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)

Forty-one patients completed the study where Visken was added to the treatment regimen of patients whose blood pressures were poorly controlled on methyldopa or who were experiencing side-effects with methyldopa. Supine blood pressure was reduced from 177/108 mm Hg before Visken therapy to 159/96 mm Hg after twelve weeks of taking Visken. The dose of methyldopa was reduced from a mean 921 mg at the start to 445 mg at the end. Fourteen patients were able to stop methyldopa therapy. The number of side-effects reported was reduced as the study continued and fifteen patients commented that they felt better on Visken. Nine patients did not complete the trial, three of these because of side-effects, viz insomnia, lethargy and sleep disturbances.
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PMID:The addition of Visken to methyldopa therapy in hypertension: a multicentre study. 102 42

An electro-behaviour dissociation was described, at first by animals next about the man, in experiment testing and in the drug addictions. This non concordance appear as lesser if it is be considered not only the sleeping waves but also all the electrical signs of the vigil state: non-existent, fluctuating, limited in topography, behind the stimulation, incomplete or emphasized. In this view we study some pathological states: narcotic and alcoholic addictions, confusion and pre-senile illness. Sometimes it is the abnormal sleep (coma or amazement) which alter the vigil state: absent, decreased, etc. Sometimes the vigilance is "numbed", the behaviour and the recording are those of lethargy. Sometimes also, the drowsiness has insomnia characteristics, associating a deep sleep loss, a reactivity to stimulations at once emphasized and undiscriminated, and "strangeness" insurmontable for the consciousness (perplexity, delusions, nightmare and level anomalies).
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PMID:[Alterations of arousal in some psychopathologic states]. 134 49

A new antidepressant Fluoxetine, a serotonin re-uptake inhibitor, was tried on 26 resistant depressed patients. There were four drop out due to severe side effects. Improvement was noticeable soon after the first week and was maximum within 3 weeks of medication in 14 (63.6%) patients while in 8 (36.4%) patients it was as late as 6-12 weeks. The decline in improvement after three weeks in 7(31.8%) patients, needs attention in future studies. Bradycardia in 2 patients above the age of sixty indicate that the drug should be used with caution in elderly. GIT disturbance, insomnia, anorexia, restlessness and lethargy were common side effects. A well planned double blind study is recommended before its place is assigned in our patient population.
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PMID:Early experience with fluoxetine. 176 70

The cases presented here, along with a preliminary body of clinical literature, suggest that, in conjunction with other factors, cyclosporine has an etiologic role in the production of a variety of organic mental disorders, including delirium, generalized anxiety disorder, hallucinosis, and organic mood disorder-depressed. The cases in this report were chosen in part because they illustrate definable organic syndromes. Other transplant recipients may experience less severe or isolated symptoms, such as sleep-wake reversal, insomnia, anxiety, lethargy, or mild confusional states that do meet full criteria for organic mental syndrome but that appear to be related to cyclosporine. Persecutory delusions may also occur in both floridly delirious patients and in patients with only minimal disorientation. Mental state aberrations most commonly begin within 2 weeks of treatment with cyclosporine, and, frequently, most acute symptoms resolve within a few weeks of onset. However, in more severely delirious patients or in patients with medical courses complicated by other problems, symptoms may continue longer. In particular, difficulties with memory and with the acquisition of new information may persist for several weeks. Less commonly, mental syndromes may also occur following longer periods of treatment with cyclosporine. Individual vulnerability appears to vary widely, and many patients demonstrate mental complications at cyclosporine levels that are in the moderate therapeutic range for immunosuppression. In addition, patients who have recently been started on cyclosporine and who demonstrate high therapeutic, rapidly rising, or toxic serum levels may be at greatest risk. Other risk factors may include intravenous administration, hypomagnesemia, hypocholesterolemia, and concurrent methylprednisolone bolus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cyclosporine-associated organic mental disorders in liver transplant recipients. 200 44

A young, previously healthy woman presented with increasing muscle pain, lower limb swelling, fatigue and eosinophilia. She had consumed L-tryptophan tablets (one to two at night) over the preceding five months for management of her insomnia. Her condition slowly deteriorated and she developed generalised oedema and severe lethargy. A white blood cell count was 21.3 x 10(9)/L with 43% eosinophils (Normal range: 4.0-11.0 x 10(9)/L with 1-6% eosinophils. A biopsy specimen of the deep fascia and gastrocnemius muscle demonstrated fasciitis and myositis. The patient failed to recover after cessation of L-tryptophan use but her condition improved rapidly without significant sequelae after systemic treatment with corticosteroids.
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PMID:Eosinophilia-myalgia syndrome associated with L-tryptophan use. 199 19

Hartnup disease is an inborn abnormality of renal and intestinal transport involving the neutral amino acids. Intermittent pellagra-like rash, attacks of cerebellar ataxia and psychiatric disturbance are characteristic symptoms of this disease. We described here a patient with adult-onset Hartnup disease who presented unique neuropsychiatric symptoms but no dermatologic symptoms, and reported features of amino acids transport in this patient and his family. The patient, a man aged 37 years, was referred to us because of lasting daytime bruxism. He is the second child of healthy parents who are first cousin; his elder brother who has been mentally retarded became bed-ridden and died at 32 years of age. His younger brother is completely healthy. Although the patient's development in infancy has been slightly retarded, he completed compulsory 9-year education. At 29 years of age, he experienced episodes of diplopia, ataxic gait and insomnia, and at 33 years of age, of transient stupor. There had been no history of photosensitivity or dermatitis. On neurological examination, there were trunkal ataxia, increased muscular tone and decreased mental activity besides bruxism. These symptoms remained unchanged despite of several medications including trihexyphenidyl, diazepam, halloperidol, tiapride and sulpiride. Two months later, the patient became stuporous; bruxism and hypertonicity became exaggerated. Myerson's sign, sucking reflex and grasp reflex in both hand appeared. There was no dermal lesion. A cranial computed tomography revealed a small calcification in the right frontal subcortical region and a single photon emission tomography indicated possible bifrontal hypoperfusion. Electroencephalograms demonstrated non-specific slowing. Somatosensory evoked potentials and nerve conduction velocities were normal. There were constant indicanuria and amino-aciduria.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Adult-onset Hartnup disease presenting with neuropsychiatric symptoms but without skin lesions]. 258 82

Quazepam is a trifluoroethyl benzodiazepine hypnotic with a half-life of 27 to 41 hours, which has been shown to induce and maintain sleep in the short to long term (up to 4 weeks) treatment of patients with chronic or transient insomnia. Although its hypnotic efficacy has been well characterised against placebo, there are few clinical studies in comparison with established hypnotics, particularly over long term administration. However, preliminary evidence suggests that quazepam 15 to 30 mg is as effective as flurazepam and triazolam in usual therapeutic doses, and causes minimal rebound insomnia following its withdrawal, unlike rapidly eliminated benzodiazepines such as triazolam. The lack of rebound phenomena is likely to be attributable to the 'carryover' effects occurring after discontinuation of quazepam, which has pharmacologically active metabolites with half-lives of elimination similar to or longer than that of the parent drug. Probably because of the long half-lives of quazepam's metabolites, daytime sedation, fatigue and lethargy are the most frequently reported side effects. These side effects are most intense with the 30 mg dose and least with the 7.5mg dose, which has not been studied extensively. Hence, quazepam is an effective hypnotic which may be particularly suitable for short or medium term use in patients in whom withdrawal effects or rebound insomnia may be especially bothersome. Further definition of certain characteristics of its profile--such as its long term use and potential for development of tolerance or dependence, effects on psychomotor skills, efficacy of the 7.5mg dose, and suitability in elderly patients and patients with chronic organic diseases--will assist in more clearly defining its ultimate place in therapy.
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PMID:Quazepam. A preliminary review of its pharmacodynamic and pharmacokinetic properties, and therapeutic efficacy in insomnia. 289 93

Hypnotic efficacy and safety of 3 weeks of daily doses of 2 mg lorazepam or 30 mg flurazepam were compared in a double-blind cross-over study in eight chronic insomniacs between the ages of 29 and 60 years. Subjects were monitored in the sleep laboratory twice weekly for a total of 25 nights. Also, subjective estimates of sleep, vigilance tests, and adverse effects were recorded throughout the study. Findings indicated lorazepam performed better than flurazepam in most sleep parameters. With lorazepam there was improvement from baseline in percentage of sleep time (P less than .05); in total wake time after sleep onset (P less than .01) and in last third of night (P less than .05); in percentage of stage 2 (P less than .05) (weeks 1, 2, 3) and in percentage of night in stage 4 (weeks 2 and 3). Only total wake time from baseline improved (P less than .05) with flurazepam (week 2). Objective and subjective sleep parameters did not correlate well for either drug. Neither drug impaired REM sleep or vigilance test performance. Side effects (grogginess, lethargy; flurazepam only) were few and none was unexpected; neither rebound insomnia nor early morning insomnia occurred with either drug. In summary, both lorazepam 2 mg at bedtime and flurazepam 30 mg at bedtime were found to be effective and safe for treating chronic insomnia, as measured by parameters of sleep and daytime functioning. Lorazepam had more favorable effects on sleep than did flurazepam.
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PMID:Comparison of lorazepam and flurazepam as hypnotic agents in chronic insomniacs. 328 Jun 15

Alzheimer's disease is a slowly progressive disorder involving deterioration of both intellect and personality. The neuropathological features of Alzheimer's disease include abundant neurocortical senile plaques and neurofibrillary tangles. Drug therapies of Alzheimer's disease have been based on empirical observations of the signs and symptoms of the disease and have included the use of hypnotics to reverse insomnia or inverse sleep rhythms; anxiolytics to relieve anxiety, tension and restlessness antipsychotics to "tranquilize" or control psychotic symptoms, such as delusions and hallucinations; stimulants to overcome withdrawn behavior or lethargy; and lastly, antidepressants to control depression. Our growing knowledge of neuropathological and neurochemical changes associated with normal aging and Alzheimer's disease has made it possible to explore and develop pharmacologically-based therapies in Alzheimer's disease. Recent research has revealed behavioral symptoms associated with underlying biochemical changes in either the cholinergic, dopaminergic/ GABAergic (gama-aminobutyric acid) noradrenergic, serotoninergic, neurochemical and/or neuropeptidergic systems. Pharmacological strategies involving manipulation of these systems as a means of relieving Alzheimer's disease symptoms will be reviewed from several perspectives, e.g., those involving transmitter substitution, enzyme inhibition and direct specific receptor stimulation.
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PMID:Pharmacotherapy in Alzheimer's disease: basis and rationale. 354 Oct 49

Temazepam is a benzodiazepine derivative indicated for the treatment of insomnia. Pharmacokinetic studies of the hard capsule formulation indicate that the mean time to peak is 2.99 hours and the mean elimination half-life is 14.7 hours. Sleep laboratory studies have demonstrated improvements in all sleep parameters except sleep onset latency. Clinically, patients report improvements in all sleep parameters including sleep onset latency. The efficacy of temazepam compares favorably with barbiturates, glutethimide, nitrazepam, lorazepam, oxazepam, and flurazepam. It has not been compared with diazepam in the clinical setting. Side effects include drowsiness, dizziness, and lethargy. The incidence of hangover effects from 15- and 30-mg doses is relatively low. Temazepam has no proven advantages over other benzodiazepine hypnotics. The major issues that need further clarification include temazepam's sleep induction properties and the relative incidence of hangover and rebound insomnia when compared with longer-acting benzodiazepines.
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PMID:Temazepam (Restoril, Sandoz Pharmaceuticals). 612 97


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