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51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent advances in neuropharmacology and neuroimaging are mapping the topography of symptoms in major depressive disorder (MDD). Different malfunctioning neuronal circuits apparently mediate different symptoms in MDD. Since all patients with MDD do not have the same symptoms, this implies that they may not all have the same malfunctioning circuits. Furthermore, since MDD patients treated with antidepressants commonly experience residual symptoms that prevent them from attaining complete remission, this implies that not all circuits are successfully targeted by treatment in such patients. A new neurobiologically informed treatment strategy for such patients calls for targeting residual symptoms by augmenting antidepressants with agents capable of boosting specific neurotransmitters in the hypothetically malfunctioning circuits. With this approach, the frequently residual symptoms of sleepiness, fatigue, and executive dysfunction can be targeted with bupropion, atomoxetine, modafinil, atypical antipsychotics, and stimulants.
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PMID:Brain circuits determine destiny in depression: a novel approach to the psychopharmacology of wakefulness, fatigue, and executive dysfunction in major depressive disorder. 1465 30

Patients with major depressive disorder commonly experience fatigue and cognitive/executive dysfunction. These problems may be symptoms of the depression and persist despite effective antidepressant treatment, or these problems may emerge as adverse effects of some antidepressant treatments. A number of augmentation strategies can be employed to manage fatigue or cognitive/executive dysfunction, but the efficacy of these augmentation strategies must be researched further.
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PMID:Symptoms of fatigue and cognitive/executive dysfunction in major depressive disorder before and after antidepressant treatment. 1465 33

Modafinil is a wake-promoting agent approved by the Federal Drug Administration for the treatment of narcolepsy. Preliminary evidence indicates that modafinil may improve fatigue and excessive sleepiness associated with a variety of conditions. The purpose of this study was to investigate the utility of modafinil as an adjunctive treatment of depressed patients. Subjects with a history of major depression with partial response on a stable therapeutic dose of an antidepressant were eligible to participate. All subjects endorsed complaints of significant fatigue and/or excessive sleepiness on clinical assessment. Modafinil was added to their existing regimen at a dose of 100 to 400 mg/d for 4 weeks. Subjects were assessed at 2-week intervals for improvement using the standard depression scales (HDRS, BDI, CGI), fatigue scales (VASF, FSI), and a neuropsychologic battery. Thirty-five subjects were entered and 31 subjects completed the 4-week trial. Significant improvements were seen across all 3 measures of depression (HDRS, BDI, CGIS) and both measures of fatigue (VASF, FSI). On the neurocognitive battery, significant gains in the Stroop Interference Test were seen at 4 weeks, whereas the other cognitive tests showed no change. Modafinil may be a useful and a well-tolerated adjunctive agent to standard antidepressants in the treatment of major depression.
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PMID:A prospective trial of modafinil as an adjunctive treatment of major depression. 1470 53

The purpose of this report is to study serotonin reuptake of the brain in a severely overtrained athlete by using single-photon emission computed tomography (SPECT). A 26-year-old team athlete increased his training volume (by 200 %) and intensity markedly in a new high-level team. After two months, he started to feel continuous fatigue. He had tinnitus in his left ear, he felt disturbing palpitation and had pollacisuria. After four months, he started to suffer from insomnia. He still continued to play for another three months, after which he was unable to play. He could only sleep for 3 to 4 hours per night. Only minor abnormalities could be found in extensive physical and laboratory examinations. The athlete had a severe overtraining state. In the brain SPECT scans, using the specific radioligand for serotonin transporter imaging ( (123)I labelled 2beta-carbomethoxy-3beta-[4-iodophenyl]-nortropane), low activity areas were detected in the midbrain, anterior gingulus, and left frontal and temporo-occipital lobes. In a psychiatric examination, the patient was found to have signs of major depression, which he hardly recognized himself. We conclude, that that the severe overtraining state could have been related to decreased serotonin reuptake in the brain and signs of major depression.
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PMID:Abnormal serotonin reuptake in an overtrained, insomnic and depressed team athlete. 1498

During Depression Screening Day in Uppsala, Sweden, 127 adolescents, 23 boys and 104 girls, in the ages 13-20 years were investigated. We found that 44 (34.6%) fulfilled the criteria for a major depression according to DSM-IV criteria and 42 (40.4%) of the girls and 2 (9.5%) of the boys had an ongoing depression. All depressive symptoms, except increased appetite, were significantly more common in the depressed as compared to the non-depressed adolescents. The most common symptoms were fatigue, decreased interest and concentration difficulties. When the adolescents with major depression were compared to adults with major depression, rated by means of self-rating with the Montgomery Asberg Depression Rating Scale, depressions among adolescents and adults were very similar. However, sleep disturbances and decreased initiative were less frequent among the adolescents while decreased appetite was more common. Many of the patients with major depression found had mild symptoms but 21 (44.7%) were regarded being in need for medical treatment.
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PMID:[Depression common among young people with somatic disorders. Fatigue, lack of emotional engagement, increased need of sleep are some of the warning signals]. 1498 44

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

BACKGROUND: Depression is underdiagnosed in the primary care setting. Physical symptoms such as aches, pains, and gastrointestinal disturbance are frequently associated with major depressive disorder (MDD) and are often the presenting symptoms. Duloxetine, a dual-reuptake inhibitor of serotonin and norepinephrine, may have a positive effect on physical symptoms in addition to efficacy in treating emotional symptoms of depression. METHOD: Efficacy was evaluated in 6 double-blind, placebo- and/or active comparator-controlled trials of duloxetine for patients with MDD (DSM-IV criteria). Efficacy in depression was determined primarily using the 17-item Hamilton Rating Scale for Depression (HAM-D-17). Secondary efficacy measures included subscales of the HAM-D-17 and assessment of physical symptoms. Safety evaluations included adverse events, vital signs, laboratory analyses, and electrocardiograms. Safety was evaluated by pooling the data from the MDD trials and a study of duloxetine in nondepressed patients. RESULTS: Duloxetine demonstrated significant differences from placebo on core mood symptoms, physical symptoms (e.g., back pain), and global functioning as early as week 1 of treatment. The estimated probabilities of remission in the studies that demonstrated efficacy ranged from 43% to 57%. The most frequently observed adverse events for duloxetine-treated patients included nausea, dizziness, insomnia, fatigue, and somnolence. Duloxetine did not prolong corrected QT intervals, and the rate of sustained elevations of blood pressure did not differ significantly from placebo. CONCLUSION: In these studies, duloxetine was safe and effective in the treatment of both emotional and physical symptoms of MDD. Based on dose assessments, 60 mg q.d. appears to be the optimum starting and therapeutic dose.
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PMID:Duloxetine: A New Treatment for the Emotional and Physical Symptoms of Depression. 1515 43

High doses of antidepressants are often used for treatment-resistant depression. Venlafaxine, a dual serotonin and noradrenaline reuptake inhibitor, has been shown to have a tolerable side-effect profile in previous studies using doses of up to 375 mg/day. We investigated the tolerability of higher than currently recommended doses of venlafaxine using the UKU side-effect rating scale. Seventy outpatients fulfilling DSM-IV criteria for major depressive disorder were recruited into two demographically matched groups according to their daily dosage of venlafaxine: high dose n = 35 (> or = 375 mg/day, range 375-600 mg, average 437 mg/day) or standard dose n = 35 (< 375 mg/day, range 75-300 mg, average 195 mg/day. Clinical characteristics were noted and the UKU side-effect rating scale was administered to a subsample of patients. The most frequently reported complaints in both groups were increased fatigue (48%), concentration difficulties (48%), sleepiness/sedation (37%), failing memory (44.4%) and weight gain (29.6%). Apart from weight gain, the complaints were found to be experienced significantly more severely by the high-dose group. Six patients discontinued venlafaxine due to intolerable side-effects but only two of these patients were on a high dose. There was a tendency for mildly raised blood pressure in 10% of patients on an average dose of 342 mg/day. However, no difference between the two groups was found. This preliminary open study demonstrates that venlafaxine is tolerated at higher than British National Formulary recommended doses (i.e. up to 600 mg daily). However, increased frequency and severity of reported side-effects in the high-dose group are not associated with increased rates of discontinuation.
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PMID:Tolerability of high-dose venlafaxine in depressed patients. 1526 Sep 8

The aim of this study was to investigate depressive symptomatology across distinct major psychiatric disorders. A total of 1351 subjects affected by major depressive disorder (MDD = 389), bipolar disorder (BP = 511), delusional disorder (DD = 93) and schizophrenia (SKZ = 358) were included in our study. Subjects were assessed using the Operational Criteria for Psychotic Illness checklist (OPCRIT). The most frequently represented depressive symptoms in MDD were Loss of energy/tiredness, Loss of pleasure, Poor concentration, and Sleep disorders. Compared with MDD, BP had higher occurrences of Agitated activity, Excessive sleep, and Increased appetite and/or Weight gain, as well as lower Loss of pleasure. In our sample, 32.3% and 26.8% of DD and SKZ, respectively, had quite consistent depressive symptomatology, with at least four or more depressive symptoms. The most common depressive symptoms were Sleep disorders, Poor concentration and Loss of energy/Tiredness, followed by Psychomotor symptoms in SKZ only. Excessive self-reproach, Suicidal ideation, and Appetite and/or Weight changes were more specific to mood disorders. Finally, compared with SKZ, DD suffered from more depressive symptoms and had more severe depressive symptomatology. A quite consistent level of depressive symptomatology is therefore present in subpopulations of delusional and schizophrenic subjects other than in affective subjects. We identified some symptoms that are common across all major psychoses and symptoms that are more specific to each group.
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PMID:Depressive syndrome in major psychoses: a study on 1351 subjects. 1526 8

Chronic fatigue syndrome (CFS) is a disabling condition characterized by subjective fatigue, mental and physical fatigability, a whole range of somatic symptoms and a poor quality of sleep. Its physiopathology is largely unknown. Several clinical and biological differences were observed between CFS and major depression. A classical conceptualization of masked (or somatized expression of) depression is therefore no longer tenable. Sleep anomalies were reported in all studies published to date. However, these sleep anomalies do not seem to explain a major part of the symptomatology of CFS. The contribution of sleep abnormalities to the development and chronicity of CFS should be further studied. CFS can be considered as a somatoform condition. CFS is like most functional disorders a clinically and biologically heterogeneous condition. The best available treatment to date is cognitive-behavioural therapy.
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PMID:Review of clinical and psychobiological dimensions of the chronic fatigue syndrome: differentiation from depression and contribution of sleep dysfunctions. 1531 Apr 82


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