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

There is a suggestive evidence for a relationship between central 5-HT and the occurrence of certain types of depressions. This evidence is derived from three sources: postmortem studies; measurement of CSF 5-HIAA; accumulation of CSF 5-HIAA after transport blockade by probenecid. Disturbances of central 5-HT metabolism are not typical for any depression but for certain types of vital (endogenous) depression. This implies that the group of vital depression, though tending towards homogeneity in terms of symptomatology, is heterogenous in biochemical terms and comprises patients with and without disorders in central 5-HT metabolism. It is plausible that disorders of the 5-HT metabolism play a role in the pathogenesis of depression, instead of resulting from them. This statement is based on the following findings: (i) 5-HTP can abolish or alleviate the depressive syndrome or some of its elements. (ii) This 5-HTP effect can be potentiated by clomipramine (Anafranil), a relative selective inhibitor of 5-HT reuptake. (iii) There exists a negative correlation between 5-HT turnover in the CNS and the therapeutic effect of clomipramine. The alleged distrurbances in central 5-HT are more likely to be predisposing than of direct causative significance. This assumption is based on two observations: (i) In more that 50% of cases, the 5-HT turnover remains low after clinical recovery, the patient being drug-free. (ii) There is suggestive evidence that abolition of the 5-HT deficit (by means of 5-HTP) exerts a prophylactic effect in uni-and bipolar depression.
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PMID:The Harold E. Himwich Memorial Lecture. Significance of biochemical parameters in the diagnosis, treatment, and prevention of depressive disorders. 30 32

SAdness and normal grief are distinguished from pathological grief and depression by intensity, duration, precipitating events, and the quality of psychopathological features. Depression is evaluated as a final common pathway of potential psychodynamic, genetic, psychosocial, physiological, and personality characteristics or events. The clinical entity of depression is diagnosed by describing some of each of the affective, behavioral, and cognitive changes concomitant with depression. The clinical entity of depression is further differentiated for purposes of treatment into the categories of bipolar depression (manic-depressive illness), unipolar depression (psychotic depressive reaction or involutional melancholia), neurotic depression, and secondary depression (secondary to somatic disease, drugs, or to other psychiatric disorders). The immediate treatment depends on the type of depression diagnosed. Unipolar and bipolar depressions respond to specific pharmacologic therapy and supportive care. Neurotic and characterologic depressions respond to supportive or insight psychotherapy with possible brief adjunctive anti-anxiety or hypnotic medication. All of the treatment modalities, with the possilbe exception of insight psychotherapy, can be effected very adequately by the primary care physician who is given clear diagnostic and assessment guidelines with specific treatment approaches.
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PMID:The depressed patient. 42 80

In the last two decades, there has been rapid progress in the pharmacologic treatment of affective disorders. In Part I of this review, drugs mainly used for depression (tricyclic antidepressants and monoamine oxidase inhibitors) were discussed. Here, lithium carbonate, the most effective drug for manic-depressive illness (bipolar depression) is the focus. Its indications, mode of action, pharmacokinetics, dosage, and side effects are discussed. A section on drug interactions with lithium deals with the combination effect of lithium used with antidepressant and other psychotropic agents.
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PMID:Series on pharmacology in practice. 1. Drugs that alter mood. II. Lithium. 44 9

Fifteen elderly depressed patients were treated by 36-hour sleep deprivation (SD). The depression was unipolar in 3 cases, bipolar in 3, and secondary in 4. Nine of the 15 patients responded to SD, and 6 had a remission (1 with SD alone and 5 with SD plus an antidepressant drug). Some of the remaining 6 patients might have responded if the treatment had not been interrupted for various reasons. These favorable results in elderly patients were better than anticipated. SD was well tolerated, although in one patient with bipolar depression a manic attack was precipitated. The effectiveness of SD poses interesting theoretic questions.
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PMID:Sleep deprivation in the treatment of elderly depressed patients. 93 79

Optimal treatment of mood disorders and prevention of suicide requires biological and psychosocial methods, therapeutic alliance and psycho-education. In moderate unipolar depression an antidepressant may be sufficient, if necessary potentiated by another antidepressant or triiodothyronine. In moderate bipolar depression lithium or carbamazepine are preferred. In severe unipolar and bipolar depression the combination of an antidepressant and lithium (or carbamazepine) or electroconvulsive therapy (ECT) is indicated, in psychotic depression neuroleptics, too. Non-selective monoamine oxidase inhibitors (MAOIs) are the most potent antidepressants. Moderate acute mania and mixed state may respond to lithium, carbamazepine or valproate only. In severe cases a neuroleptic and lithium are combined, or these drugs may be combined with carbamazepine or valproate. Electroconvulsive therapy is preferable in acute mixed states with marked confusion or depression. In chronic mixed state and rapid cycling, withdrawal of antidepressants and neuroleptics should be tried. Most patients will need a combination of lithium and carbamazepine or valproate. Added to these drugs, antidepressants are less risky. Adding thyroxin may stabilize rapid cycling. The combination of lithium and an antidepressant is the most potent prophylaxis in unipolar disorder and bipolar disorder dominated by depression.
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PMID:[Affective disorders. Drug treatment and electroconvulsive therapy]. 135 73

Fifteen patients with endogenous unipolar and bipolar depression were treated with imipramine and, if necessary, one of benzodiazepine or neuroleptic. Total serum concentrations of imipramine (IMI) and its active metabolite desipramine (DMI) were measured in steady-state by FPIA method . Severity of depression was assessed using the Hamilton Depression Rating Scale. IMI + DMI serum concentration monitoring appeared to be useful in every case. It helped to arrive more quickly at the optimal dosage, confirmed the suspicion of overdosage or noncompliance. In nonresponders group, it helped with the earlier decision of changing brands of tricyclic antidepressant or it contributed to intensify the diagnostic process which detected the additional pathology.
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PMID:[Clinical usefulness of monitoring serum levels of imipramine and desipramine in patients treated for endogenous depression]. 178 Mar 75

We evaluated positron emission tomography (PET) in the differential diagnosis of depression and Alzheimer's disease. The local cerebral metabolic rate for glucose (LCMRGlc) in the parahippocampal gyrus-hippocampus and the dorsolateral prefrontal cortex were determined. The ratio of the LCMRGlc in those two regions was examined in patients with unipolar depression, bipolar depression, and Alzheimer's dementia. An analysis of variance revealed significant overall intergroup differences in values for both hemispheres. Student's t test showed significant differences in LCMRGlc for both unipolar and bipolar depression as compared with Alzheimer's dementia. These data indicate that PET may be useful in the differential diagnosis of dementia vs. depression.
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PMID:Changes in glucose metabolism in dementia of the Alzheimer type compared with depression: a preliminary report. 178 Mar 92

The effects of antidepressant drugs on phase switching was studied in 602 individuals treated for endogenous depression. Altogether 869 depressed phases were evaluated retrospectively--there were 470 depressed phases in the course of bipolar affective disorder and 399 of unipolar disorder or with the undefined course. Switching from depression to mania was observed in patients with bipolar disorder--in 27.9% of cases of bipolar depression and in 21.5% of bipolar patients. Most frequently the switching was observed during management of depressed phase with amitriptyline (24.4% of treatments with this drug). The results point to a role of cholinergic system in pathophysiology of switching out of depression into mania during treatment with antidepressant drug.
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PMID:[Transition from the depressive stage to the manic stage during the treatment with antidepressive drugs]. 182 82

The effectiveness and good acceptability of tianeptine have been demonstrated in episodes of major depression without melancholia or signs of psychosis which are the valided indications of the tianeptine. In a way of research program, a multicenter study was conducted in 30 patients with D.S.M. III criteria for major depression with melancholia and signs of endogenicity as defined by the Newcastle scale. The patients were treated in a double-blind trial for 42 days. Administration of a placebo for 4 days prior to beginning the study was designed to eliminate rapid responders to placebo. The antidepressant effectiveness was evaluated on the Hamilton (HDRS), Montgomery and Asberg (MADRS) and global clinical impression (GCI) scales. The effect was satisfactory and statistically significant. Seventeen of the 30 patients (57 percent) included in this study improved with tianeptine (CGI-item 2). Results were comparable whatever the diagnosis established on DSM III criteria: bipolar depression, major depression, recurrent or isolated forms. The acceptability evaluated from patient complaints, measurement of blood pressure and laboratory tests was very satisfactory. Treatment was withdrawn in 14 patients with no subsequent withdrawal symptoms. These findings show that tianeptine can be prescribed with success for major depression episodes with melancholia (DSM III) and signs of endogenicity, although it cannot be concluded that patients should be given this treatment in first intention for this type of depression.
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PMID:[Tianeptine in episodes of major depression with melancholia and signs of endogenicity]. 183 16

By means of a review of genetic, biological and neurophysiological studies, we attempted to validate the DSM III-R depressive disorder categories. Genetic studies support the distinction between bipolar and recurrent major (unipolar) depression although genetic heterogeneity and variable phenotypic expressivity have been suggested in bipolar depression. Biological and neuroendocrine abnormalities in depression seem to relate more to a particular symptomatological profile than to a specific depressive subtype including the bipolar-unipolar dichotomy. For example, catecholamines and serotonin metabolism seem to reflect respectively psychomotor status and aggressiveness in depression. Using genetic and biological criteria, major depression with psychotic features is the best validated category of the four main DSM-R major depressive subclasses or specifications (psychotic, chronic, melancholic, seasonal). Psychotic depression seems to constitute the most coherent subgroup and biological abnormalities such as dexamethasone non suppression and shortened REM latency are very often observed. An important confounding variable in these biological validation studies is the severity of the depressive state. Psychotic depression is considered to be a more severe depressive subtype and also shows marked biological disturbances. Conversely, in seasonal depression, a less severe depressive subtype, CSF monoamine metabolism abnormalities, dexamethasone non suppression and shortened REM latency could not clearly be demonstrated. Genetic studies show that early onset dysthymia and cyclothymia could be part of the affective spectrum and some maintain that these two clinical entities are attenued forms of bipolar or recurrent major depression.
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PMID:[Biological psychiatry and current classifications of depressive disorders]. 186 51


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