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)

In a 12-week controlled study ethopropazine was compared to benztropine in the treatment of parkinsonism induced by fluphenazine enanthate in 60 schizophrenic outpatients. Ethopropazine and benztropine were found to be equally effective in controlling parkinsonian symptoms and were as efficacious as procyclidine, their previous antiparkinsonian drug. However, benztropine treated patients had a significant increase in tardive dyskinesia compared to their condition during procyclindine treatment, and significantly more anxiety and depression than ethopropazine treated patients. This suggests that benztropine is not the anticholinergic drug of choice in the treatment of neuroleptic-induced parkinsonian symptoms, because of its more toxic central and peripheral atropinic effect.
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PMID:Ethopropazine and benztropine in neuroleptic-induced parkinsonism. 3 69

The clinical, pathological, and neurochemical characteristics of a newly recognized inherited neurological disorder are reported. Lethargy and mental depression are early symptoms, followed by mild parkinsonism and progressive weight loss. Failure of automatic respiratory control develops and may result in sudden death. Advanced degeneration of the substantia nigra, cell loss and gliosis of the basal ganglia, and focal gliosis in the medulla are seen on pathological study. Degeneration of the nigrostriatal dopaminergic system is evidenced by low levels of tyrosine hydroxylase, dopamine, homovanillic acid, and L-dopa decarboxylase in postmortem brain samples. Taurine concentrations in fasting plasma and CSF are somewhat depressed; brain contents of taurine are within normal limits.
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PMID:Familial fatal Parkinsonism with alveolar hypoventilation and mental depression. 4 4

The effects of the ergoline derivative, lergotrile mesylate, on the serum levels of PRL, GH, TSH, LH, FSH, cortisol, and blood sugar were studied in six normal males. The effects of lergotrile mesylate on the serum levels of GH and PRL were also studied in eight patients with acromegaly and in two with idiopathic hyperprolactinemia. In the normal subjects, 2 mg oral lergotrile lowered basal PRL levels after 90 min and markedly impaired the PRL response to TRH (200 micrograms iv); the mean peak value +/- SE was 8.3 +/- 1.1 micrograms/liter, compared to the control value of 66.6 /+- 11.3 micrograms/liter. Lergotrile raised serum GH levels in five of the six subjects to peaks of 8-49 micrograms/liter, compared to 2-8 micrograms/liter after placebo. In three subjects, the GH response to lergotrile was attenuated by the prior administration of the dopamine antagonist, metoclopramide (10 mg orally). Lergotrile had no effect on FSH and LH levels under basal conditions or after the gonadotrophin-releasing hormone (GnRH; 100 micrograms iv). Circulating TSH levels were unaltered basally but impaired after TRH. Blood sugar levels were unaltered; serum cortisol was elevated in five of six subjects; there was a brief depression of diastolic blood pressure, but no change in pulse rate. The side effects after lergotrile were variable, with drowsiness as a consistent feature. These actions are similar to those of bromocriptine (an ergot derivative treatment of hyperprolactinemia and acromegaly, to suppress PRL and GH secretion, and in parkinsonism. Therefore, it may be expected that lergotrile could fulfill these clinical uses; however, in the studies comparing the effects of single oral doses of lergotrile (2 mg) and bromocriptine (2.5 mg) on GH and PRL secretion in patients with acromegaly and hyperprolactinemia, lergotrile in the dose used has been found to have an earlier onset and shorter duration of action.
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PMID:Effect of the dopamine agonist, lergotrile mesylate, on circulating anterior pituitary hormones in man. 4 63

Forty-five patients with parkinsonism were carefully matched for age and sex with 45 chronically disabled control patients with a significantly more severe grade of physical handicap. Depression was measured by the Hamilton Rating Scale, and it was found that the parkinsonian group was very significantly more depressed than the control group (p less than 0-0001). Depression scores in both groups were unaffected by the patients's sex or by the severity of the disability. Analysis of the individual ratings of the Hamilton Scale showed that parkinsonian patients had significantly higher scores on items relating to suicide, work and interests, retardation, psychic anxiety, general somatic symptoms, and loss of insight. It was concluded that patients with parkinsonism suffer a degree of depression which cannot be solely a reaction to the stress of physical disability. This finding is discussed with reference to the monoamine hypothesis of depressive illness.
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PMID:Depression in patients with Parkinsonism. 13 Jan 80

The use of tetrabenazine to treat the movement disorder of Huntington's chorea and other dyskinesias is described. Tetrabenazine produced moderate to marked improvement in the movement disorder in 79% of a series of 40 Australian patients. The most commonly reported side effects were depression, drowsiness and Parkinsonism.
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PMID:Tetrabenazine for involuntary movement disorders. 15

An historical review is presented of the evolution of the clinical apomorphine treatment. Some of the results from the last 10 years of psychopharmacological research have led us to the hypothesis that there exists a close relationship between abstinence and craving symptoms in drug and alcohol addicts, and that anxiety, depression, and tremor symptoms in Parkinsonism (and dementia senilis), are due to disturbances of the same, mainly dopaminergic, pathways in the CNS. In such cases, by means of effective preparations for oral use, we have utilized the synergistic effect of small amounts of apomorphine, L-dopa, and decarboxylase inhibitor with considerable therapeutic effect.
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PMID:Apomorphine revived: fortified, prolonged, and improved therapeutical effect. 35 69

The present investigation examined the biochemical interaction of bromocriptine and levodopa with respect to monoamine and gamma-aminobutyric acid metabolism in the brain. Rats were treated with levodopa, 250 mg per kilogram of body weight intraperitoneally, with or without carbidopa, 25 mg per kilogram, 1 or 2 hours before sacrifice. Some were also given bromocriptine, 5.0 mg per kilogram, 4 hours before sacrifice. Rats were killed 1 and 2 hours after levodopa and brain levels of gamma-aminobutyric acid and monoamines, and their metabolites were measured. Dopamine levels and metabolism were not markedly altered when bromocriptine was added to levodopa treatment. The level of serotonin, which was reduced 25 to 40 percent by levodopa alone, was close to normal with the combination treatment. Serotonin metabolism was also enhanced by the addition of bromocriptine as shown by increased levels of 5-hydroxyindoleacetic acid. The results suggest that bromocriptine not only may improve the motor disorder of parkinsonism but also may reduce some side effects of levodopa therapy, such as depression, which could be due to serotonin depletion.
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PMID:Interaction between bromocriptine and levodopa. Biochemical basis for an improved treatment for parkinsonism. 57 99

The AA. study 60 cases of Parkinsonism treated with levodopa associated to G31,406 (dibenzazepnic derivative), to amantadine and to a placebo. Drug-associations: 1) L-dopa + G 31.406, of anticataleptic effect, probably because of its anticholinergic activity and adrenergic central and/or dopaminergic stimulating action; 2) L-Dopa + chl. amantadine; 3) L-dopa + placebo. The patients were previously under exclusive use of L-dopa. The assay verifies: a) if there is any benefit with these associations and in what proportions; b) incidence and intensity of side effects; c) comparative study. The assay also intends to evaluate the effect of the G 31.406 on the depression which usually occur in Parkinsonians.
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PMID:The L-dopa sparing effect of G 31,406 in the treatment of parkinson's disease. 79 28

Pharmaco-psychiatry has contributed to the study of mood regulation mechanisms (thymo-regulation). Anti-manic neuroleptics may induce depressions: anti-depressants may cause mood inversion (with artificial "bipolarity"), and lithium has an action upon alternating disorders of the mood. Correlations with the extrapyramidal syndromes are to be noted: parkinsonism going along with depression, and the antiparkinsonian action with the stimulation of mood. The extent of the role played by neuro-hormones, beta-inhibitors, and releasing-factors is still under discussion. The theoretical notion of mood regualtion makes it possible to single out a special type of psycho-stimulation implying manifold applications.
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PMID:[Psychotropic drugs and mechanisms of mood regulation]. 81 83

The author reviews the association between Parkinson's disease and depression and presents evidence to support the hypothesis that depression may be not only reactive but biochemically related to the disease. A psychotically depressed patient with parkinsonism responded positively to ECT as shown by improvement on a depression rating scale, two extrapyramidal rating scales, and handwriting samples. The beneficial effect on parkinsonian signs occurred before the improvement in depression, which suggests that ECT has a specific antiparkinsonian effect. Possible explanations for this observation based on biochemical theories of depression are discussed.
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PMID:Parkinson's disease, depression, and ECT: a review and case study. 83 44


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