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

Treatment of depression in elderly patients is not generically different from treatment of depression in younger age cohorts. Because of certain age-related physical, physiological, and biochemical factors, however, drug prescription for geriatric patients must be modified in several respects. Tricyclic antidepressants are the principal agents in treatment, but their side effects tend to be magnified in the elderly. Dosage should initially be lower than with younger patients and increased in gradual increments. Lithium, MAO inhibitors, and neuroleptics are appropriate in some cases, but additional precautions are necessary. Because the elderly are liable to multiple system decompensation, they are likely to be prescribed multiple pharmacological agents. Drug-drug interactions involving antidepressant medication present a variety of therapeutic problems and can threaten life. Depression in late life can be treated pharmacologically, but both the therapeutic and deleterious activities of the drugs can be altered by compromised organ systems.
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PMID:Pharmacotherapy in older depressed patients. 0 82

A relationship between brain monamines and endogenous depression is suggested by observations on the mode of action of drugs producing or alleviating depressive symptoms. For example, reserpine is capable of faithfully mimicking the clinical picture of endogenous depression, which may be related to monoamine depletion. On the other hand, antidepressant drugs, e.g. the monoamine oxidase inhibitors, the tricyclic antidepressants and the monoamine precursors appear to increase the availability of monoamines at postsynaptic receptor sites. The different classes of antidepressant agents in general appear to potentiate each other's actions, according to animal data and clinical observations. Studies on the mode of action of tricyclic antidepressants with different profiles and on monoamine precursors suggest that 5-hydroxytryptamine is primarily involved in the control of mood, and noradrenaline in psychomotor activity. Clincial investigations initiated by the drug studies have demonstrated changes in monoamine metabolism in endogenous depression. The available evidence thus suggests a causal relationship between disturbances in monoamine metabolism and depression.
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PMID:The contribution of drug research to investigating the nature of endogenous depression. 1 May 84

Depression is both a common and a greatly undertreated illness in the United States today. The focus of this review is a definition of the characteristics of four subtypes of depression which appear to be differentially sensitive to four different classes of medications. The tricyclic antidepressants should be used for patients with unipolar depression and vegetative symptoms. Lithium appears to be most effective for bipolar depressives. The monoamine oxidase (MAO) inhibitors are best used for patients with atypical depression. Antipsychotic medications appear to be useful for depressed patients with psychotic symptoms or agitation. Recent pharmacokinetic and biochemical data, including serum lithium levels, plasma tricyclic levels, and the predictive ability of pretreatment urinary 3-methoxy-4-hydroxyphenylglycol (MHPG) levels are also reviewed.
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PMID:Subtypes of depression--diagnosis and medical management. 1 27

The biological mechanisms through which oral contraceptives influence the central nervous system and produce depression were examined. Oral contraceptives reduce the level of serotonin and norepinephrine available at the central adrenergic receptor sites, alter folate and B12 levels, and perhaps influence hypothalamic releasing hormone levels. The level of serotonin is influenced in the following manner. The estrogens in oral contraceptives increase tryptophan available for the brain to convert to serotonin and tryptamine. Depression is associated with lower levels of serotonin, tryptamine, and perhaps tryptophan in the brain. Estrogens in oral contraceptives may also alter pryridoxal phosphate which in turn affects the production of serotonin. Oral contraceptives possibly lower norepinephrine levels by 1) decreasing tyrosine; 2) influencing coenzymes necessary to norepinephrine production; and 3) increasing monoamine oxidase levels. Oral contraceptives apparently inhibit the metabolism of folate and B12, and lower levels of these substances are associated with depressive symptoms. Decreased norepinephrine and serotonin levels may inhibit the release of gonadotrophin-releasing hormones, and these hormones may in turn influence behavior. Recommendations to clinicians were: 1) patients should be screened for a history of depression prior to prescribing oral contraceptives; 2) pill users should be monitored for depression; and 3) 25 mg daily of pyxidoxine should be administered if a patient taking oral contraceptives is deficient in B6.
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PMID:Oral contraceptives and depressive symptomatology: biologic mechanisms. 3 42

This paper reviews the diagnosis and medical treatment of the major affective disorders. Patients with severe mood disturbances are frequently seen by the family physician. The diagnosis may be delayed since the patient may focus predominantly on somatic concerns which may mimic physical illness. The characteristics, course, and differential diagnosis of depression and mania are discussed. Antidepressants and lithium therapy greatly improve the prognosis of these disorders; monoamine oxidase inhibitors and neuroleptics are indicated for special subtypes of depression. Dosage schedules, interactional effects, adverse and toxic effects are reviewed for tricyclic antidepressants and lithium.
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PMID:Primary affective disorders. 3 9

In a group of depressed patients who had either been treated with or considered suitable for monoamine oxidase (M.A.O.) inhibitor therapy, a highly significant decrease in conjugated tyramine output was observed after an oral tyramine load compared with normal controls. However, there was no difference in conjugated isoprenaline output between the two groups after isoprenaline ingestion, even though this amine is almost solely metabolised by what is likely to be the same conjugation mechanism. Whilst some explanation in terms of altered gut motility is conceivable, it seems more likely that the apparent deficit in tyramine conjugation in depression represents an increase in functional M.A.O. activity. Consequently, this enzyme would metabolise a greater proportion of available amine, causing a proportionately large decrease in the smaller conjugate pool.
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PMID:Is there an increase in monoamine-oxidase activity in depressive illness? 4 26

Tryptophan and 5-hydroxytryptophan have now been extensively investigated in affective disorders. There is now very good evidence that tryptophan increases the antidepressant activity of monoamine oxidase inhibitors. The antidepressant activity of tryptophan and 5-hydroxytryptophan has also been the subject of numerous investigations. There is evidence that patients with decreased cerebrospinal fluid concentration of 5-hydroxyindoleacetic acid respond particularly favourably to this treatment. The therapeutic activity of tryptophan has led to the investigation of the plasma concentration of tryptophan. Free plasma tryptophan, that is tryptophan unbound to plasma protein, appears decreased. There is also evidence that tryptophan and 5-HT transported are abnormal in depression.
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PMID:[Indoleamine precursors in depression (author's transl)]. 9 9

A case report is described wherein the monoamine oxidase inhibitor phenelzine was administered for 10 months at different doses. Drug treatment in the initial part of the study was double blind. Weekly psychotherapy was instituted at the point of symptomatic recovery. At a reduced dose, in month 3, the patient experienced a relapse in depression. While platelet monoamine oxidase inhibition was greater than 80 per cent the patient was well, but at the point of relapse, inhibition was 14 per cent. Clinical ratings at relapse (Beck and SCL-90 scales) revealed greater readiness by the patient to report psychological discomfort compared with the original interview. The combined effects of psychotherapy and pharmacotherapy were felt to be responsible for this change. However, psychotherapy in this form and duration did not prevent relapse, which depended upon maintaining an adequate dose of phenelzine.
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PMID:Single case study. Complementary effects of phenelzine and psychotherapy in long term treatment of depression. 11 5

Drugs which increase brain levels of serotonin (5-HT) have frequently been found to cause a decrease in voluntary ethanol consumption. Results obtained with parachlorophenylalanine (pCPA), which decreases 5-HT, have been less consistent. The present investigation compared the effects of pCPA on alcohol selection with those of pargyline, a monoamine oxidase inhibitor which increases brain levels of 5-HT. Ingestion of a 10% ethanol solution was assessed in male C57BL/6J mice given daily injections of 250 or 300 mg/kg pCPA, 50 mg/kg pargyline, or saline. An additional control group received no treatment. A two-bottle preference procedure was employed, and ethanol and water intake were recorded during a pretreatment period (11 days), a treatment period (8 days), and a posttreatment period (10 days). Like other agents which increase 5-HT, parygyline produced a depression in ethanol intake which lasted beyond the time of drug administration. pCPa had no effect on ethanol ingestion either during the period of drug administration or afterwards.
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PMID:Reduction of alcohol selection by pargyline in mice. 13 69

Hospitalized bipolar and unipolar endogenously depressed patients who showed an antidepressant response to the monoamine oxidase (MAO) inhibitor, tranylcypromine sulfate, relapsed (ie, depression returned) when relatively small doses of parachlorophenylalanine (PCPA) were added for brief periods. Considered together with our findings that PCPA similarly reversed the antidepressant effects of the tricyclic drug, imipramine hydrochloride, implications are (1) serotonergic mechanisms are likely involved in the antidepressant effects of both the tricyclic drugs and MAO inhibitors in man and (2) this indolamine may also play a role in the endogenous clinical state of depression.
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PMID:Parachlorophenylalanine reversal of tranylcypromine effects in depressed patients. 13 50


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