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)

Patients meeting the social phobia criteria of the revised third edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-III-R) on the DSM-III-R Structured Clinical Interview (n = 101) entered a long-term moclobemide treatment study. These patients were treated for 2 years with moclobemide (phase I) followed by drug withdrawal, in most cases abruptly (phase II). Those who relapsed entered phase III for a further period of 2 years of treatment. During phase I 40 patients (39.6%) withdrew due to inefficacy or relapse. Two patients were removed from the study because of other diagnoses (borderline or schizophreniform). At the end of phase I the remaining patients (58.4%) were rated as not ill (45.5%) or minimally ill (11.9%). Effort was taken to achieve the maximum dose of moclobemide (750 mg/day) and the mean (+/-SD) dose was 723.3 +/- 67.7 mg/day (month 21). A marked decrease in symptoms in the patients who responded was recorded on the Liebowitz Scale for Social Phobia, Clinical Global Impressions. Hamilton Anxiety Scale and Hamilton Depression Scale. Non-response was mainly associated with co-morbidity, especially alcohol abuse, axis II disorders, and a history of major depression or secondary dysthymia. The drug was well tolerated; the more frequent side effects were mild and occurred mainly in the first 2 months of phase I, including nausea, headaches or insomnia. In phase II there was a relapse rate of 88% and 51 patients entered phase III; these patients are still being treated.
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PMID:The long-term treatment of social phobia with moclobemide. 892 15

Drug-induced parkinsonism (DIP) is frequent. The list of drugs able to induce parkinsonism is long and probably incomplete, because new drugs, with previously unknown antidopaminergic activity, are constantly being added. Not all the drugs have the same potency for inducing parkinsonism. We classify these drugs in three groups: (1) drugs with obvious antidopaminergic activity which regularly induce parkinsonism; (2) drugs able to induce parkinsonism in particular individuals and (3) drugs which may aggravate Parkinson's disease treated with levodopa. The reports of isolated cases of parkinsonism induced by widely-used drugs (drugs in group 2) may be the result of either an idiosyncratic side effect or a misdiagnosis of parkinsonism. The antidopaminergic activity of the drugs of this group is weak and not sufficiently demonstrated. Maybe, in these cases, the blockage of other neurotransmitters different from dopamine plays a role in the induction of parkinsonism. Probably, the number of patients with DIP is higher than reported or detected, because many patients suffer from weak symptoms that quickly disappear after drug withdrawal. One of the main points of interest is knowing the list, because all these drugs, specially those of group 1, should be avoided or used with caution in the treatment of some common symptomatic problems in patients with Parkinson's disease, such as depression, arterial hypertension, diabetes mellitus and cardiac disorders. The precautions should extent to other populations especially susceptible to suffer from DIP, such as the elderly or patients with other neurodegenerative disorders, such as Alzheimer's disease.
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PMID:Drugs inducing or aggravating parkinsonism: a review. 913 99

Although fluoxetine might be more effective than placebo for treating adolescent depression without major comorbidity, little is known about the response of depressive symptoms to antidepressants in adolescents with comorbid conduct disorder (CD) and substance use disorders (SUD). Male adolescents, who remained or became depressed after > or = 1 month of abstinence from abused substances during residential treatment for SUD, were treated in an open trial for > or = 7 weeks with a fixed dose of 20 mg of fluoxetine. The eight adolescents (ages 14-18 years) with CD, SUD, and major depression were not in drug withdrawal or receiving other pharmacotherapy. A > or = 50% improvement was observed in mean scores on Ten Point Depression Scale rated by clinician (p < 0.01) and patients (p < 0.01), Carroll Self-Ratings for depression (p < 0.02), and Severity of Illness scores on the Clinical Global Impression (p < 0.01). Of the eight adolescents, seven showed marked improvement and wished to continue fluoxetine after the trial. Side effects were mild and transient. No subject required dosage reduction or discontinuation of medication because of side effects. Fluoxetine appeared useful in treating substance-dependent delinquents whose major depressions persisted or emerged after 4 weeks of abstinence. These preliminary findings justify a controlled trial in such youths.
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PMID:Fluoxetine in drug-dependent delinquents with major depression: an open trial. 933 94

We investigated the sleep electroencephalogram (EEG) and the nocturnal secretion of prolactin and cortisol in 25 normal subjects and 12 male inpatients with major depression before treatment and after remission and drug withdrawal. In the depressed patients, sleep-EEG disturbances persisted after recovery, whereas the cortisol concentration decreased. Prolactin variables in the patients did not differ between the two time points (i.e. before treatment and after remission). Compared with the normal subjects, the patients had significantly higher cortisol concentrations. The above findings were not altered when age was used as a covariate in statistical analysis. Our data suggest that neither depression nor aging exerts distinct effects on prolactin secretion.
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PMID:Nocturnal secretion of prolactin and cortisol and the sleep EEG in patients with major endogenous depression during an acute episode and after full remission. 933 99

A program for withdrawal of sedative/hypnotic medication was investigated in elderly women, ages 64 to 91. The sleep cycles of 10 drug withdrawal (DW) and 10 non-drug withdrawal (N-DW) subjects were monitored for a 24-hour period for 5 successive weeks, using a nonintrusive recording procedure. The first 2 baseline weeks were followed by 1 week of half-dose, then 2 weeks of full withdrawal for the DW group. The results indicated no demonstrable effect on sleep, sleep complaints, levels of depression, or daytime sleepiness on the DW group. The conclusion is that the procedure of withdrawal from sleep medication over a 2-week period, combined with the use of a substitute pill to maintain the ritual of nightly pill-taking, is appropriate and effective for long-term elderly users.
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PMID:A procedure for withdrawal of sleep medication in elderly women who have been long-term users. 981 75

The effect of subcutaneous administration (10, 15 and 20 mg/kg body weight/day, for 21 days; and 20 mg/kg body weight/day, for 28 days) of 17 alpha-cyanomethyl-17 beta-hydroxy- estra-4, 9-dien-3-one (STS 557) on the male reproductive organs of the Parkes strain mouse was investigated. The effect of the treatment on the testis was not uniform; both regressed and normal seminiferous tubules were observed in the same section of the organ. Furthermore, the histological changes observed in the seminiferous tubules in testes of STS 557--treated mice were not different in different dosage groups. In general, in moderately affected seminiferous tubules, the germinal epithelium was thin and consisted of Sertoli cells, spermatogonia, spermatocytes and spermatids; such tubules showed presence of many vacuoles in the epithelium. In severe cases, the tubules had collapsed and were lined by mainly Sertoli cells, spermatogonia and spermatocytes. The treatment also caused marked depression in motility and concentration of spermatozoa in cauda epididymidis, weight of accessory sex glands and in the levels of sialic acid and fructose in the epididymis and seminal vesicle, respectively. By 56 days of drug withdrawal, the alterations induced in the reproductive organs returned to control levels, suggesting that STS 557 treatment induces reversible alterations in the male reproductive organs of Parkes strain mouse.
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PMID:Effect of 17 alpha-cyanomethyl-17 beta-hydroxy-estra-4, 9-dien-3-one on reproductive organs of the male laboratory mouse. 1008 81

Previous antiparkinson drug withdrawal studies involving white subjects have yielded inconclusive findings, whereas there is a paucity of data concerning Asian patients. A double-blind, placebo-controlled, randomized trial using gradual withdrawal of antiparkinson medication was conducted to evaluate the need for maintenance antiparkinson therapy for clinically stable Chinese patients with chronic schizophrenia. Seventy-five schizophrenic subjects who had received a diagnosis according to DSM-IV who had been ill for at least 5 years and on antipsychotic and antiparkinson medication for a minimum of 2 years entered the study. After baseline assessment, 58 subjects were matched according to age, sex, age at onset, length of illness, dose and length of antipsychotic and antiparkinson medication, and the presence of various extrapyramidal side effects. Randomly assigned dose-reduction and control groups were formed consisting of 29 subjects each. Trihexyphenidyl (THP), the only oral antiparkinson drug used in the study, was reduced by 1 mg every 2 weeks, whereas other psychotropic medication remained unchanged. Monthly assessment was performed using the Brief Psychiatric Rating Scale, Hamilton Rating Scale for Depression, Abnormal Involuntary Movement Scale, Simpson-Angus Scale, Barnes Akathisia Rating Scale, and the Nursing Observation Scale for Inpatient Evaluation-30. Complete withdrawal of THP was possible in 25 (90%) of the 28 subjects who completed the study, whereas considerable dose reduction was achieved in the remaining 3 subjects. There were no significant differences between dose reduction and control groups on any of the rating scales at the completion of the study. Our results suggest that long-term prophylactic administration of antiparkinson medication is unnecessary in the treatment of the majority of Chinese patients with chronic schizophrenia because withdrawal was accomplished without adverse mental or motor effects.
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PMID:Gradual withdrawal of long-term anticholinergic antiparkinson medication in Chinese patients with chronic schizophrenia. 1021 15

The symptom of "diminished interest or pleasure" in rewarding stimuli is an affective symptom of nicotine and amphetamine withdrawal, and a core symptom of depression. An operational measure of this symptom is elevation of brain reward thresholds during drug withdrawal. We report here that acute co-administration of fluoxetine, a selective serotonin reuptake inhibitor, and p-MPPI, a serotonin-1A receptor antagonist, alleviated the diminished interest in brain stimulation reward observed during withdrawal from nicotine or amphetamine in rats (i.e., increased reward). By contrast, the same drug combination treatment did not reduce the somatic signs of nicotine withdrawal indicating symptom-specific neurobiological abnormalities. Surprisingly, the same treatment had opposite effects in control rats where reductions in reward were produced, suggesting that animal models should be based primarily on studying specific deficits that are pathognomic of a psychiatric disorder. The reversal of the affective aspects of drug withdrawal by a treatment that enhances serotonin neurotransmission indicates that decreased serotonergic function may mediate the reward decrements characterizing nicotine and amphetamine withdrawal, and that these symptoms may be homologous to a core symptom of non-drug-induced depressions.
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PMID:Fluoxetine combined with a serotonin-1A receptor antagonist reversed reward deficits observed during nicotine and amphetamine withdrawal in rats. 1137 19

Clomipramine (CLI), a REM sleep suppressant, alleviates symptoms of depression in adults but produces depressive behaviors if applied neonatally. Both effects of CLI as applied to adults and to neonates have been interpreted as consequences of its involvement in REM sleep deprivation. However, the paradox of these conflicting effects remains to be understood. The current study attempts to find the possible answer by studying the effects of CLI on postnatal sleep. Eight postnatal rats were evaluated polysomnographically for nine days. Four rats were treated with CLI, 40 mg/kg/day for six days, and four rats were treated with equivolume saline during the same period. The results showed that 1) CLI treatment did not reduce the time of phasic muscle activity which appears during slow wave EEG as it did during REM sleep; 2) during treatment, rats treated with CLI had 44.66%-68.62% REM sleep reduction, varied according to age; 3) REM sleep reduction during treatment was generally compensated by non-REM sleep, so that total sleep (and wakefulness) was comparable to that experienced by rats treated with saline; 4) an obvious REM sleep rebound was observed after drug withdrawal at the age of P19. These results suggest that 1) the stage that shows phasic muscle activity simultaneously with a high amplitude EEG is not REM sleep and is likely to be independent from non-REM sleep in terms of the percentile change; 2) REM sleep reduction without a corresponding increase in wakefulness in postnatal rats is likely the mediator of postnatal RSD in the production of adult depression; and 3) the neuronal bases responsible for REM rebound function by the end of the postnatal third week.
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PMID:Clomipramine suppresses postnatal REM sleep without increasing wakefulness: implications for the production of depressive behaviors. 1190 26

Depression and suicide have been reported in association with multiple sclerosis (MS). Some studies show that interferon beta may increase the depression rate. We report a case of depression and suicidal ideation in coincidence with the start of increased doses of interferon beta-1a and their complete reversal following the drug withdrawal. The patient was a 21-year-old man with MS and no past history of affective disorders who was given interferon beta-1a in the dose of 11 microgram three times per week. As a new relapse occurred the dose of interferon beta-1a was increased to 22 microgram three times a week. The patient then observed increased worry, irritability and a sense of discouragement as well as recurring suicidal thoughts. His mood was rapidly restored following interferon beta-1a withdrawal. This case suggests that patients with MS may develop depression and suicidal thoughts when treated with high doses of interferon beta-1a.
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PMID:Interferon beta-1a-induced depression and suicidal ideation in multiple sclerosis. 1236 37


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