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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reports of frequency and interpretation of intellectual and mood disorders differ in multiple sclerosis (MS). Forty-one patients with MS defined according to MacAlpine's criteria were evaluated by psychometric tests (WAIS) and neuropsychologic examinations (study of language, gnosic and praxic activities, dynamic gestural organization, memory and learning) together with, in 24 of them, the AMDP psychopathologic rating scale. Intellectual disorders were noted in 65 p. 100 of patients. Although more frequent in severe and chronic forms they were nevertheless of early onset since more than a half of the patients with onset of disease less than 5 years ago were affected. Their semiology was fairly homogeneous, combining disturbances of dynamic gestural organization (decomposition or simplification) and memory and learning deficiencies without anomalies of instrumental functions or usual psychometric mental deterioration. Application of the AMDP scale failed to reveal any psychotic type of disorders. Mood disturbances were predominant, affecting 60 p. 100 of the subpopulation studied (24 cases) and combining, in an unexpected manner: dysphoria, euphoria and depression. Only euphoria appeared to be correlated with intellectual disorders. Frequency of both intellectual and mood disorders was similar to that reported in other series published. The relative homogeneity of semiology, seen by the correlation between the different disturbances (decomposition and simplification, plateau learning curve and euphoria) and the unusual grouping of these effects, is suggestive of their organic basis. In addition, signs and symptoms resemble the neuropsychological expression of frontal lobe lesions and certain lesions of central grey nuclei.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Intellectual and mood disorders in multiple sclerosis]. 367 62

All depressive syndromes include physical as well as psychological features. Physical symptoms in major "endogenous" depression are well known. In other forms, called masked depressions, various physical disorders are the patients main complaint and may be misleading. Localized pain and paresthesia are common. Behaviour disorders may mask depression in adolescents. Mood disturbances (loss of interest, anhedonia) as well as the personal and family histories, should be precisely assessed in order to establish diagnosis. Masked depression is not a minor form of depressive syndrome and antidepressant drugs should be used in correct doses over a sufficient period of time.
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PMID:[Masked depression and paucisymptomatic depression (author's transl)]. 627 36

Despite the high prevalence of postpartum depressive disorders, many signs and symptoms of this illness are dismissed as normal physiologic changes associated with childbirth. Prompt recognition and treatment are imperative in order to limit the negative impact on both the mother and infant. Mood disturbances may have a minor functional impact that respond well to social support (eg. postpartum blues) or cause significant functional compromise requiring more aggressive therapy (eg. postpartum depression). The most extreme case of postpartum depressive disorder, postpartum psychosis, occurs when patients develop psychosis, mania, or thoughts of infanticide. Depression during pregnancy or the presence of risk factors suggests the need for careful follow-up. If postpartum depression develops, psychotherapy is the first-line treatment. Antidepressant treatment may be warranted for some patients, and the risks and benefits to both the mother and infant should be considered in the decision to institute pharmacotherapy.
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PMID:Postpartum depressive disorders. 896 9

Mood disturbances have been identified in association with changes in levels of reproductive hormones. The use of hormonal measures in the diagnosis of reproductive endocrine-related mood disorders is highly variable, ranging from necessary in perimenopausal depression to irrelevant in premenstrual syndrome. This article describes our view of the use of hormonal measures for diagnostic and research purposes in perimenopausal depression and premenstrual syndrome. We suggest that the understanding of these disorders lies in as yet unidentified contextual factors rather than in hormonal excesses or deficiencies.
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PMID:Hormone measures in reproductive endocrine-related mood disorders: diagnostic issues. 980 56

Mood disturbances and depression are supposed to have a negative impact on patients' outcome in malignant tumour disease. On the other hand, poor prognosis in cancer patients is associated with chronic immune challenge which is paralleled by enhanced degradation of the essential amino acid tryptophan and thus decreased plasma tryptophan concentrations. Because tryptophan is precursor for the biosynthesis of the neurotransmitter serotonin (= 5-hydroxytryptamine, 5HT), low tryptophan concentrations will lead to decreased availability of serotonin which finally increases the susceptibility for the development of mood disturbances and depression in the patients. Thus, the development of depression in cancer patients may result from chronic cellular immune stimulation. In conclusion, a more aggressive tumour rather than depression will be responsible for worse outcome of cancer patients and will be associated with a more drastic challenge of the immune system, as a side effect leading to neurotransmitter disturbances.
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PMID:Immune reaction links disease progression in cancer patients with depression. 1090 30

Mood disturbances are common sequelae of traumatic brain injury (TBI), but the scientific database for such disorders is very limited in descriptive, prognostic, and treatment data. Post-TBI symptoms often cross diagnostic boundaries and include cognitive loss, amotivation, psychosis, mood, changes, or other domains. The treating physician must be mindful that clear diagnostic boundaries may not exist. Premorbid level of functioning commonly affects post-TBI level of functioning. When setting treatment goals, this must be considered. Patients who had lower levels of psychosocial functioning before the injury may not fare as well afterwards. Treatment of post-TBI mood symptoms should proceed after a full diagnostic work-up including imaging and electroencephalographic (EEG) studies, neuropsychologic testing, and physical and laboratory examinations. Once the diagnostic picture is established, treatment should then proceed with a multidisciplinary team (physician, social worker, neuropsychologist, and others). For the medications, consider both target symptoms and side effects; start medications with low doses and raise slowly, give full therapeutic trials before switching or adding second agents, avoid benzodiazepines if possible, limit anticholinergic or antidopaminergic agents, and avoid providing large quantities of lethal medications. When starting medications for the treatment of mood disorders following TBI, several general principles of treatment in this population should be considered, including: balancing treatment of target symptoms with the potential for adverse effects; making use of side effects to treat comorbid problems when present (ie, relatively antidepressant for depression and marked insomnia); using a "start low, go slow" approach; continuing dose escalation to full therapeutic levels (ie, completing therapeutic trials) before switching or adding augmenting agents; avoiding agents with predictable and functionally important adverse effects (ie, benzodiazepines, strongly anticholinergic or antidopaminergic agents); and avoiding prescription of large and potentially lethal quantities of medications.
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PMID:Emotional Disturbances Following Traumatic Brain Injury. 1173 4

This review examines the frequency of depression complicating Parkinson's disease (PD), its aetiology and clinical features, and also how it may be recognised and treated. Studies investigating the frequency of depression in PD have yielded figures ranging between 2.7% and 70%. Methodological differences account for much of the disparity. The aetiology of depression in PD is complex, and probably relates to both biological and exogenous factors. Dysfunction of multiple neurotransmitter systems, including the serotonergic system, may be involved. Mood disturbances resulting from deep brain stimulation of the subthalamic nucleus may provide a fruitful area for future research, and assist our understanding of the neural networks involved in mediating depression. Several recent studies have confirmed that depression in the PD patient is a major determinant of quality of life and that this is closely related to dysfunction in other clinically important health areas. The validity for many existing scales in the screening, diagnosis, and monitoring of depression in the PD patient has not been established. The Montgomery-Asberg Depression Rating Scale and the Hamilton Rating Scale for Depression appear to have good diagnostic sensitivity and specificity when compared with DSM-IV criteria. Recommendations for the optimal drug treatment of depression in PD are difficult to give, due to an inexplicable dearth of sizeable, placebo-controlled studies. A majority of physicians would probably now opt for a selective serotonin reuptake inhibitor in the depressed PD patient. There is no good evidence that these drugs are associated with a worsening of motor features, but they should probably not be coprescribed with selegiline, because of the risk of causing a potentially serious serotonin syndrome. Several studies have suggested that depression in the PD patient is associated with a more rapid deterioration in cognitive and motor functions, perhaps as a surrogate marker for more extensive brainstem cell loss.
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PMID:Beyond the iron mask: towards better recognition and treatment of depression associated with Parkinson's disease. 1211 90

Androgenic-anabolic steroids (AAS) are synthetic derivatives of the male hormone testosterone. They can exert strong effects on the human body that may be beneficial for athletic performance. A review of the literature revealed that most laboratory studies did not investigate the actual doses of AAS currently abused in the field. Therefore, those studies may not reflect the actual (adverse) effects of steroids. The available scientific literature describes that short-term administration of these drugs by athletes can increase strength and bodyweight. Strength gains of about 5-20% of the initial strength and increments of 2-5 kg bodyweight, that may be attributed to an increase of the lean body mass, have been observed. A reduction of fat mass does not seem to occur. Although AAS administration may affect erythropoiesis and blood haemoglobin concentrations, no effect on endurance performance was observed. Little data about the effects of AAS on metabolic responses during exercise training and recovery are available and, therefore, do not allow firm conclusions. The main untoward effects of short- and long-term AAS abuse that male athletes most often self-report are an increase in sexual drive, the occurrence of acne vulgaris, increased body hair and increment of aggressive behaviour. AAS administration will disturb the regular endogenous production of testosterone and gonadotrophins that may persist for months after drug withdrawal. Cardiovascular risk factors may undergo deleterious alterations, including elevation of blood pressure and depression of serum high-density lipoprotein (HDL)-, HDL2- and HDL3-cholesterol levels. In echocardiographic studies in male athletes, AAS did not seem to affect cardiac structure and function, although in animal studies these drugs have been observed to exert hazardous effects on heart structure and function. In studies of athletes, AAS were not found to damage the liver. Psyche and behaviour seem to be strongly affected by AAS. Generally, AAS seem to induce increments of aggression and hostility. Mood disturbances (e.g. depression, [hypo-]mania, psychotic features) are likely to be dose and drug dependent. AAS dependence or withdrawal effects (such as depression) seem to occur only in a small number of AAS users. Dissatisfaction with the body and low self-esteem may lead to the so-called 'reverse anorexia syndrome' that predisposes to the start of AAS use. Many other adverse effects have been associated with AAS misuse, including disturbance of endocrine and immune function, alterations of sebaceous system and skin, changes of haemostatic system and urogenital tract. One has to keep in mind that the scientific data may underestimate the actual untoward effects because of the relatively low doses administered in those studies, since they do not approximate doses used by illicit steroid users. The mechanism of action of AAS may differ between compounds because of variations in the steroid molecule and affinity to androgen receptors. Several pathways of action have been recognised. The enzyme 5-alpha-reductase seems to play an important role by converting AAS into dihydrotestosterone (androstanolone) that acts in the cell nucleus of target organs, such as male accessory glands, skin and prostate. Other mechanisms comprises mediation by the enzyme aromatase that converts AAS in female sex hormones (estradiol and estrone), antagonistic action to estrogens and a competitive antagonism to the glucocorticoid receptors. Furthermore, AAS stimulate erythropoietin synthesis and red cell production as well as bone formation but counteract bone breakdown. The effects on the cardiovascular system are proposed to be mediated by the occurrence of AAS-induced atherosclerosis (due to unfavourable influence on serum lipids and lipoproteins), thrombosis, vasospasm or direct injury to vessel walls, or may be ascribed to a combination of the different mechanisms. AAS-induced increment of muscle tissue can be attributed to hypertrophy and the formation of new muscle fibres, in which key roles are played by satellite cell number and ultrastructure, androgen receptors and myonuclei.
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PMID:Effects of androgenic-anabolic steroids in athletes. 1524 88

Manganese exposure reportedly may have an adverse effect on CNS function and mood. Sixty-two welders with clinical histories of exposure to manganese were compared to 46 matched regional controls chosen at random from a telephone directory. The following tests were given: Wechsler Adult Intelligence Scale (WAIS-III), Wechsler Memory Scale (WMS-III), Boston Naming, WRAT-3, Cancellation H, Trail Making Tests A and B, Auditory Consonant Trigrams, Stroop, Rey-Osterreith, Animal Naming, Controlled Oral Word Association (COWAT), Test of Memory Malingering, Rey 15-item, Fingertapping, Grooved Pegboard, Dynamometer, Visual Attention Test, Lanthony d-15 Color Vision, Vistech Contrast Sensitivity, and Schirmer strips. The controls were administered a shorter battery of tests and the Rey-Osterreith, Animal Naming and some of the subtests of the WAIS-III, WMS-III were not administered. Mood tests, given to both groups, included the Symptom Checklist-40, Symptom Checklist-90-R, Profile of Mood Scale, Beck Depression Inventory II, and Beck Anxiety Inventory. Forty-seven welders and 42 controls were retained for statistical analysis after appropriate exclusions. Results showed a high rate of symptom prevalence and pronounced deficits in motor skills, visuomotor tracking speed and information processing, working memory, verbal skills (COWAT), delayed memory, and visuospatial skills. Neurological examinations compared to neuropsychological test results suggest that neuropsychologists obtain significantly more mood symptoms overall. Odds ratios indicate highly elevated risk for neuropsychological and neurological symptomatology of manganism. Mood disturbances including anxiety, depression, confusion, and impaired vision showed very high odds ratios. Neurological exams and neuropsychological tests exhibit complementarity and differences, though neuropsychological methods may be more sensitive in detecting early signs of manganism. The present study corroborates the findings of our previous study in another group of welders.
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PMID:Manganese exposure: neuropsychological and neurological symptoms and effects in welders. 1634 29

Our objective was to identify determinants of health-related quality of life (HRQoL) in a cohort of Brazilian patients with Parkinson's disease (PD). Patients were evaluated by means of the Hoehn and Yahr staging (H&Y), Unified Parkinson's Disease Rating Scale (UPDRS), Schwab and England scale (S&E), Mini-Mental State Exam, Geriatric Depression Scale, and Hospital Anxiety and Depression Scale (HADS). HRQol was assessed using the MOS-Short-Form 36 (SF-36), the Parkinson's disease Questionnaire (PDQ-39), and the Scales for Outcomes in Parkinson's Disease-Psychosocial Questionnaire (SCOPA-PS). 144 patients were evaluated (mean age 62 years; 53.5% men; mean duration of illness 6.6 years; median H&Y, 2 (range: 1-4). Mean SCOPA-PS and PDQ-39 Summary Index (SI) were 39.2 and 40.7, respectively. Both, PDQ-39 and SCOPA-PS SIs correlated at a moderate level (r = 0.30-0.50) with H&Y, S&E, total UPDRS, HADS subscales, and SF-36 Physical and Mental Components. PDQ-39 and SCOPA-PS were closely associated (r = 0.73). HRQoL significantly deteriorated as H&Y progressed, as a whole. Mood disturbances, disability, motor complications, and education were independent predictors of HRQoL in the multivariate analysis model. In PD Brazilian patients, HRQoL correlated significantly with diverse measures of severity. Depression showed to be the most consistent determinant of HRQoL, followed by disability, motor complications, and education years. There was a close association between the PDQ-39 and SCOPA-PS summary scores.
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PMID:Determinants of quality of life in Brazilian patients with Parkinson's disease. 1751 79


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