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)

The authors compared the antimanic effects of clonidine with lithium carbonate in a double-blind crossover design with 24 volunteers. Lithium was observed to be more effective than clonidine. Some patients reported experiencing hypotension (N=8) and depression (N=7) while taking clonidine.
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PMID:Comparison of clonidine and lithium in the treatment of mania. 309 18

In our investigations on rats was proofed the qualification of substances 2-Cyanoethyl Urea (CEH), Thymus-Extract and Lithium-carbonate for a potential reducing or shortening of the leucocyte-depression after whole-body irradiation. Intravenous applications of 2-Cyanoethyl Urea in Wistar rats showed no effect not only in the increase of leucocytes but also in variation in portions of leucocytes. In our investigations we could not influence radiogenic phase of leucopenia by application of CEH after 7 Gy whole-body irradiation. Intramuscular injections of thymus extract don't influence the number of leucocytes in peripheral blood in irradiated Wistar rats. The differential blood-count was uninfluenced. Increase in concentration of thymus extract and also higher frequency of the applications effect no changes in blood-count. Leucocyte depression after whole-body irradiation was independent of the application modus of thymus extract. Lithium-carbonate shows a significant increase of leucocytes in peripheral blood in dependence of dosage and frequency of application. After whole-body irradiation with 7 Gy under lithium therapy it was shown that on day 6th after irradiation leucocyte number was significantly higher than in controls. Radiogenic leucopenia phase was reduced significantly by lithium.
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PMID:[Modification of radiogenic leukopenia]. 312 8

Lithium has been used successfully to enhance the effectiveness of tricyclic and other antidepressants, monoamine oxidase inhibitors, and combinations of antipsychotics and antidepressants. The safety and efficacy of adding lithium to the treatment regimen was examined in 14 elderly patients with refractory depression. Seven of the 14 had a complete recovery, and three showed a partial response. Side effects, including peripheral weakness, severe fine tremor, and neurotoxicity, necessitated the discontinuation of lithium in three patients. In two other patients with side effects, lower dosages of lithium relieved their symptoms. Lithium augmentation appears to be a promising treatment for geriatric depressed patients who are unresponsive to or cannot tolerate other standard therapies.
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PMID:Lithium augmentation for treatment-resistant depression in the elderly. 315 Sep 26

Five depressed patients who had shown no improvement with trials of antidepressants from several chemical families, including fluoxetine, responded when lithium was given in conjunction with fluoxetine. Lithium augmentation of fluoxetine may represent a useful strategy in refractory depression.
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PMID:Possible synergism between fluoxetine and lithium in refractory depression. 326 13

Lithium salts, in particular the carbonate and citrate, were formerly in widespread use, forming part of alkaline salt mixtures which were used for treatment of the many disorders belonging to the uric acid diathesis. Among these disorders were mania, depression, acute mania, acute melancholia and periodic depression. Satisfactory prophylactic effects on periodic depression were directly claimed. Daily doses of 3 to 26 mmol of lithium were recommended as standards. Only slight or moderate symptoms of poisoning were reported in a very few cases during the period in question (1860 to 1930), when the popularity of these lithium-containing prophylactic drugs with a favourable therapeutic index was at its peak. Lithium intoxication was not a serious clinical problem until 1949 when Cade introduced his fortuitously effective, but nevertheless high, dosage regimen which was continued until signs of recovery from mania appeared. For the maintenance dose, Cade in principle recommended, but seldom adhered to, 17 mmol/day. Chronic lithium intoxication starts insidiously with silent affliction of the kidneys followed by 'prodromal' symptoms, and when moderate severity has been reached, an accelerating renal vicious circle with decreasing kidney function is imminent. After this point the chronic intoxication resembles acute intoxication. Active detoxification at this, or an earlier stage, leaves the patient with a good chance of recovery. At a later stage, with the occurrence of oliguria, semi-coma or coma, and latent convulsive movement, recovery is less certain. There is no specific antidote for the toxic effects of lithium. Haemodialysis is the most effective treatment for acute lithium poisoning. For patients with impaired, or potentially impaired renal function, peritoneal dialysis may be an alternative, but less effective, treatment. Forced diuresis demands unimpaired renal function, and is little more effective than withdrawal of treatment, supplemented with correction of water and electrolyte balance. Sodium overloading is not recommended. Patients on lithium prophylaxis are treated on an outpatient basis. Prevention of intoxication depends on cooperation between patient and clinician, and possibly on the use of smaller, low risk dosages in most patients.
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PMID:Clinical features and management of lithium poisoning. 328 25

The therapeutic effects of lithium in depression are reviewed. The acute antidepressant effect of lithium alone is neither as impressive nor as predictable as its antimanic action, nor is it equivalent to that of tricyclic antidepressants. In patients who are 'refractory' to tricyclics or monoamine oxidase inhibitors, combined treatment with lithium may augment antidepressant response. Lithium is an effective prophylactic treatment in both unipolar and bipolar disorder and in the latter is the drug of choice. Aspects of monitoring, such as range of therapeutic plasma levels, dosage regimen and adverse effects, are discussed. Current evidence suggests that, in patients who fail to respond to lithium or are unable to tolerate side-effects, carbamazepine should be considered.
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PMID:Lithium in depression: a review of the antidepressant and prophylactic effects of lithium. 332 26

The epidemiology, pathophysiology, diagnosis and clinical features, and treatment of unipolar (depressive) and bipolar (manic-depressive) affective disorders are described. Disturbances of mood are the most common psychiatric disorders in adults, with 18-23% of women and 8-11% of men having at least one major depressive episode. Genetic factors are important in both depression and manic-depressive illness. Depression is characterized by a persistent dysphoric mood accompanied by feelings of sadness or hopelessness nearly every day for at least two weeks. The essential feature of a manic episode is an elevated, expansive, or irritable mood associated with symptoms such as hyperactivity and lack of judgment. Treatment involves nonpharmacologic and pharmacologic interventions. Psychotherapy in patients with depression is most useful in improving social functions, while antidepressant drugs reduce relapse rates. Electroconvulsive therapy is indicated in depressed patients at immediate risk of suicide or extreme incapacitation. Tricyclic antidepressants (amitriptyline, imipramine, doxepin, notriptyline, desipramine, trimipramine), second-generation antidepressants (maprotiline, amoxapine, trazodone, bupropion), monoamine-oxidase inhibitors (phenelzine, isocarboxazid, tranylcypromine, pargyline), and lithium are useful in treating patients with affective disorders. Tricyclic agents are the mainstay of treatment for depression; newer second-generation agents should be used in specific subgroups of patients. Lithium is the drug of choice for prophylaxis in bipolar patients, whereas combinations of lithium and tricyclic agents are useful during acute episodes of depression in bipolar patients. Major affective disorders occur commonly and require a careful balance of pharmacologic and nonpharmacologic interventions for proper therapy.
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PMID:Current concepts in clinical therapeutics: major affective disorders, Part 1. 351 59

The authors report two cases of Bipolar Affective Disorder which were responsive to Lithium therapy in the past, but could no longer be treated with Lithium due to hyperparathyroidism in the first case and noncompliance in the second. In both cases, successful control of hypomania was achieved with Verapamil, but treatment of depression required the addition of Trazodone. The rationale for employing a calcium channel blocking agent, such as Verapamil, in bipolar illness is reviewed.
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PMID:Verapamil in bipolar illness. 373 Oct 14

Pharmacologic agents currently used or being studied for the treatment of schizophrenia are reviewed. Neuroleptic medications are still the mainstay of treatment, but recent studies suggest new approaches to dosage and to the treatment of acute psychosis. Lithium is beneficial in psychotic illnesses with acute onset and a remitting course, regardless of the acute psychotic symptoms. Antidepressant agents may ameliorate depression in psychotic patients, but do not improve psychotic symptoms or social withdrawal. Propranolol's reported antipsychotic action has not been confirmed by controlled studies, but the drug may have a role in treating organic psychoses. The benzodiazepines, clonidine, and carbamazepine all merit more investigation as possible treatments for psychosis. The implications of differential treatment response among schizophrenic patients are discussed.
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PMID:The pharmacologic treatment of schizophrenia: a progress report. 614 Jul 50

Electrocortical and behavioral arousal are separate phenomena subserved by different neural substrata operating in parallel. A comprehensive theory of 'activation' must take into account the relationships between the electrical and behavioral activating systems. In pathological or experimentally induced states paradoxes, resolvable by a theory positing functional interaction between these systems, arise. EEG arousal is directly mediated, in both the waking and sleeping state, by cholinergic mechanisms. Antidepressant withdrawal precipitates cholinergic overdrive; this would account for the apparent disturbances of REM sleep occurring when antidepressants are stopped. Generally, cholinergic overdrive would produce behavioral inhibition but in particular instances it triggers marked psychomotor arousal by mobilizing a 'limbic activating system'. The existence of a monoaminergic 'limbic activating system', system 'A', with the properties attributed to it in this paper, is supported by both clinical and laboratory observations. System 'A' theory provides a parsimonious means of adequately explaining many phenomena. This theory also has in its favor explanatory power and scope. The Cholinergic-Monoaminergic Interaction Theory of antidepressant withdrawal induced activation and of rapidly-cycling manic-depressive illness maintains that system 'A' and a cholinergic inhibitory system interact dynamically, and that excessive monoaminergic function can precipitate excessive cholinergic function and a dearth of monoaminergic function (due to autoregulation) and hence depression. Likewise, excessive cholinergic function is posited to activate monoaminergic systems and hence to secondarily cause behavioral activation. Rapidly-cycling manic-depressive patients, according to the model, develop alternating cholinergic and monoaminergic overdrive states because the homeostatic mechanisms which should serve to maintain, within normal limits, the composite of cholinergic inhibitory and monoaminergic activating influences are defective. Consequently, rather than reaching a reasonable balance compatible with adaptive function there is oscillation between extremes. Each oscillatory movement is actually a move towards the 'golden mean' and is induced by deviation from this ideal but the defective homeostatic mechanisms promote ' perpetual ' overshooting. Lithium and ECT may be useful in the treatment of rapidly-cycling patients as both treatments may down-regulate muscarinic receptors, and otherwise modify cholinergic and monoaminergic systems in ways promoting homeostasis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Antidepressant withdrawal-induced activation (hypomania and mania): mechanism and theoretical significance. 614 95


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