Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The authors review the literature describing acute symptomatology produced by the gradual or abrupt withdrawal of heterocyclic antidepressants, monoamine oxidase inhibitors (MAOI) and neuroleptics. 2. Withdrawal of heterocyclic antidepressants and antipsychotic agents causes similar symptomatology. Symptoms produced by the discontinuation of these drugs include nausea, emesis, anorexia, diarrhea, rhinorrhea, diaphoresis, myalgias, paresthesias, anxiety, agitation, restlessness, and insomnia. 3. Psychotic relapse is often presaged by anxiety, agitation, restlessness, and insomnia. Prodromal symptoms are distinguished from the effects of neuroleptic withdrawal by a temporal relationship of the latter to reductions in the dosage or discontinuation of antipsychotic agents. 4. Withdrawal of MAOIs can result in severe anxiety, agitation, pressured speech, sleeplessness or drowsiness, hallucinations, delirium, and paranoid psychosis. 5. MAOI withdrawal phenomena resemble the symptoms produced by the discontinuation of chronically administered psychostimulants. 6. The capacity of MAOIs to exert amphetamine-like effects presynaptically and the propensity of somatic treatments for depression to subsensitize presynaptic receptors regulating the release of catecholamines provide a basis for the development of psychotic symptoms upon the withdrawal of MAOI. Evidence for this hypothesis is reviewed.
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PMID:Heterocyclic antidepressant, monoamine oxidase inhibitor and neuroleptic withdrawal phenomena. 196 71

Depression is a common complication of anxiety disorders. Major depressive disorder may be the primary diagnosis, the patient having been unaware of depressed affect until anxiety became less prominent. Depression may also be a comorbid condition, appearing because anxiety lowers the threshold for its development or as a result of use of central nervous system depressants or intercurrent medical illnesses. Depression may also be a response to psychosocial consequences of anxiety or its resolution. In some anxious patients, depression is a later stage in the development of a dysregulated stress response. Initial treatment of depression involves therapy for organic causative factors and psychosocial problems. Medications that may be useful for both depression and anxiety include cyclic antidepressants, monoamine oxidase inhibitors, and possibly azapirones and benzodiazepines. Combined anxiolytic-antidepressant treatment may be necessary for some patients.
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PMID:Understanding and treating depression in anxious patients. 197 23

Modern treatment of mental depression started with the availability of monoamine oxidase (MAO) inhibitors and tricyclic antidepressants. These drugs also contributed to the early development of psychopharmacology. Attempts to improve the anti-tuberculous action of the hydrazine derivative isoniazid by developing derivatives thereof led to the synthesis of iproniazid. Its introduction as the first modern antidepressant was based on three unexpected actions of the drug: MAO-inhibition, 'reversal' of reserpine-induced sedation, and the presence of psychostimulation as a clinical side effect in man. However, the initial success of iproniazid and other MAO inhibitors, hydrazides and non-hydrazides, was curtailed by the occurrence of undesirable side effects such as potentiation of the blood-pressure elevating action of food amines. The tricyclic antidepressants were a development of the class of antihistamines, one of which, chlorpromazine, showed neuroleptic activity. A congener of this compound, imipramine, was discovered by clinical observation to have unexpected antidepressant effects. The clinical success of this drug (which is still in use) led to the development of a successful series of other tricyclic and non-tricyclic antidepressants. Progress in the elucidation of possible mechanisms of the action of the tricyclic compounds has helped this development. Recent advances in basic research have also induced a revival of MAO-inhibitors since, due to the discovery of MAO-subtypes, inhibitors with higher specificity and fewer undesirable side effects are now available.
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PMID:The discovery of antidepressants: a winding path. 199 42

We employed a study design that permitted a double-blind 12-week contrast of imipramine hydrochloride and phenelzine sulfate therapies in patients who met Columbia University criteria for atypical depression and were unresponsive to 7 weeks of treatment with placebo. These patients were found to benefit selectively from therapy with monoamine oxidase inhibitors compared with tricyclic drug therapy. This supports our observation about treatment response in depressed patients with reversed vegetative features. The design we utilized in this study has not previously been reported, to our knowledge. It was hypothesized that it would offer the advantage of the removal of a portion of placebo responders and serve to replicate our original findings. Treatment response to therapy with both imipramine and pheneizine in placebo nonresponders was uniformly lower (roughly 20% less than corresponding rates for patients who did not participate in the initial 6-week placebo trial). This is consistent with the view that the lower response rates were a result of the removal of some "placebo" responders in the drug groups. We think this is a useful design that should be considered in all studies of placebo and two active treatment regimens.
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PMID:Response to phenelzine and imipramine in placebo nonresponders with atypical depression. A new application of the crossover design. 200 33

The clinical significance of chronic mild depression (dysthymia) is well recognized, but has not been the focus of extensive research. In particular, basic research on the phenomenology and treatment of these conditions is limited. Clinical lore suggests that psychotherapy, rather than pharmacotherapy, is the treatment of choice. This is based more on a theoretical understanding of chronic depression as a personality disorder rather than on actual treatment studies. This paper reviews the literature on the pharmacotherapy of dysthymia. The results provide substantial evidence for the efficacy of antidepressants in dysthymia, although the treatment response is less than that typically found in major depression. Furthermore, the findings suggest the possibility that monoamine oxidase inhibitors (MAOIs) may be superior to tricyclic antidepressants (TCAs) in the treatment of dysthymia, although this needs to be more rigorously evaluated. Some of the methodological problems with these studies are discussed. Additional areas of research, including the clinical and biological indicators of drug response, the use of non-TCA, nonMAOI drugs, the effects of pharmacological intervention on the development and maintenance of chronicity, and the comparison of and interaction between pharmacotherapy and psychotherapy are identified and suggested for future study.
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PMID:Pharmacotherapy of dysthymia: a review. 205 46

Lithium carbonate is the drug of choice for the management of bipolar disorder, but 20% to 40% of patients do not exhibit adequate response to this agent. Moreover, adjunctive therapy with tricyclic antidepressants and monoamine oxidase inhibitors (for depression) and neuroleptics (for mania) is widely prescribed in most lithium clinics. These agents, however, may precipitate or exacerbate the subsequent phase of the illness. More recently, carbamazepine, an anticonvulsant drug, has shown promise in the management of bipolar illness. Used either alone or in combination with lithium, carbamazepine has been associated with a response rate of approximately 65% in more than 500 patients enrolled in controlled and uncontrolled studies. The drug's antimanic effects have been clearly demonstrated, but its antidepressant effects must undergo further examination. Other anticonvulsants (such as valproate) appear highly effective. The high-potency benzodiazepines (such as clonazepam) and calcium channel blockers (such as verapamil) are also being evaluated in this patient population.
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PMID:Non-lithium treatment for bipolar disorder. 211 6

Fluvoxamine, a potent and selective serotonin uptake inhibitor, effectively reduced compulsive handwashing and other rituals in a patient previously refractory to behaviour therapy, clomipramine, MAO inhibitors and other pharmacotherapy. Treatment effect was delayed but broadly patholytic, reducing anxiety and depression scores as well as ratings of obsessiveness.
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PMID:Successful fluvoxamine treatment of a case of refractory obsessive-compulsive disorder. 212 85

The effect of moclobemide, a short-acting, reversible, preferential type-A MAO inhibitor (300 mg daily in three divided doses), on the sleep of eight depressed patients was assessed by polysomnographic recordings in a 4-week therapeutic trial. Six patients showed an improvement greater than 50% on the Hamilton Depression Rating Scale. Compared to placebo, patients receiving moclobemide showed improved sleep continuity as judged by the decrease in wake time after sleep onset and total wake time, particularly during the intermediate and late stages of drug administration. Total sleep time increase was comprised of larger amounts of stage 2 NREM sleep. REM sleep latency was significantly increased and REM sleep % decreased during the drug administration period. However, in contrast to the older, non-selective and selective MAOIs, moclobemide had a mild REM sleep suppressant effect.
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PMID:The effects of moclobemide on nocturnal sleep of depressed patients. 214 41

The evidence that catecholestrogens are formed in the brain and exert behavioral effects in animal models suggest that these steroids might have psychotropic activities. In the present investigation, the formation and metabolism of catecholestrogens were studied in depressed patients. Twenty-four-hr urine samples were collected from 6 male patients (59 +/- 8 years) with endogenous retarded depression (subtype primary, endogenous, and recurrent according to Research Diagnostic Criteria) and from 12 male control subjects (51 +/- 4 years). The patients were treated with the monoamine oxidase inhibitor tranylcypromine (10-40 mg/day for 3-4 weeks). The concentrations of primary estrogens, 4- and 2-hydroxyestrogens and 2-methoxyestrogens, were measured in the urine samples after multiple chromatographic separation steps by radioimmunoassay. In the depressed patients, the excretion rates of 4-hydroxyestrogens were significantly lower than in control subjects. The ratio 2-methoxyestrogens:2-hydroxyestrogens as an index for 2-O-methylation was 3.8 +/- 1.6 in patients and 1.8 +/- 0.7 in controls. The increased methylation and reduced 4-hydroxylation rates of patients were not affected by treatment with tranylcypromine though the psychopathological state was improved by 46%. Therefore, it seemed unlikely that the observed alterations were pathognomonically relevant in these depressed patients. The alterations in the formation and methylation of catecholestrogens show that the depressed patients exhibited remarkable metabolic disturbances. The functional role of these disturbances remains to be clarified.
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PMID:Formation and metabolism of catecholestrogens in depressed patients. 217 30

Platelet imipramine binding was measured in 25 unmedicated depressed patients and 25 age- and sex-matched healthy controls. In the patients, the measurement was repeated after 3 weeks and 2 months of imipramine treatment leading to clinical recovery. No significant differences in imipramine binding were found between controls and unmedicated patients. In the latter, imipramine administration produced a progressive change in the binding characteristics, increasing the apparent Kd and decreasing the number of binding sites (Bmax). The results suggest that platelet imipramine binding is not altered in depression and that changes in this parameter are the consequence of the presence of imipramine in the blood stream. However, such changes accompany changes in other biological parameters, such as platelet monoamine oxidase and serotonin uptake, seen in the same patients throughout imipramine treatment, suggesting that the drug acts on a wide range of normal or altered serotonin-related cellular mechanisms while it accelerates the clinical recovery from depression.
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PMID:Platelet imipramine binding in endogenous depressed patients and controls: relationship to platelet MAO and 5HT uptake during successful imipramine treatment. 217 40


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