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The relationships between mood change, obstetric experience and alterations in plasma cortisol, beta-endorphin (beta-EP) and corticotrophin-releasing hormone (CRH) were examined in a prospective study of 97 primiparous Australian women. Psychological measures were administered between the 28th week of pregnancy and the 3rd postnatal month, including the Profile of Mood States (POMS) and the Montgomery Asberg Depressive Rating Scale (MADRS). Blood samples were collected for cortisol, beta-EP and CRH assay on most of these occasions and during labour. Factor analysis was used to identify key subsets of psychological variables for use in the subsequent analyses. 'Mood disturbance' and 'tiredness' factors peaked at 38 weeks' gestation, while 'difficulty falling asleep' was greatest around the time of birth. Cortisol, beta-EP and CRH concentrations rose significantly as pregnancy advanced and peaked at birth; plasma CRH correlated with plasma cortisol (r = 0.54) and beta-EP (r = 0.32). Women with the highest 'mood disturbance' and MADRS depression scores at 28 weeks' gestation received significantly more pain relief during labour. Those women whose mood deteriorated from 38 weeks' gestation to postnatal day 2 had larger falls in plasma beta-EP after delivery (p less than 0.01) than those women whose mood improved or remained constant. Women in this mood-deteriorated subgroup also had significantly higher MADRS depression scores at 3 months (p less than 0.01). Mild antenatal depression (MADRS greater than 13) occurred in 5.2% of women and mild postnatal depression in 4.7%. Overall, these data suggest a role for circulating CRH in the regulation of maternal cortisol secretion and significant relationships between maternal postnatal mood states and beta-EP and between antenatal mood states and obstetric events.
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PMID:Mood changes, obstetric experience and alterations in plasma cortisol, beta-endorphin and corticotrophin releasing hormone during pregnancy and the puerperium. 213 27

Women with postpartum health problems do not readily initiate consultation, making it necessary for those providing care to devise methods by which problems can be identified. By taking detailed accounts of each woman's labour and delivery details when planning postpartum care, some morbidity could be preempted and its effect limited. Postnatal care requires a planned structure which could be modelled on current antenatal care organisation. All women could routinely be seen at three or six months post-delivery. Care could be given by midwives, with referral to GPs where necessary. Fatigue could put women at greater risk of developing postpartum depression, but few women spontaneously report fatigue as a health problem. Limiting the effects of childbirth on maternal health will have important implications for the future use of the medical services.
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PMID:Identifying morbidity in postpartum women. 769 1

The aim of the study was to assess the psychological impact of nipple pain in lactating women. Forty-eight lactating women with nipple pain completed mood scales at their first visit and following resolution of their pain, and 65 lactating women without nipple pain completed one set of mood scales. At the first visit, the mean score on the Edinburgh Postnatal Depression Scale (EPDS) in the nipple pain group was 12.4 and the control group was 7.6 (p < 0.0001). Eighteen women (38%) scored above the threshold for depression (> 12), compared to nine in the control group (14%): p < 0.01. Following pain resolution, the mean score on the EPDS decreased to 7.3 (p < 0.001); and six women (16%) scored 13 or over on the EPDS, significantly less than initially (p < 0.05). Similarly, on the Profile of Mood States (POMS), the nipple pain group scored significantly higher than control group on all mood factors (Tension, Depression, Fatigue, Confusion, Vigor [lower]), except Anger which did not reach a level of significance. After pain resolution, POMS scores returned to similar levels as the control group. In conclusion, both the EPDS and POMS indicated women with nipple pain were experiencing high levels of emotional distress. However, once the pain had resolved their distress also resolved.
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PMID:Psychological aspects of nipple pain in lactating women. 886 Aug 87

Postpartum thyroid dysfunction (PTD) occurs in approximately 5% to 10% of all women within 1 year following delivery and is usually due to intrinsic thyroid disease rather than hypothalamic or pituitary lesions. The most common etiology of PTD, which may resemble postpartum depression, is autoimmune thyroid disease (chronic or Hashimoto's thyroiditis). Women with Graves' disease who experience symptom exacerbation in the postpartum period account for a small percentage of cases. Clues to PTD include nonspecific symptoms such as tiredness, fatigue, depression, palpitations, and irritability. On physical examination, tachycardia may be noted. Goiters are detected in the majority of cases. The disease course varies; most patients experience a phase of hypothyroidism that takes 2 to 6 months to resolve, but some develop permanent hypothyroidism within 5 years of the diagnosis.
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PMID:Evaluating and Managing Postpartum Thyroid Dysfunction. 974 99

While becoming a mother can be a fulfilling and joyful experience, 10-28% of women are affected by an intense emotional response commonly called postpartum depression. This phenomenon is distinguishable from the "transitory baby blues" and is often characterized by crying, confusion, fatigue, depression, insomnia, difficulty caring for the baby and self, and suicidal thoughts. Research on postpartum depression has largely concentrated on investigating its possible causes and predictors utilizing quantitative methodology. Women are the experts of their own lives, yet their voices are missing in the existing body of knowledge about depression after childbirth. In this exploratory qualitative study, I used a feminist perspective to explore the experiences of eight women who had recovered from postpartum depression. A three-stage model emerged that demonstrated how women made sense of that time in their lives. The findings of this study provide a contextual picture of women's experiences with depression after childbirth. The knowledge created has important implications for informing the practice of professionals and the implementation of policy and programs that meet the needs of new mothers and their families.
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PMID:Out of the darkness and into the light: women's experiences with depression after childbirth. 1035 Nov 69

The stress system coordinates the adaptive responses of the organism to stressors of any kind.(1). The main components of the stress system are the corticotropin-releasing hormone (CRH) and locus ceruleus-norepinephrine (LC/NE)-autonomic systems and their peripheral effectors, the pituitary-adrenal axis, and the limbs of the autonomic system. Activation of the stress system leads to behavioral and peripheral changes that improve the ability of the organism to adjust homeostasis and increase its chances for survival. The CRH and LC/NE systems stimulate arousal and attention, as well as the mesocorticolimbic dopaminergic system, which is involved in anticipatory and reward phenomena, and the hypothalamic beta-endorphin system, which suppresses pain sensation and, hence, increases analgesia. CRH inhibits appetite and activates thermogenesis via the catecholaminergic system. Also, reciprocal interactions exist between the amygdala and the hippocampus and the stress system, which stimulates these elements and is regulated by them. CRH plays an important role in inhibiting GnRH secretion during stress, while, via somatostatin, it also inhibits GH, TRH and TSH secretion, suppressing, thus, the reproductive, growth and thyroid functions. Interestingly, all three of these functions receive and depend on positive catecholaminergic input. The end-hormones of the hypothalamic-pituitary-adrenal (HPA) axis, glucocorticoids, on the other hand, have multiple roles. They simultaneously inhibit the CRH, LC/NE and beta-endorphin systems and stimulate the mesocorticolimbic dopaminergic system and the CRH peptidergic central nucleus of the amygdala. In addition, they directly inhibit pituitary gonadotropin, GH and TSH secretion, render the target tissues of sex steroids and growth factors resistant to these substances and suppress the 5' deiodinase, which converts the relatively inactive tetraiodothyronine (T(4)) to triiodothyronine (T(3)), contributing further to the suppression of reproductive, growth and thyroid functions. They also have direct as well as insulin-mediated effects on adipose tissue, ultimately promoting visceral adiposity, insulin resistance, dyslipidemia and hypertension (metabolic syndrome X) and direct effects on the bone, causing "low turnover" osteoporosis. Central CRH, via glucocorticoids and catecholamines, inhibits the inflammatory reaction, while directly secreted by peripheral nerves CRH stimulates local inflammation (immune CRH). CRH antagonists may be useful in human pathologic states, such as melancholic depression and chronic anxiety, associated with chronic hyperactivity of the stress system, along with predictable behavioral, neuroendocrine, metabolic and immune changes, based on the interrelations outlined above. Conversely, potentiators of CRH secretion/action may be useful to treat atypical depression, postpartum depression and the fibromyalgia/chronic fatigue syndromes, all characterized by low HPA axis and LC/NE activity, fatigue, depressive symptomatology, hyperalgesia and increased immune/inflammatory responses to stimuli.
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PMID:Hypothalamic-pituitary-adrenal axis, neuroendocrine factors and stress. 1237 95

This paper summarizes the current knowledge concerning the biosynthesis of neurosteroids in the human brain, the enzymes mediating these reactions, their localization, and the putative effects of neurosteroids. The presence of the steroidogenic enzymes cytochrome P450(SCC), aromatase, 5alpha-reductase, 3alpha-hydroxysteroid dehydrogenase, and 17beta-hydroxysteroid dehydrogenase in the human brain has now been firmly established by molecular biological and biochemical studies. Their presence in the cerebral cortex and in the subcortical white matter indicates that various cell types, either neurons or glial cells, are involved in the biosynthesis of neuroactive steroids in the brain. The following functions are attributed to specific neurosteroids: modulation of GABA(A), N-methyl-d-aspartate (NMDA), nicotinic, muscarinic, serotonin (5-HT(3)), kainate, glycine and sigma receptors, neuroprotection and induction of neurite outgrowth, dendritic spines, and synaptogenesis. We still do not know whether and how the steroidogenic enzymes are involved in the pathophysiology of the nervous system. The first clinical investigations in humans produced evidence for an involvement of neuroactive steroids in conditions such as fatigue during pregnancy, premenstrual syndrome, postpartum depression, catamenial epilepsy, and depressive disorders. Further and improved knowledge of the biochemical pathways of neurosteroidogenesis and their actions on the brain may enable new perspectives in the understanding of the physiology of the human brain as well as in the pharmacological treatment of its disturbances.
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PMID:Neurosteroid biosynthesis in the human brain and its clinical implications. 1499 41

Postpartum depression (PPD) is an irritable, severely depressed mood that occurs within 4 weeks of giving birth and possibly as late as 30 weeks postpartum. Manifestations include crying spells, insomnia, depressed mood, fatigue, anxiety, and poor concentration. Patients may experience mild, moderate, or severe symptoms. Many psychosocial stressors may have an impact on the development of PPD. Recent studies conclude that the majority of factors are largely social in nature. The greatest risk is in women with a history of depression or other affective illness and in those who have experienced depression during past pregnancies. Women with significant risk factors should be followed closely in the postpartum period. The severity of symptoms and degree of impairment guide the approach to treatment. Treatment should begin with psychotherapy and advance to pharmacotherapy if needed; however, many patients benefit from concomitant treatment with both psychotherapy and medication. Common forms of psychotherapy include interpersonal therapy and short-term cognitive-behavioral therapy. Postpartum depression demands the same pharmacologic treatment as major depression does, with similar doses as those given to patients with nonpuerperal depression. It is essential to use an adequate dose of antidepressants in a duration sufficient to ensure complete recovery. Mothers should continue medication for 6 to 12 months postpartum to ensure a complete recovery. Inadequate treatment of depression puts women at risk for the sequelae of untreated affective illness, and the depression may become chronic, recurrent, and/or refractory. Family physicians are key players in the detection and treatment of PPD owing to the nature of the disease and the tendency for new mothers to negate their feelings as something other than a treatable psychiatric illness.
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PMID:A Review of Postpartum Depression. 1501

The postpartum is a high-risk period for the occurrence of anxious and depressive episodes. Indeed, during the first few days after delivery, mothers can present postpartum blues symptomatology: fatigue, anxiety, disordered sleeping and a changing mood. Postpartum depression is characterised by a changing mood, anxiety, irritability, depression, panic and obsessional phenomena. It occurs in approximately 10 to 20% mothers. The exact prevalence depending on the criteria used for detection. The first symptoms usually appear between the fourth and sixth week postpartum. However, postpartum depression can start from the moment of birth, or may result from depression evolving continuously since pregnancy. We can add that the intensity of postpartum blues is a risk factor that can perturb maternal development. So it is important for health professionals to dispose of predictive tools. This study is a validation of the French version of the EPDS. The aims of the study were to evaluate the postpartum depression predictive value at 3 days postpartum and to determine a cut-off score for major depression. Subjects participating in this study were met in 3 obstetrical clinics in, or in the vicinity of, Toulouse. Mothers with psychological problems, under treatment for psychological problems or mothers whose babies present serious health problems were excluded from the study. The EPDS was presented to 859 mothers (mean age=30.3; SD=4.5) met at one of the clinics at 3 days postpartum (period 1). They had an EPDS mean score of 6.4 (SD=4.6); 258 (30%) mothers had an EPDS score 9. 82.6% of these mothers experienced a natural childbirth and 17.3% a caesarean section; 51.5% gave birth to their first child, 36.2% to their second child and 12.3% to their third or more. All subjects were given a second EPDS with written instructions to complete the scale during the period 4 to 6 weeks postpartum and return it for analysis (period 2). Between the 4 to 6 weeks postpartum period, 722 mothers replied again to the EPDS. 131 mothers had an EPDS score 11 (mean age=30.3; SD=4.8). They had an EPDS mean score of 13.6 (SD=3.3). Mothers with probable depression were interviewed and assessed, using the Mini (Mini Neuropsychiatric Interview, Lecrubier et al. 1997), the SIGH-D (Structured Interview Guide for the Hamilton Depression Scale) and the BDI (Beck Depression Inventory) in order to diagnose a major depressive episode. They had a HDRS mean score of 13.7 (SD=5.1) and a BDI mean score of 13.6 (SD=5). At 3 days postpartum, we observed that 258 mothers (30%) had an EPDS scores 9 and 164 mothers (19%) had an EPDS scores 11. Between 4 and 6 weeks postpartum, we observed 18.1% of postpartum depression (EPDS 11) and 16.8% (EPDS 12) of major postpartum depression. The analysis of the sensitivity and the specificity at 3 days postpartum provides a cut-off score of 9 (Sensibility: 0.88) (Specificity: 0.50) as predictive of postpartum depression, for this cut-off score, the type I error is low (5.8%) but the type II error is more higher (18.9%). The analysis of the sensitivity and the specificity between 4 and 6 weeks postpartum provides a cut-off score of 12 (Sensibility: 0.91) (Sensibility: 0.74) for the detection of major postpartum depression. Factor analysis shows at 3 days postpartum that the internal structure of the scale is composed of two subscales. The first factor F1 "anxiety" accounts 28% of the variance and the second factor F2 "depression" accounts 20% of the variance. Between 4 and 6 weeks postpartum, factor analysis suggests an unidimensional model in the evaluation of postpartum depression which is better than a two factor model. This factor accounts 40% of the variance. The scale has a good predictive value, and we can observe a significant correlation with the EPDS periods 1 and 2 (r=0.56; p<0.05). This result shows that the depressive mothers mood intensity predicts a future depressive risk. Furthermore, correlations between EPDS and BDI (r=0.68; p<0.05) and EPDS and HDRS (r=0.67; p<0.05) show a good convergent validity. The reliability study confirms the good internal consistency of the EPDS, at 3 days postpartum and in the postpartum depression -symptomatology evaluation (Cronbach's Alpha>0.80). In conclusion, this scale demonstrates good validity and is fast and easy use in obstetrical services, allowing early detection of women who risk to develop postpartum depression and, in the first week of postpartum, of mothers who suffer from a major postpartum depression. The use of the EPDS for an early screening of the risk of postnatal depression which is essential considering the consequences that postnatal depression can have on the development of the infant, on the quality of the relationship within the couple and on other social relationships. Mothers at risk for postnatal depression should be controlled and surveyed by the health professionals in obstetrical clinics.
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PMID:[A study of the Edinburgh Postnatal Depression Scale (EPDS) on 859 mothers: detection of mothers at risk for postpartum depression]. 1553 13

The primary aim of this study was to explore the feasibility of applying diagnostic criteria for cancer-related fatigue syndrome (CRFS) in patients with advanced cancer. A secondary aim was to assess the use of screening instruments for fatigue and depression in this population. Patients with advanced cancer (n=16) were interviewed using the Diagnostic Interview for CRFS and a semi-structured psychiatric interview. Subjects also completed the Bi-dimensional Fatigue Scale (BFS) and the Edinburgh Postnatal Depression Scale (EPDS) as screening instruments. The prevalence of psychiatric disorders was 50% (8/16). The EPDS was found to have a sensitivity of 67% and a specificity of 100% for detecting depression. The prevalence of clinically significant fatigue symptoms was 62.5% (10/16). The BFS was found to have a sensitivity of 70% and a specificity of 64% for detecting clinically significant fatigue. The prevalence of CRFS was 12.5% (2/16).
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PMID:Investigation of diagnostic criteria for cancer-related fatigue syndrome in patients with advanced cancer: a feasibility study. 1687 11


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