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Query: UMLS:C0015672 (fatigue)
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Nineteen patients, each hospitalized with a major depressive episode, were deprived of sleep for one night. Ten patients responded with clear improvement in depressive symptoms; the substantial clinical change was transient, usually lasting one day. Those who responded had significantly higher initial depression ratings (P less than .01) and tended to be older than nonresponders who experienced mild increases in irritability, fatigue, and discomfort following sleep deprivation. Amine metabolites, 5-hydroxyindoleacetic acid (5HIAA), and homovanillic acid (HVA) were not substantially affected by sleep deprivation, although there was a significant interaction of clinical response and direction of 3-methoxy-4-hydroxyphenylglycol (MHPG) change. Sleep deprivation thus produces acute, but only transient improvement in a selected group of severely depressed patients; it appears to be an important tool in the study of the affective disorders.
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PMID:Effects of sleep deprivation on mood and central amine metabolism in depressed patients. 126 78

Depression has been reported to be common in patients with coronary artery disease (CAD), using a variety of criteria for the diagnosis of depression. However, many studies have relied solely on the presence of symptoms such as a dysphoric mood and fatigue in making a diagnosis of depression. Both fatigue and dysphoric mood are also associated with medical illnesses, and psychiatric diagnoses based on such nonspecific symptoms may lack the specificity necessary to predict the need for psychiatric treatment. To assess the incidence of depression likely to require and respond to psychiatric treatment, 50 patients documented to have CAD by coronary angiography underwent psychiatric diagnostic interviews. Current research-based criteria (DSM-III) were used to make diagnoses of major depressive disorder. In addition, the applicability of a brief screening inventory the (Beck depression inventory) for detecting the presence of depression in these patients was tested. Nine patients (18%) met criteria (DSM-III) for major depressive episode. Depression was not related to the extent of CAD, age or use of beta blockers. There was a relation between depression and smoking. Only 2 of the 9 depressed patients had been diagnosed previously and were being treated for depression. When a score of greater than or equal to 10 on the Beck depression inventory was used to distinguish patients with depression, it had moderate sensitivity (78%) and specificity (90%) for the identification of depression.
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PMID:Major depressive disorder in coronary artery disease. 368 79

In an acute trial, three different dosages (60, 300, and 600 micrograms) of the endocrinologically inert but behaviorally active corticotropin 4-9 (ACTH4-9) fragment ebiratide were given to three patients with clinically probable Alzheimer's disease and five patients with a major depressive episode who were psychomotorly retarded. The drug was given intravenously in a double-blind, placebo-controlled, crossover design, and cognitive as well as psychopathologic assessments were carried out predrug and postdrug treatment. In summary, no adverse effect of the ACTH fragment was detected. In this explorative study, none of the patients improved cognitively, as measured by neuropsychologic testing. However, all patients, regardless of underlying disorder, reported a decrease of the feeling of tiredness or loss of energy, respectively. They felt more vigorous and alert. This occurred after any of the three doses of ACTH4-9, but not after placebo. In concert with reports from other studies, it is concluded that the ACTH4-9 fragment ebiratide may have activating properties in humans. However, given acutely, it does not seem to have antidementia or antidepressive efficacy.
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PMID:Behavioral effects of a synthetic corticotropin 4-9 analog in patients with depression and patients with Alzheimer's disease. 839 47

One hundred and twenty seven patients with major depressive episode were included in a double-blind, four-week, prospective, randomized, multi-centre parallel-group trial comparing moclobemide and imipramine. The dose of moclobemide was 150-525 mg/day and that of imipramine 50-175 mg/day; the mean daily doses during the last week of treatment were 307 mg and 100 mg of moclobemide and imipramine, respectively. The decrease of the total scores of the Hamilton Depression Scale (HDRS) as well as the Overall Assessment of Efficacy by the Investigators showed significant amelioration of depression in both treatment groups (p < 0.001). No significant differences were found between the moclobemide and imipramine groups with regard to treatment outcome. The onset of the antidepressant activity was faster in the moclobemide group as measured by the Assessment of the Investigators. This difference was not observed when the therapeutic index figures calculated on the basis of the changes in the HDRS scores were scrutinized. Treatment-emergent side effects were somewhat more frequent during imipramine than during moclobemide treatment. Nevertheless, a total of only four patients discontinued the trial prematurely because of poor tolerability. Imipramine-treated patients reported more anticholinergic side effects, whereas tiredness and headache were observed more frequently in the moclobemide-treated patients. Restlessness, nervousness and sleep disturbances were noted with equal incidence in both patient groups.
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PMID:Moclobemide versus imipramine in depressed out-patients: a double-blind multi-centre study. 846 35

Klinefelter's syndrome (KS) concerns men and is usually characterized by tallness, underdeveloped testes and sterility. It is generally due to the 47,XXY genotype, ie one extra X chromosome in each cell. Its estimated frequency among newborn boys is 1/500 to 1/700. It seems that 64% KS would be undiagnosed. Abnormally low levels of testosterone blood values are very common in this syndrome. In this case, replacement androgen therapy should be initiated (ideally at the age of 11-15) which prevents osteoporosis and enhances secondary sexual features. Case report - Since early childhood, Mr X has been shy, passive with few friends. When he was 13 years old, the school physician noted a delay of puberty and referred him to an endocrinologist who diagnosed KS. Androgen therapy was introduced but rapidly stopped, because the boy and his parents thought it was useless. Mr X consulted a psychiatrist at the age of 21. He presented a schizo-affective disorder with influence syndrome, auditory and visual hallucinations, labile mood with disinhibited and depressive periods. He was admitted in a psychiatry ward of a general hospital. An endocrinologist confirmed the diagnosis of KS and found very low blood testosterone levels. Besides lithium and risperidone which had already been introduced before the hospitalization, androgens (testosterone undecanoate) were very progressively given to Mr X with a daily psychiatric evaluation. One month after discharge, a major depressive episode led to the adjunction of citalopram. After one year of follow-up, Mr X shows increased social adjustment and enhanced interest; the influence syndrome has partially regressed and his mood is more stable. Discussion - In the years '60 and '70, systematic screenings in psychiatric hospitals have detected 1.3% KS among hospitalized boys, ie 10 times more than in the general population, and 0.6 to 1% KS among hospitalized men. A large variety of psychiatric disorders have been described. Boys presenting KS are usually described as shy, with little energy and initiative, and few friends. They cry more often than compares. Neuropsychological studies demonstrate significantly lower verbal IQ than controls, while performance IQ is generally normal and global IQ is in the normal range with large individual variations. Language acquisition is always delayed. However, agressiveness is not increased. In his follow-up study of 20 years, Nielsen at al found more psychiatric disorders among KS patients, compared to a group of hypogonadal patients at first examination (mean age=27 years). After 20 years follow-up, however, no significant difference remained between the two cohorts concerning the frequency of psychiatric hospitalizations or mental diseases. Several hypotheses have been proposed to explain psychological aspects of KS such as low levels of androgens during foetal and child development, personality disorder related to hypogonadism, delay of mitosis of cells with an extra X chromosome, but none of them is able to explain the specificity of psychological problems associated with KS. Concerning therapeutic aspects, specialists prone substitutive androgen therapy in case of too low testosterone blood levels, from the time of increase in FSH (around the age of 11-15). It prevents osteoporosis, backache and excessive tiredness often found in males with KS; testosterone also improves social drive, mood, concentration and ability at work. If KS diagnosis is made at adult age, androgen therapy has also shown some efficacy, though less than if started earlier. Due to the oral and written language problems of KS boys between 5 and 12 years of age, Graham et al. recommend anticipatory guidance for these boys. In addition, they insist on the importance of the information of the parents, language therapy, the reduction of the length of the instructions given by schoolmasters and specially stimulating and stable childhood conditions. Though it is generally thought that androgens increase agressiveness, we found no consistent data in litterature proving that the restoration of physiological androgen blood levels increases crimes nor aggressiveness. In the contrary, Miller and Sulkes described four cases of KS men presenting chronic fire-setting behaviors. Testosterone was introduced. For three of them, follow-up was available: their behavior seemed improved and none of them recurred. However, the initiation of androgen therapy for patients with severe psychiatric illness should be done very carefully. Conclusion - The Klinefelter's syndrome is frequent and, if not diagnosed (which seems to be the most common case), these men have higher risks to develop psychiatric disorders. Therefore, child psychiatrists and psychiatrists should evoke that diagnosis when they examine boys or men who present typical physical traits of KS (tallness, underdevelopped testes) associated to school problems and/or psychiatric disorders. Indeed, if the diagnosis is confirmed by an endocrinologist and a genetic testing, psychological follow-up and testosterone undecanoate treatment (in case of abnormal testosterone blood levels) should be initiated. This therapy generally improves physical well-being and improves mood, concentration, capacity at work. There is no consistent data in the litterature proving that restoring physiological testosterone blood levels would be dangerous for KS men presenting severe psychiatric troubles. However, this should be discussed in each situation with caution, and androgens should be introduced very progressively.
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PMID:[What is the interest of Klinefelter's syndrome for (child) psychiatrists?]. 1209 88

Helping oncologists to identify and treat depression is an important step in improving the overall care of people with cancer. In previous work performed in our community-based, ambulatory oncology outreach network, we validated a depression screening tool, put into place depression screening programs, and taught oncologists how to follow up on screening with brief, reliable clinical interviews. Subsequently, we provided these oncologists with a fluoxetine-based antidepressant algorithm to follow for the treatment of their depressed patients. In this article, we report on the initial experience identifying and treating 35 ambulatory oncology patients who were screened with the Zung Self-rating Depression Scale (ZSDS). Structured follow-up interviews by their oncologist determined whether the patients qualified for a diagnosis of a major depressive episode. These patients then received 1 of 4 treatments based on the algorithm (no treatment, fluoxetine alone, fluoxetine plus bedtime doxepin, or fluoxetine plus methylphenidate). Patients were matched by their oncologist to a prototype patient for each treatment arm based on their symptomatic presentation (i.e., patients requiring a side effect minimization approach were to be placed on fluoxetine alone; patients who had significant insomnia, weight loss, or neuropathic pain were placed on the fluoxetine plus doxepin regimen; those with prominent fatigue were to receive fluoxetine plus methylphenidate). Patients were followed weekly for one month, and then every two weeks for two more months, with telephone assessments of their depression, associated symptoms and overall quality of life. Results suggested that oncologists most often chose the simplest regimen (fluoxetine alone) but that patients uniformly benefited in terms of improved mood and overall quality of life throughout the 12 weeks of follow-up. Our initial experience suggests that oncologists can be empowered to recognize and treat depression in their patients with a screen-and-intervene approach. Such an approach may benefit patients, and, if kept simple, can be incorporated into day-to-day care of people with cancer.
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PMID:Use of a depression screening tool and a fluoxetine-based algorithm to improve the recognition and treatment of depression in cancer patients. A demonstration project. 1245 13

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

Changes in neuroendocrine function may predispose menopausal women to psychological disturbances characterized by depressed mood, anxiety, irritability, fatigue, insomnia, forgetfulness and decline in libido. The acute tryptophan depletion paradigm was employed to examine the serotonergic contribution to mood and cognitive function in menopausal women who were within 4 weeks of recovery from an episode of major depression. Menopausal women whose depression was responsive to treatment with oestradiol, the selective serotonin reuptake inhibitor fluoxetine, or a combination of both treatments underwent assessment of mood and verbal memory on active tryptophan depLetion and sham depletion test days. Although performance on the delayed paragraph recall subtest of the Wechsler Memory Scale was impaired by tryptophan depletion, no subjects experienced a relapse of depression or a significant worsening of mood. Results from this pilot study indicate that menopausal women who have recently recovered from a major depressive episode do not experience a worsening of mood with acute tryptophan depletion, despite the existence in this sample of some known risk factors for depressive relapse as a result of these procedures. While preliminary, the results suggest that serotonin may be less critical to the pathogenesis of depression during the menopause.
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PMID:The resistance to depressive relapse in menopausal women undergoing tryptophan depletion: preliminary findings. 1689 41

Diagnosis of a major depressive episode by the Diagnostic and Statistical Manual of Mental Disorders of the American Psychiatric Association requires 5 out of 9 symptoms to be present. Therefore, individuals may differ in the specific symptoms they experience and reach a diagnosis of depression via different pathways. It has been suggested that depressed women more often report symptoms of sleep disturbance, appetite or weight disturbance, fatigue, feelings of guilt/worthlessness and psychomotor retardation than depressed men. In the current study, we investigate whether depressed men and women differ in the symptoms they report. Two samples were selected from a sample of Dutch and Australian twins and siblings. First, Dutch and Australian unrelated depressed individuals were selected. Second, a matched epidemiological sample was created consisting of opposite-sex twin and sibling pairs in which both members were depressed. No sex differences in prevalence rates for symptoms were found, with the exception of decreased weight in women in the sample of unrelated individuals. In general, the similarities in symptoms seem to far out-weigh the differences in symptoms between men and women. This signifies that men and women are alike in their symptom profiles for major depression and genes for depression are probably expressed in the same way in the two sexes.
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PMID:Sex differences in symptoms of depression in unrelated individuals and opposite-sex twin and sibling pairs. 1703 42

Although most treatment research on bipolar disorder has focused on mania, depressive episodes occur more frequently among patients with bipolar disorder. Here, we report the results of 2 identically designed, 8-week, multicenter, randomized, double-blind, placebo-controlled studies (CN138-096 and CN138-146) to evaluate the efficacy and safety of aripiprazole monotherapy in outpatients with bipolar I disorder experiencing a major depressive episode without psychotic features. Patients were randomized to placebo or aripiprazole (initiated at 10 mg/d, then flexibly dosed at 5-30 mg/d based on clinical effect and tolerability). The primary end point was mean change from baseline to Week 8 (last observation carried forward) in the Montgomery-Asberg Depression Rating Scale total score. In Studies 1 and 2, respectively, 186 and 187 patients were randomized to aripiprazole, and 188 and 188 to placebo. Although statistically significant differences were observed during Weeks 1 to 6, aripiprazole did not achieve statistical significance versus placebo at Week 8 in either study in the change in Montgomery-Asberg Depression Rating Scale total (primary end point). In addition, despite early statistical separation on the Clinical Global Impressions Bipolar Version Severity of Illness-Depression score (key secondary end point), aripiprazole was not superior to placebo at end point. Aripiprazole was associated with a higher incidence of akathisia, insomnia, nausea, fatigue, restlessness, and dry mouth versus placebo. More patients discontinued with aripiprazole versus placebo in Study 1 (46.8% vs 35.1%) and Study 2 (41.2% vs 29.8%). Aripiprazole monotherapy-as dosed in this study design-was not significantly more effective than placebo in the treatment of bipolar depression at end point (Week 8).
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PMID:Aripiprazole monotherapy in nonpsychotic bipolar I depression: results of 2 randomized, placebo-controlled studies. 1820 35


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