activate the HPA axis directly. The benzodiazepine antagonist flumazenil does not increase stress hormones, but this agent does not reliably induce panic attacks. Pharmacological agents that increased anxiety in both normal subjects and panic patients raised stress hormone levels; among them are the alpha2-adrenergic antagonist yohimbine, the serotonergic agents 1-(m-chlorophenyl) piperazine (mCPP) and fenfluramine, as well as the psychostimulant agent caffeine. Therefore, the panic attack does not seem to activate the HPAaxis, in contrast to anticipatory anxiety.

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Drug-free symptomatic panic patients, drug-treated nonsymptomatic patients and healthy controls were submitted to simulated public speaking. Subjective anxiety, cognitive impairment and discomfort measured by the visual analog mood scale as well as skin conductance level were higher in symptomatic patients than in controls at the beginning of the experimental session, nonsymptomatic patients lying in between. Subjective sedation, spontaneous fluctuations of skin conductance, heart rate and blood pressure were similar in the three groups. Preparation and performance of speech decreased sedation while increasing anxiety, cognitive impairment, level and fluctuations of skin conductance, heart rate and blood pressure. Anxiety, cognitive impairment and conductance level were less increased in symptomatic patients than in controls. Electrodermal activity, but not cardiovascular measures of sympathetic arousal correlated with anticipatory anxiety. Chronic treatment with serotonin uptake inhibitors attenuated the differences between panic patients and controls, supporting the participation of serotonin in panic disorder.

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Anxiety and salivary cortisol were measured in subjects performing simulated public speaking (SPS), a procedure that has been neurobiologically related to panic disorder. The subjects were divided into three groups: 18 symptomatic panic patients, 16 nonsymptomatic, drug-treated panic patients, and 17 healthy controls. In the experimental session, subjective anxiety (Visual Analogue Mood Scale) and the total score of the Bodily Symptom Scale (BSS) were higher in symptomatic patients than in controls, with nonsymptomatic patients in between. Measures of cortisol taken at home showed that the level was higher at 9:00 h than at 23:00 h in every group, indicating a normal circadian regulation of the hypothalamic-pituitary-adrenal (HPA) axis in panic patients. Also in every group, the level of cortisol was high at the beginning of the experimental session and decreased after 70 min. This fall parallels the decrease in anxiety and BSS ratings, and appears to reflect habituation of initial, anticipatory anxiety. Preparation and performance of speech raised anxiety and BSS scores to the initial levels, but failed to increase cortisol measured over 60 min, starting at the end of the speech. Therefore, SPS does not seem to activate the HPA axis, as reported in panic attacks.

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