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)

To assess the potential hazards of flurazepam (Dalmane) therapy of insomnia in the elderly, the relation of dosage and patient age to the frequency of flurazepam-attributed adverse reactions was studied in 2,542 hospitalized medical patients. Adverse reactions, predominantly unwanted residual drowsiness, were reported in 78 flurazepam recipients (3.1%). None of the adverse reactions were serious. The frequency of reported toxicity increased with average daily dose, ranging from 1.3% among those receiving less than 15 mg/day to 12.3% at doses of 30 mg/day or more (p less than 0.001). Toxicity increased with age, progressively from 1.9% among those under 60 to 7.1% among those 80 or over (p less than 0.001). Unwanted effects of high-dose flurazepam were observed much more commonly in the elderly. Only 2.0% of those 70 years of age or older experienced adverse reactions at doses under 15 mg/day, as opposed to 39.0% at 30 mg or more per day. Low doses of flurazepam appear to be safe for elderly individuals, but they are susceptible to unwanted central nervous system depression at high doses.
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PMID:Toxicity of high-dose flurazepam in the elderly. 1 61

An uncontrolled clinical study with WIN 27,147-2 was conducted with 10 hospitalized depressed psychiatric patients. There was statistically significant improvement in the total scores of the HAM-D, BPRS and Zung; in the scores of all the factors of the HAM-D and Zung; in the scores of the anxiety/depression and activation factors of the BPRS, and in the scores of 6 of the 18 items of the BPRS. Judged by clinical global impression, 9 of the 10 patients were very much improved and 1 patient much improved. The most frequently occurring adverse effects were dry mouth, sweating, drowsiness and insomnia.
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PMID:WIN 27,147-2 in the treatment of depression. An uncontrolled clinical study. 1 70

Bipolar manic-depressive illness is a chronic disease in which patients experience recurrent episodes of mania and depression. Patients often change from a nonverbal, retarded depression of many months' duration to a hyperactive, psychotic, manic condition during the switch. The time required for the switch from depression into mania varies from 5 minutes to a couple of days. Just before it happens, pateints experience marked insomnia and decreased rapid eye movement sleep. It is hypothesized that specific changes in brain monoamine metabolism precede the switch. Alterations in neurotransmitter metabolites, as measured in urine and cerebrospinal fluid, may precede and accompany it. The switch into mania can be precipitated by environmental stresses or by drugs that act by increasing functional brain monoamines. Drugs that reverse the manic state all share the common property of affecting biogenic amines. The switch into mania is viewed in the context of a longitudinal cyclic process and may be further studied with specific pharmacologic agents that block drug-induced maniclike states in man.
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PMID:The switch process in manic-depressive psychosis. 2 15

Following 4 weeks of treatment with ORF-8063 a polyfluorinated benzodiazepine derivative, 8 hospitalized patients manifesting a primary pathology of anxiety showed marked general improvement. 2 other persons were treated, but for shorter periods: 9 and 14 days. Both are included in the pre-post analysis. Mean optimal dosage was 66.5 mg. The five instruments used to measure therapeutic effect showed pre- to posttreatment change with high level of statistical significance in serveral of the pathological factors. When measures of change are considered, patients showed more improvement related to psychic than somatic components of anxiety. Change data also indicates more patients improvement in anxiety than depression. Side effects reported more were dizziness, faintness and insomnia; these were reported in 8 patients. 6 patients noted drowsiness, and 4 noted excitement. 5 persons tolerated optimum dosages with no extreme reactions; 5 others (including the 2 subjects who terminated treatment early) were unable to maintain optimum dosages because of side effects.
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PMID:The treatment of anxiety with a polyfluorinated benzodiazepine derivative. 2 34

Sleep is affected in depression; insomnia is common, sleep of normal duration and hypersomnia less common. All-night studies have shown changes of the two types of sleep. Deep non-REM sleep is abolished during the course of the illness and sometimes also after remission. Paradoxical sleep, which may be reduced or increased in duration, starts sooner after the onset of sleep. According to Kupfler, ease of production of that sleep is specific to primary depression, unipolar or bipolar. A possible relationship between paradoxical sleep and certain types of depression is suggested by the fact that the tricyclic and MAOI antidepressant drugs and lithium reduce or suppress that sleep. Finally, deprivation of paradoxical sleep by repeated waking during the night has been put forward as a form of treatment. Despite the heterogeneous nature of depression, findings at present which show paradoxical sleep pressure provide a pathophysiological basis for the biological problems posed.
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PMID:[Depression and sleep (author's transl)]. 4 63

Intermittent hyperthyreosis occurs under various forms of stress, especially heat stress. The clinician may diagnose such cases as masked or apathetic hyperthyroidism or "forme fruste" hyperthyreosis or thyroid autonomy. As most routine and standard tests may here yield inconsistent results, it is the patients' anamnesis which may provide the clue. Our Bioclimatology Unit has now seen over 100 cases in which thyroid hypersensitivity towards heat was the most prominent syndrome: 10-15% of weather-sensitive patients are affected. The patients complain before or during heat spells of such contradictory symptoms as insomnia, irritability, tension, tachycardia, palpitations, precordial pain, dyspnoe, flushes with sweating or chills, tremor, abdominal pain or diarrhea, polyuria or pollakisuria, weight loss in spite of ravenous appetite, fatigue, exhaustion, depression, adynamia, lack of concentration and confusion. Determination of urinary neurohormones allows a differential diagnosis, intermittent hyperthyreosis being characterized by three cardinal symptoms: 1. tachycardia -- every case with more than 80 pulse beats being suspect (not specific); 2. urinary histamine -- every case excreting more than 90 mug/day being suspect. Again the drawback of this test is its lack of specificity, as histamine may also be increased in cases of allergy and spondylitis; 3. urinary thyroxine -- every case excreting more than 20 mug/day T-4 being suspect. This is the only specific test. Therapy should make use of lithium carbonate and beta-blockers. Propyl thiouracil is rarely required.
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PMID:Intermittent hyperthyreosis -- a heat stress syndrome. 5 84

St Christophers' Hospice near London is now internationally known as a special centre for the care of terminally ill patients. In these cases, the relief of symptoms is paramount, and prominent among those symptoms is pain. Such pain can almost always be relieved without euphoria or lessening of consciousness. More than 60% of patients admitted to St Christopher's complain of pain, and the scheme of management outlined below results in substantial or complete relief of pain in all of them. Addiction does not occur when control of the patient's pain is part of the pattern of total care. The author considers management of pain of varying severity, together with associated symptoms such as vomiting, anorexia, dry mouth and hiccup, dyspnoea, cough, anxiety and depression, insomnia, constipation and diarrhoea.
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PMID:Drug control of common symptoms in the terminally ill patient. 6 49

Information which has emerged thus far relates to the overall transmitter mechanisms of sleep. The data, while conflicting, point to the involvement of many neuroregulators at numerous integrative levels of the process. However the long term question still remain: what triggers and maintain sleep, what stops sleep, what occurs to the body and brain during sleep--in essence, why sleep? These questions are now problems for behavioral neurochemists, whereas in a previous era, they were problems for philosophers. Unfortunately, our answers to date, while in another idiom, have hardly been more complete or satisfying. To answer these questions, it will be necessary to understand, in detail, the manner in which neurobiochemical processes relate to the functional physiology of sleep. Although existing studies have given invaluable insight into the neurochemical anatomy of sleep, we have only recently acquired the technical and biochemical expertise necessary to investigate sleep as it occurs normally. Future research must focus on the dynamic changes associated with the regulatory mechanisms of neurotransmitters. Many questions can be asked. With sleep transitions, what changes occur in transmitter content, synthesis, or release? Are there changes in metabolic pathways, reflecting a shift from intra- to interneuronal metabolism? What changes occur in pre- and postsynaptic neurotransmitter receptors to affect sensitivity? What constraints do genetic (245) and environmental (246) factors impose upon these mechanisms? Knowledge of such parameters will allow us to construct more complete models of the neuroregulatory basis of sleep and waking. However, as we acquire this knowledge, we must avoid the temptation of assuming causation when the evidence merely shows correlation. Neuroregulation are involved in the control of number different behaviors; and, at present, we have few, if any, methods of establishing causative links between a specific neuroregulator and a specific behavioral state. Yet, even without an understanding of what "causes" sleep, we may be able to develop pharmacological agents which permits discrete alteration of sleep mechanisms in a more physiological and specific manner. This potential for manipulation of sleep is of obvious importance in illnesses such as insomnia, narcolepsy, and sleep apnea (247, 248). In addition, it may be valuable in the treatment of such conditions as psychosis and depression, where sleep disturbances are an important component of the illness. For example, delirium tremens might be best understood as a psychotic episode which is the result of an aspect of sleep emerging into wakefulness. The range and breadth of both the basic questions and the potential application of sleep research portend an exciting future for this field.
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PMID:Neuroregulators and sleep mechanisms. 16 54

Sleep is a vital human physiologic process. Insomnia can be caused by obsession and depression states, pain, or worry over everyday problems. Because of their pharmacologic action, alcohol and high doses of soporifics used as remedies may produce REM-deficit sleep and actually prolong insomnia. If the true cause of sleeplessness is not recognized and properly treated, insomnia may develop into a severe sleep problem. Since benzodiazepines and chloral hydrate do not suppress REM sleep, they are the medications of choice in the therapy for insomnia.
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PMID:Insomnia and the physiology of sleep. 20 31

Thirthy-three alcoholics, aged between 31 and 82 years, were treated for 7 to 30 days with tiapride. The dosage was 600 mg/day (200 mg 3 times daily) by mouth or 100 to 800 mg/day I.M. Out of 27 cases of tremor treated, there were 25 favourable results, one average result and one nil result. Insomnia and character disorders, e.g. anguish, depression, nightmares, hallucinations, were improved during the first few days of treatment in 27 cases out of 30. Out of 12 cases of algo-paresthesia of the lower limb treated, the were 9 good or excellent results, 2 average results and 1 nil result. A favourable result was observed in 7 cases out of nine in vomiting, water brash (3 cases out of 4), and in 16 cases out of 20 in anorexia. No clinical or laboratory disturbance attributable to tiapride was noted in our patients whose general health was often very poor.
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PMID:[Tiapride and alcoholic disorders of central origin. Apropos of 33 cases]. 21 35


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