This multicenter study compared the efficacy and safety of citalopram and placebo in a population of moderately to severely depressed patients with melancholia. This randomized, double-blind, parallel-group study compared citalopram (flexible dose; 20-80 mg/day) with placebo in 180 psychiatric outpatients with a DSM-III diagnosis of major depression or bipolar disorder, depressed, who also met DSM-III criteria for melancholia. Following a 1-week placebo washout period, patients meeting study entry criteria were randomized to 4 weeks of double-blind treatment with either citalopram or placebo. Efficacy measures included the Hamilton Rating Scale for Depression (HAM-D), the Clinical Global Impressions (CGI) Scale, and the Zung Self-Rating Depression Scale. Patients treated with citalopram showed significantly greater improvement at endpoint than placebo patients on the HAM-D, CGI, and Zung scales. On the HAM-D, citalopram patients exhibited significantly greater improvement than placebo patients after 1 week of double-blind treatment and at all subsequent study visits. Endpoint analyses of the HAM-D subscales demonstrated that citalopram produced significant improvement of the psychomotor retardation, cognitive disturbance, sleep disturbance, and melancholia symptom clusters. Nausea, dry mouth, somnolence, dizziness, and increased sweating were reported at higher rates by citalopram-treated patients than by placebo-treated patients, but there were no significant citalopram-placebo differences in the incidence of activation (e.g., anxiety, nervousness, insomnia) or sexual dysfunction. Analysis of electrocardiograms, vital signs, and laboratory tests did not reveal any clinically significant effects of citalopram treatment. The results of this study indicate that citalopram is safe and effective in the treatment of depressed patients with melancholia, and is associated with a favorable side effect profile and a potentially rapid onset of action.
Since 1948 a number of papers published in Great Britain have demonstrated the feasibility of studying the incidence and prevalence of both major and minor psychiatric disorders in general practice (3, 4, 7, 8, 10, 11, 14, 16, 17, 18). Few, however, have focused on the health of West Indian immigrants in Great Britain, some 125,000 of whom have entered the country since that time (2, 12, 13, 20). This paper reports on the results of a six-month psychiatric morbidity survey of a group general practice in Brixton, the main purpose of which was to collect and compare data on the illness and consultation patterns of West Indian and English patients attending the same general practice.
The cardiovascular effects of bupropion hydrochloride and nortriptyline were compared in a double-blind, randomized, 6-week trial in adult outpatients with major depression. After a 1-week placebo phase, 58 patients were randomized to treatment with bupropion (225-450 mg/day) and 57 to nortriptyline (75-150 mg/day). Nortriptyline-treated patients had statistically significant heart rate increases at each assessment as determined by RR intervals on electrocardiogram (14.5-18 bpm). Bupropion-treated patients had small but statistically significant increases in supine diastolic blood pressure of 5.6 mm Hg on day 7 and 7.5 mm Hg on day 28. A few patients in each treatment group had orthostatic changes, but only nortriptyline-treated patients had symptomatic orthostatic hypotension. A slowing of cardiac conduction and possibly of rate-corrected repolarization occurred in patients treated with nortriptyline that did not occur in patients treated with bupropion. Compared to nortriptyline, bupropion appears to have a wider safety margin with regard to cardiovascular effects. This may be particularly true in the elderly, in patients with preexisting cardiovascular disease, or in overdose.
To compare the safety and efficacy of paroxetine (n = 167) and placebo (n = 169), data from 4 centres using the same protocol were pooled. A double-blind parallel group design was used, with therapy lasting 6 weeks. Significant differences between paroxetine- and placebo-treated patients were found on the major efficacy outcome variables by week 2 and on all efficacy variables by week 4 of the study. Improvement on the sleep factor of the Hamilton Rating Scale for Depression was found after 7 d. Observer and patient global efficacy ratings were in agreement by week 4. No serious adverse events occurred, and paroxetine had no clinically significant effects on vital signs or laboratory safety data. Side effects were more common on paroxetine and were similar to other serotonin reuptake inhibitors. In general, these were well tolerated and did not lead to dropout. Symptoms of increased arousal were not seen during early therapy.
In a multicenter, placebo-controlled, clinical trial, the efficacy of Limbitrol was compared with that of its components, amitriptyline and chlordiazepoxide. All patients had a diagnosis of primary depression. Data from 279 patients were evaluated using the Hamilton depression scale, the Beck depression inventory, and physician and patient global change measures. Statistically significant differences favoring Limbitrol occurred after 1 week of treatment, and a trend in favor of Limbitrol continued throughout the remaining 3 weeks. In most efficacy comparisons, the combination was as good as, or better than, amitriptyline alone. It was superior to chlordiazepoxide alone after 2 and 4 weeks of treatment. Each component produced an independent contribution to the total therapeutic effect: the chlordiazepoxide effect was more prominent in the first 2 weeks and the amitriptyline effect in the latter 2 weeks. A trend favoring amitriptyline over chlordiazepoxide was evident by week 4. The overall incidence of side effects was comparable in both Limbitrol- and amitriptyline-treated groups. Limbitrol-treated patients exhibited more sedation, but significantly fewer Limbitrol patients discontinued treatment prematurely because of side effects.
Psychiatrists have for long paid attention to mental illness in different communities and cultures. In Java, Kraepelin noted that melancholia and mania were rare and that depressive reactions rarely contained elements of sinfulness (9). Later, Bleuler commented upon differences between English and Irish patients and between Bavarian and Saxon patients (2). Others have described various “culture-bound” syndromes such as amok, the windigo psychosis of the Cree, Salteaux and Ojibwa, latah and Arctic hysteria (23, 5, 8, 11, 26). More recently Tooth has described a special category of “delusional” states in West Africans while Carothers has reported on “ill-defined” states and “primitive” psychoses among the West Africans (22, 4). Other workers have stressed the significance of cultural factors in the distribution of mental illness. Seligman noted in 1929 that confusional states were more common than systematized insanities among the Papuans of New Guinea and could not find any cases of manic depressive illness (17). Berne noted that toxic confusional psychoses rather than the schizophrenias were the predominant illness among hospitalized Malay (1). Carothers related Westernization to an increase in manifest paranoid behaviour among patients in Kenya (4). Similarly Spiro noted that the Ifaluk in the Carolines had violent paranoid outbursts only after Japanese occupation and Slotkin emphasized the paranoid schizophrenia phenomena among acculturated Menomini (20, 19). Opler found that lower class Filipinos had a high proportion of affective disorders and catatonic confusional states among the Hawaiian hospitalized, while Carothers and Tooth in Africa both found statistically low incidences of depression and suicidal states with relatively high rates of confusional states among African natives (13, 4, 22).
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.