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Query: UMLS:C0917801 (insomnia)
 10,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

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

The responsibility of the folate deficiency in some neuropsychiatric disorders is recent knowledge. The role of the folate on the nervous system is not yet well definite, but the action on the metabolism of the amino-acids, on the purine and the pyrimidine synthesis and on the metabolism of the catecholamins are certainly essential. The neuropsychiatric diseases secondary to the folate deficiency are numerous: dementia, schizophrenia like syndromes, insomnia, irritability, forgetfulness, endogenous depression, organic psychosis, pueperal psychosis, peripheral neuropathy, myelopathy (spinal cord syndrome and/or pyramidal tract damage), restless legs syndrome. Clinically the diagnosis may be difficult with sub acute combined degenration secondary to the pernicious anaemia, and the dosage of the folate (in serum, in red-cells and in cerebrospinal fluid) is necessary. The congenital defects in the uptake or utilization of the folate are associated with neuropsychiatric disturbances. The treatment is easy and safe if the vitamin B12 deficiency is eliminated and if employed with caution in epileptic patients because folate can induced seizures.
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PMID:[Folate and the nervous system (author's transl)]. 22 16

The first thioxanthene derivative without the double bind up to now considered mandatory for the antipsychotic effect, teflutixol, was administered in a phase II pilot efficacy trial to acute or subacute psychotic inpatients (mean age 36,1) during at least 5 weeks at a dosage of 3 to 20 mg p.d. once a day. The patients were abruptly switched from a haloperidol baseline therapy, which was administered on an average for 3 weeks at 15 mg p.d. Preliminary results are reported for the first 11 patients on a purely clinical basis. Despite the limitations of a small sample and of a qualitative analysis of data, it is hypothesized that teflutixol is a potent and original neuroleptic drug combining at 6 mg p.d. or less potent antidelusional, hallucinolytic and antiautistic effects. Latency and duration of action approximate 2 days. At 6 mg and above appear side-effects of the desinhibiting type (anxious and/or aggressive mood, withdrawal, flaring up of delusions, insomnia, agitation) and extrapyramidal side-effects of the akathisia type. No adrenolytic, anticholinergic or toxic effects were prominent. The patient followed up for the longest period (6 months on 3 mg p.d.) has not relapsed and has normal liver functions.
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PMID:[Preliminary note on the antiautistic, antidelusional and hallucinolytic effect of teflutixol (author's transl)]. 33 57

Over the years, oxazepam has distinguished itself clinically from other benzodiazepines by virtue of its excellent tolerance. Recent research suggests that this is due to metabolic and pharmacokinetic differences rather than an intrinsically more favourable toxic-to-therapeutic dosage ratio. Because of its excellent tolerance, dosage is very flexible, and it is, therefore, possible to utilize oxazepam in a wide spectrum of anxiety-related disorders including the psychoses. The use of oxazepam in anxiety neurosis, depressive neurosis, psychotic disorders, alcoholism, and insomnia is discussed.
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PMID:The clinical activity of oxazepam. 36 60

Increasing materialism in society is resulting in more wide spread nervous tension in all age groups. While some degree of nervous tension is necessary in everyday living, its adverse effects require that we must learn to bring it under control. Total tension is shown to have two components: a controllable element arising from factors in the environment and the inbuilt uncontrollable residue which is basic in the individual temperament. The effects of excessive or uncontrolled stress can be classified as 1) emotional reactions such as neurotic behaviour (anxiety hypochondria, hysteria, phobia, depression obsessions and compulsions) or psychotic behaviour and 2) psychosomatic reactions (nervous asthma, headache, insomnia, heart attack). Nervous energy can be wastefully expended by such factors as loss of temper, wrong attitudes to work, job frustration and marital strains. Relaxation is the only positive way to control undesirable nervous tension and its techniques require to be learned. A number of techniques (progressive relaxation, differential relaxation, hypnosis, the use of biofeedback, Yoga and Transcendental Meditation) are described and their application to dental practice is discussed.
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PMID:Tension and relaxation in the individual. 37 62

This study suggests that patients receiving daily doses of 40 mg of prednisone or its equivalent, are at greater risk for developing steroid psychosis. Psychotic reactions were twice as likely to occur during the first 5 days of treatment as subsequently. Premorbid personality, history of previous psychiatric disorder, and a history of previous steroid psychosis did not clearly increase the patient's risk of developing psychotic reaction during any given course of therapy. Steroid psychoses present as spectrum psychoses with symptoms ranging from affective through schizophreniform to those of an organic brain syndrome. No characteristic stable presentation was observed in these 14 cases reported here. The most prominent symptom constellation to appear some time during the course of the illness consisted of emotional lability, anxiety, distractibility, pressured speech, sensory flooding, insomnia, depression, perplexity, agitation, auditory and visual hallucinations, intermittent memory impairment, mutism, disturbances of body image, delusions, apathy, and hypomania. Phenothiazines administered in average daily doses of 212 mg produced excellent response in all patients studied. Of particular note was the fact that tricyclic antidepressants produced an exacerbation or worsening of the clinical state in all patients to whom they were administered.
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PMID:Presentation of the steroid psychoses. 43 94

The objectives of the study have been to evaluate the therapeutic efficacy of PLP 100-127 (6-(4-methyl-l-piperazinyl) morphanthridin) on patients with moderate to severe insomnia, to evaluate safety and tolerance of the drug and to investigate whether or not the drug may have dependence producing properties through the possible development of mental and/or physical dependence. A clinical-therapeutical long-term comparsion as a double blind cross-over investigation between PLP 100-127 and nitrazepan is presented. 30 patients at Gaustad hospital, mainly long-term patients with the diagnosis of schizophrenia, were selected for the trial, which lasted for 38 weeks. There were 9 drop outs, mainly due to relapse of psychotic symptoms. PLP 100-127 seems to have a favorable effect on moderate and severe insomnia in patients suffering from severe mental diseases. It seems to be well tolerated in these groups of patients. No signs of dependence producing properties have been observed by the observation method here presented.
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PMID:Clinical trial with a new substance (PLP 100-127) in order to asses therapeutic efficacy and dependence creating properties. 78 60

The difficulties of regular drug intake in long term treatments for psychotic patients gave rise to the need of using medicines at the longest possible intervals, facilitating thus adequate control and regularity. Penfluridol is a neuroleptic meeting that requirement: it is necessary only one dose per week. This paper reviews the results of Penfluridol in 26 patients (20 inpatients and 6 outpatients), ages between 17 and 54 with a mean of 36.8, sex feminine, and the following diagnoses: schizophrenia, paranoid: 14, simple: 8, hebephrenic: 3, catatonic: 1. The patients, divided in two groups of 13 each, had one oral dose a week, of between 10 and 100 mg, during 90 days. The first group took only Penfluridol, suppressing any other medicaments. The other group added Penfluridol to the prescriptions already in use. The results, as described in tables I and II, were evaluated according to 36 items. The general evaluation was positive with no negative biases. The side effects were scarce and temporary: insomnia in 7 cases during the first week, and extra-pyramidal symptoms in another 7 cases, that were controlled with antiparkinsonians. The conclusion is that Penfluridol is a valuable contribution to longterm treatments in psychoses.
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PMID:[Activity of a new neuroleptic, penfluridol (R-16341) in long-term treatments]. 98 50

A group of depressed women treated with amitriptyline was studied with particular attention to the speed of response in different symptoms of depression and in psychotic as compared to neurotic depressives. The findings showed rapid improvement in suicidal feelings, insomnia, and anorexia, but slower and more gradual improvement in impaired work and interests, retardation and pessimism and hopelessness. Psychotic depressives did not show substantial improvement until the third week of treatment whereas neurotic depressives improved markedly within the first week. It is suggested that the psychotic classification may be more useful as a predictor of speed of response than as a predictor of final treatment outcome.
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PMID:Rapidity of symptom reduction in depressions treated with amitriptyline. 111 90


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