Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917801 (insomnia)
 10,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oxilorphan (levo-BC-2605) is a new, long-acting, narcotic antagonist that has agonist properties. Twenty-one (21) heroin addicts in Los Angeles were detoxified and given at least one oral dose of oxilorphan. Only three (14.3%) patients took daily doses for 14 days, which was the maximal time allowed for oxilorphan administration in this study. The remainder discontinued oxilorphan because of subjective side effects or for unknown reasons. Side effects most responsible for dropouts were dysphoria, insomnia, weakness, hallucinations, nausea, drowsiness and anorexia. Oxilorphan provided 24-hour protection with a single, oral dose, but subjective side effects encountered during inductiolinical trials with oxilorphan should be attempted with other addict populations to fully determine its potential therapeutic value.
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PMID:Clinical trial in post-addicts with oxilorphan (levo-BC-2605): a new narcotic antagonist. 1 84

It was hypothesized that the metabolic effects of caffeine, which can be objectively measured (i.e. physiological, "arousal"), could be used to develop a physiological arousal model of chronic insomnia in a group of normal young adults. Twelve normal young adult males participated for 11 nights after laboratory adaptation. Subjects received 400 mg of caffeine three times a day for 7 nights and days. As predicted, the use of caffeine resulted in increased metabolic rate. Sleep efficiency was significantly reduced by caffeine and multiple sleep latency tests (MSLTs) were significantly increased. Some adaptation to the metabolic, sleep efficiency, and MSLT effects of caffeine was seen over the week of administration. Withdrawal effects (i.e. rebound sleep or sleepiness) were not seen for metabolic, MSLT or sleep variables. The data indicated that caffeine was effective in producing significant metabolic and sleep effects and that those effects were related. The results were consistent with the interpretation that a chronic decrease in sleep efficiency associated with increased physiological arousal, although producing subjective dysphoria, does not produce a physiological sleep debt.
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PMID:Caffeine use as a model of acute and chronic insomnia. 147 67

Factor structures of the 60- and 30-item versions of the General Health Questionnaire (GHQ) were explored, using data collected from 236 Japanese high-school and university students. The 60-item version produced factors interpretable as social functioning, anxiety, somatic symptoms, and severe depression; the 30-item version produced general dysphoria, social functioning, depressive thoughts, difficulty in concentration and insomnia. Although the two versions of the GHQ produced the same number of factors, their structures differed in content. Thus it may be necessary to examine the factor structures of the GHQ when using it in a study of a population containing subjects with different cultural backgrounds.
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PMID:The factor structure of the General Health Questionnaire in a Japanese high school and university student sample. 191 76

Seventeen patients with acute mania were treated with the antiepileptic agent valproate under placebo-controlled, double-blind conditions for 7 to 21 days. No other psychotropics were allowed, except for lorazepam, up to 4 mg per day, as needed for agitation or insomnia for the first 10 study days only. Of the 17 patients, 12 (71%) showed some response, ranging from a 30 percent to a 100 percent decrease in scores on the Young Mania Rating Scale (MRS). The remaining 5 patients displayed no response to valproate treatment, with increases on the MRS of 3 percent to 13 percent. Compared with nonresponders, responders had an older age of onset and a shorter duration of illness and displayed a higher average serum valproate concentration on Study Days 3 through 6, but not on Study Day 15 or at termination. Degree of valproate response was greater for those patients with more severe sleep disruption at baseline. However, the majority of factors assessed, including a history of rapid cycling and high levels of dysphoria, were not associated with response to valproate.
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PMID:Correlates of antimanic response to valproate. 192 58

Four hundred seventy-nine drug abusing adolescent patients enrolled in seven Straight, Inc. Adolescent Drug-Abuse Treatment Programs in five geographic regions across the United States were studied to determine the severity and patterns of cocaine abuse. Of these, 341 admitted to cocaine use and became part of this survey. Cocaine use was categorized as heavy, intermediate, or light. Areas examined were the addictive spectrum, psychosocial dysfunction, and psychiatric symptoms. Intermediate and heavy users of cocaine abused significantly less marijuana and inhalants than light cocaine abusers. Heavy and intermediate users were more likely to use cocaine intravenously and to use crack. They developed tachyphylaxis more frequently, progressed to weekly use in less than 3 months more frequently, and became preoccupied with obtaining and using cocaine significantly more frequently. They used more sedative hypnotics to calm themselves and engaged in more criminal behavior, such as stealing from parents and stores and passing bad checks. They had more arrests for possession of drugs, stole more cars, sold more drugs, and were more likely to trade sexual favors to obtain the drug. Heavy and intermediate users were significantly more psychiatrically disturbed than light users, becoming more suspicious, nervous, aggressive, and demonstrating increased symptoms of fatigue, sleeplessness, decreased appetite, and increasing cocaine dysphoria. All of these symptoms could be mistaken for psychiatric disorders. This study suggests that cocaine is as addictive in adolescents as in adults; possibly more so. It also causes psychosocial dysfunction and psychiatric symptoms. Further research into cocaine addiction among adolescents is indicated.
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PMID:Adolescent cocaine abuse. Addictive potential, behavioral and psychiatric effects. 258 95

Masked depression refers to a concept of a phenomenological state, either endogenous or psychogenic where somatic symptoms replace sadness: Thirty patients were evaluated by RDC (22 endogenous and 8 masked depressions) wherein in the latter dysphoria was replaced by a nonreactive persistent somatic complaint. They were rated on Beck and Hamilton Depression Scales, on Hamilton and Trait-State Anxiety Scales and the NOSIE. All patients presented with insomnia, anorexia, loss of weight, diminished libido and anhedonia. Initial ratings were similar for both diagnostic groups except for a significantly higher agitation factor and lower retardation in masked depression. Although 59.9 percent of the subjects are positive on the dexamethasone test, only 1 masked depression did not suppress secretion of cortisol. After a randomized 30-day drug trial where patients were assigned to Clomipramine or Desipramine, patients in both groups show significant improvement on rating scales but diagnostic group drug treatment interaction exists on anxiety and agitation criteria.
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PMID:[Comparison of masked and endogenous depression using psychometric scales, endocrinological markers and pharmacological responses. Masked depression versus endogenous depression]. 309 93

Metoclopramide, a substituted benzamide derivative, was orally administered to a patient with intractable hiccups. Dysphoria, akathisia, depressed mood with suicidal ideation, insomnia, racing thoughts, and labile affect were seen following the administration of metoclopramide. The episode met criteria for an organic affective syndrome. It is suggested that the mental status of patients undergoing metoclopramide therapy be monitored, since these symptoms have not been previously reported.
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PMID:Organic affective syndrome associated with metoclopramide: case report. 395 83

Eleven patients suffering from chronic insomnia were given 30 mg flurazepam for 28 nights. While EEG measures of total sleep time and sleep efficiency were improved, changes in sleep latency and intermittent waking time were small and nonsignificant. Subjective benefits in sleep were confined to the first 2 nights. There was neither increased nor decreased daytime sleepiness. Cognitive functioning was significantly decreased during the first 2 days, and patients were unaware of these changes. Simple motor tasks were relatively unaffected. Desalkylflurazepam concentrations showed significant accumulation over time, but were not predictive of sleep measures or daytime performance in individual subjects. The withdrawal period was characterized by subjectively disturbed sleep and daytime dysphoria.
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PMID:A clinical study of flurazepam. 676 26

Sleeplessness and resting pulse rate were studied in relation to behavioral treatment of 34 chronic psychotics using an 18-week ABAB research design. These arousal measures, unrelated in the base line, showed significant opposing changes during four of the first ten treatment weeks. Sleeplessness improved proportionately with clinical response, gauged by social participation, whereas pulse rates were significantly exacerbated early in treatment. When treatment was withdrawn and reinstated, pulse rates correspondingly decreased and increased significantly. These results suggested that arousal changes transcend specific drug action and are a consequence of treatment -- possibly a hindrance -- rather than its source. The systematic differences supported a distinction between two arousal processes, on responsive and one resistant to treatment. It was proposed that the elevation of autonomic arousal with treatment may reflect dysphoria from threat to psychotic homeostasis and consequent therapeutic resistance. Implications were drawn regarding clinical intervention with poor prognosis psychotics, a two-factor model of arousal disorder, and a nonunitary approach to arousal research.
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PMID:Disjunctive arousal changes as a consequence of nondrug clinical intervention. 722 74

In a double-blind, placebo-controlled study, the therapeutic efficacy of two antidepressants with different neurochemical mechanisms of action, amitriptyline and amineptine, was investigated in patients affected by anxious depression. Sixty-six patients with the primary diagnosis of major depression or bipolar affective disorder (DSM-III-R) and meeting additional operational clinical criteria such as anxiety, trepidation, restlessness, early and/or late insomnia, impulsivity, hostility, dysphoria, compulsivity, hyperperspiration, palpitation, pollakiuria and phobias were included. They were randomly assigned to three groups (n = 22) and treated either with placebo, amitriptyline (up to 100 mg/day) or amineptine (up to 200 mg/day) for 6 weeks. Patients showed better response to amitriptyline, a preferential inhibitor of serotonin reuptake, than to amineptine, a selective inhibitor of dopamine reuptake. The present results suggest that alterations in serotonergic rather than dopaminergic transmission contribute to the pathophysiology of anxious depression.
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PMID:Comparative effects of amitriptyline and amineptine in patients affected by anxious depression. 760 61


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