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

This article presents the results of a comparison between the validity of the SCL anxiety, phobic anxiety and depression scales and the GHQ-28 anxiety-/insomnia and severe depression scales in a psychiatric outpatient population. Validity was studied at a categorical level with DSM-III diagnosis, and at a dimensional level with a prototypical anxiety and a prototypical depression scale. The SCL anxiety and depression scales and the GHQ depression scale all showed good convergent and divergent validity, however the GHQ anxiety/insomnia scale showed neither convergent nor divergent validity. It is concluded that as a screening instrument, the relative shortness of the GHQ-28 is a considerable advantage over the SCL-90. However, the GHQ-12 may be an even better alternative. As a multi dimensional measure of psychopathology, the SCL-90 is to be preferred, because it covers more dimensions. If one is interested in anxiety, the SCL-90 also seems the better choice.
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PMID:Validity of the GHQ and SCL anxiety and depression scales: a comparative study. 157 83

To investigate an hypothesized link between unwanted sexual experiences in childhood and later problems with eating, 21 survivors of sexual abuse completed three questionnaires: the Eating Attitudes Test, the Sexual Events Questionnaire, and the General Health Questionnaire. These women scored high on the EAT, and scores were higher for women who reported more sexual experiences. A similar relation was found between number of sexual experiences and depression, and anxiety and insomnia, but not with somatic symptoms. The implications of these findings for intervention in sexual abuse and eating disorder cases are discussed.
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PMID:Eating attitudes in survivors of unwanted sexual experiences. 160 Apr 4

For a period of six months (april to october 1990) 361 manic-depressive in-patients or out-patients were examined and treated. 178 patients (119 females and 69 males) were suffering from depression at examination time. Among them, 34 women and 11 men had mixed mood disorders with a symptomatology near that of typical depression (major depression, according to the DSM III-R criteria) but not of mixed bipolar disorder. The main symptoms were: dysphoric mood with irritability; internal tension, psychic and sometimes physical agitation; emotional lability; head crowded with thoughouts or thoughts that vanish too quickly; sleep disorders with initial insomnia or with frequent night awakenings; suicidal thoughts or attempted suicide with impulsiveness. These patients sustained severe suffering. They were in no way slow-minded but rather talkative and expressive. Antidepressant drugs increased agitation and insomnia, and in some cases, suicidal impulses. BZDs had limited efficacy but neuroleptics given in small doses, anticonvulsants and lithium gave very effective results. A limited number of electroshocks provided rapid improvement. In many respects, depression with delirium seems a more severe form of the above-described combined depressive syndrome and responds to the same treatments. We think that this mood disorder includes excitement as an important component, although this was not clearly evident. However, it is not easy to conceive this syndrome as a mixture of depressive and manic symptoms; it should rather be regarded as another specific mood condition, either permanent or transient, situated between the two other conditions.
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PMID:[Mixed depressive syndrome]. 160 Aug 99

The potential antidepressant effects of estrogen replacement therapy were examined cross-sectionally in a population of 1190 women 50 years and older living in Rancho Bernardo, California. Of the total, 294 (24.7%) were currently using estrogen. Among women aged 50-59 years, those currently using noncontraceptive estrogen had a significantly higher rate of Beck Depression Inventory scores of 13 or higher than all untreated women of the same age and higher mean depressive symptom scores than women who had never used estrogen. However, after age 60, mean depressive symptom scores and rates of categorical depression increased significantly in the untreated women but not in the treated women. A similar pattern was found when depressive symptom measures of treated and untreated women were stratified by the number of years since last menstrual period. Greater depressive symptoms in currently treated versus untreated women aged 50-59 years may reflect treatment selection bias, as a higher proportion of symptomatic depressed climacteric women seek treatment. The decreased risk of depressive symptoms after age 60 may reflect a long-term benefit of estrogen replacement or the selective discontinuation of estrogen by depressed women. In this cohort, reports of hot flushes, moods, and insomnia as the reason for estrogen use fell in parallel with a decline in depressive symptoms with increasing age, suggesting that hormone replacement therapy provided relief of physical symptoms, ie, possible causes of psychological distress. Clinical trials are needed to confirm these observations and postulated explanations.
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PMID:Estrogen use and depressive symptoms in postmenopausal women. 160 93

Advances in neuropeptide neurobiology in the last decade are illustrated by studies of corticotropin-releasing factor (CRF), the 41 amino acid-containing peptide that controls the anterior pituitary secretion of adrenocorticotropin and other pro-opiomelanocortin products. Corticotropin-releasing factor is synthesized in both hypothalamic and extrahypothalamic perikarya in a large prohormone form, (186 amino acids), then it is processed and transported to nerve terminals where it is released in its active form by a calcium-dependent mechanism. Corticotropin-releasing factor biosynthesis can now be measured by in situ hybridization because of the elucidation of the CRF gene sequence. Once released, CRF acts on high-affinity CRF receptors, and signal transduction is mediated by activation of adenylate cyclase in certain brain areas, and perhaps by phosphoinositide hydrolysis. In other brain areas CRF is inactivated by peptidases that degrade the hormone, though these are not well characterized. A CRF binding protein has been identified in plasma, and perhaps in brain. Considerable evidence exists from cerebrospinal fluid studies, postmortem tissue receptor measurements, and CRF stimulation test studies to support the hypothesis that CRF is hypersecreted in depression, resulting in both pituitary-adrenal axis hyperactivity and certain signs and symptoms of depression, e.g., decreased libido, insomnia, and decreased appetite. There is also evidence for an involvement of CRF in the pathophysiology of anxiety disorders and in the mechanism of action of benzodiazepines. The development of selective CRF-receptor antagonists will permit direct testing of the hypothesis that CRF hypersecretion is responsible for certain of the cardinal features of affective and anxiety disorders.
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PMID:New vistas in neuropeptide research in neuropsychiatry: focus on corticotropin-releasing factor. 161 Apr 87

Mood and health reports from 65 administrative and clerical staff were obtained daily over a period of several weeks. Three mood factors emerged from the aggregated data which appear to be most suitably labelled: happiness, tense depression and hostile depression. Subjects high on hostile depression suffered more from colds. Subjects scoring highly on tense depressed mood reported more insomnia, head and neck aches. The results, especially in regard to hostile depression, are discussed in a wider context, including possible overlap with core affective aspects of the well-known Type A coronary risk construct. Finally, psychoimmunological interpretations of the link between hostile depression and vulnerability to colds are considered.
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PMID:Mood states and minor illness. 163 22

Several developments in serotonin neuropharmacology have implications for psychiatric disorders and have already begun to impact their treatment. Selective inhibitors of serotonin uptake, which enhance serotonergic function by preventing the removal of serotonin from the synaptic cleft via the membrane transporter, have been introduced for the treatment of depression and may be effective in other disorders. Precursor loading can increase serotonin concentrations in the synaptic cleft, and tryptophan--which has been available in health food stores and drug stores--had become increasingly used for self-medication of depression, insomnia, and premenstrual syndrome. Conversion to serotonin is not the major metabolic pathway for tryptophan, and large increases in other tryptophan metabolites (such as quinolinic acid, a substance that is excitotoxic at high concentrations) accompany small increases in extracellular serotonin. The recent epidemic of the eosinophilia-myalgia syndrome associated with tryptophan now appears due to a trace contaminant in the product from a single manufacturer. A major advance in serotonin pharmacology has been the elucidation of serotonin receptor heterogeneity. At least seven receptor subtypes (5-HT1A, 5-HT1B, 5-HT1C, 5-HT1D, 5-HT2, 5-HT3, 5-HT4) have been identified in brain. Direct-acting agonists and antagonists can have selective affinity for specific receptor subtypes. Selective activation of 5-HT1A receptors seems to cause anxiolytic and possibly antidepressive effects. Selective antagonists of 5-HT2 or 5-HT3 receptors may be useful in treating anxiety and schizophrenia. Drugs that enhance serotonergic function suppress aggression in animals, but the specific receptor subtypes involved are not known. The advances being made in serotonin pharmacology will help define the role of this brain neurotransmitter in psychiatric and other disorders and can be expected to lead to further therapeutic advances.
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PMID:Role of serotonin in therapy of depression and related disorders. 167 51

Although over 20 years of clinical experience with benzodiazepine hypnotics have demonstrated their relative safety, flurazepam, temazepam, triazolam, and quazepam do not have identical safety profiles. Dose-related central nervous system (CNS) depression such as daytime sedation and psychomotor impairment may be expected because they are an extension of the therapeutic action of these agents. Therefore, drug dose is an important factor in determining the expected frequency and severity of these side effects. Also, it is important for a clinician not to assume that these unwanted CNS effects relate only to the length of a drug's half-life. Half-life does appear to be an important determinant of the presence or absence of rebound insomnia.
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PMID:A review of the safety profiles of benzodiazepine hypnotics. 168 Jan 24

An association between the ingestion tryptophan and a syndrome characterized by scleroderma-like skin abnormalities, fasciitis, and eosinophilia has recently been recognized in the United States. We report the clinical and histopathological findings in nine patients and the results of biochemical analyses of tryptophan metabolism in seven patients with this syndrome. Edema of the extremities, frequently accompanied by pruritus, paresthesia, and myalgia, developed in the nine patients (six women and three men; age range, 30 to 66 years) 1 to 18 months after the start of therapy with tryptophan (1.5 to 3.0 g daily) for insomnia, depression, or obesity. Five patients were taking drugs (benzodiazepines) known to inhibit hypothalamic-pituitary-adrenal function, and one had adrenal insufficiency. All had blood eosinophilia in the acute phase of their illness (mean eosinophil count [+/- SD], 3.62 +/- 2.87 X 10(9) cells per liter). All had histopathological changes in the dermis and subcutaneous tissue typical of scleroderma, and seven patients had eosinophils. The fascia was inflamed and fibrotic, and adjacent skeletal muscle often showed perifascicular inflammation. Tryptophan was discontinued in all patients, and eight received prednisone. The cutaneous symptoms improved, but only two patients had complete resolution of their illness. The patients had plasma levels of tryptophan before and after an oral dose of tryptophan that were similar to those in normal subjects. Plasma levels of L-kynurenine and quinolinic acid, which are metabolites of tryptophan, were significantly higher in four patients with active disease than in three patients studied after eosinophilia had resolved or in five normal subjects (P less than 0.001)--findings consistent with the activation of the enzyme indoleamine-2,3-dioxygenase. This illness resembles eosinophilic fasciitis and probably represents one aspect of the recently reported eosinophilia-myalgia syndrome. The development of the syndrome may result from a confluence of several factors, including the ingestion of tryptophan, exposure to agents that activate indoleamine-2,3-dioxygenase, and possibly, impaired function of the hypothalamic-pituitary-adrenal axis.
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PMID:Scleroderma, fasciitis, and eosinophilia associated with the ingestion of tryptophan. 231 25

Somatic symptoms are one of the leading reasons for medical outpatient clinic visits, with the most common symptoms having a prevalence of 10% or more. However, the usual diagnostic workups are often unproductive, with less than 1 in 5 symptoms having an organic explanation after the initial physical examination and laboratory testing. Therapy appears more effective for some symptoms than for others. Of patients with unspecified pain or gastrointestinal complaints, greater than 70% state that some type of treatment has been helpful, whereas less than 50% of individuals with fatigue, dizziness, numbness, insomnia, sexual dysfunction, anxiety, or depression report any relief. Future educational efforts and research need to focus on that majority of symptoms that are either psychiatric or unexplained, in order to improve our current evaluation and management strategies.
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PMID:Symptoms in medical patients: an untended field. 173 31


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