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)

1. The spontaneous activity of hippocampal theta cells in head-restrained cats was recorded during slow-wave sleep (SWS), paradoxical sleep (PS), and the attentive state of bird watching (BW). We also recorded theta cell activity during a state of insomnia with pontogeniculoocipital (PGO) waves, which was induced by the administration of p-chlorophenylalanine (PCPA), a selective inhibitor of serotonin synthesis. 2. The time-dependent structure of fluctuations in theta cell activity was evaluated by power spectral analysis and Markovian analysis. The coefficient of variation for these time series was used as a measure of the variability of theta cell activity, which indicates the relative amplitude of fluctuations. 3. During SWS, theta cell activity showed a larger variability and a flat spectrum, i.e., low Markovian properties. During PS, this activity exhibited smaller variability and high spectral density in a low-frequency band (0.01-1.0 Hz), i.e., high Markovian properties. During BW, variability, spectral and Markovian properties were intermediate. 4. The firing pattern of theta cells during PCPA-induced insomnia was similar to that during PS. However, after the administration of either a serotonin agonist, 5-Methoxy-N,N-dimethyltryptamine, or a choline antagonist, atropine sulfate, theta cell activity no longer exhibited PS-like fluctuations, revealing instead a firing pattern similar to that during SWS. 5. During PS and PCPA-induced insomnia, not only the unit activity of theta cells, but PGO activity and theta wave frequency exhibited slow fluctuations, i.e., the high spectral density in the low-frequency band (0.01-1.0 Hz). 6. Cross-correlation analyses were performed between the fluctuations in theta cell activity, theta wave frequency, and PGO activity. These fluctuations correlated with each other during both PS and PCPA-induced insomnia. Bursts of PGO waves especially contributed to these cross-correlations. 7. These results suggest, first, that the slow fluctuations of the theta cell activity during PS and PCPA-induced insomnia is the physiological expression of the removal of aminergic influences and, secondly, that they are dependent on cholinergic mechanisms, including PGO generators.
J Neurophysiol 1988 Sep
PMID:Fluctuations in spontaneous discharge of hippocampal theta cells during sleep-waking states and PCPA-induced insomnia. 297 87

Urinary cyclic adenosine monophosphate (AMP-c) was measured morning and evening in 35 patients with alcohol withdrawal syndrome (AWS). 65% of the patients revealed a higher night time than day time concentration of AMP-c in the urine, reflecting increased sympathetic adrenergic activity. The circadian rhythm was lost in 88.55% of the 35 patients. The pathogenic factors and mechanisms involved in AWS are discussed and the contribution of sympathetic adrenergic hyperactivity to the onset of the withdrawal syndrome with its concomitant depression of the cholinergic and GABAergic systems is emphasised. Finally it is suggested that insomnia and the loss of REM sleep may also contribute to the onset of the condition.
Minerva Med 1985 Sep 15
PMID:[Changes in the circadian rhythm of urinary cyclic adenosine monophosphate during the alcoholic withdrawal syndrome and related neurobiological correlations]. 299 62

Pharmacokinetic studies using a new oral quinolone ofloxacin were carried out in 12 healthy volunteers. The mean Cmax was 2.7 mg/l after the first dose of 200 mg ofloxacin rising to 3.4 mg/l after the seventh dose. The Tmax was between 1-2 h and the serum half life 5 h. Saliva concentrations matched serum levels but the absolute values were lower. Urinary concentrations ranged from 141 to 330 mg/l and the 12 h excretion was 62% after the seventh dose. Faecal concentrations were high and persisted for up to five days after the last dose. The major effect of ofloxacin on the faecal flora was the rapid and complete elimination of aerobic Gram-negative bacilli. Streptococci were generally increased but there was no change in the total anaerobic bacterial count. Pre-treatment composition of the faecal flora was re-established between 3 and 26 days after the last dose. Ofloxacin was well tolerated by the volunteers and only two complained of significant side effects, gastrointestinal disturbance and insomnia. Ofloxacin is a valuable addition to the range of antimicrobial agents available for the oral treatment of bacterial infection.
J Antimicrob Chemother 1988 Sep
PMID:Pharmacokinetics of ofloxacin and the effect on the faecal flora of healthy volunteers. 318 53

We administered countercontrol behavioral therapy for sleep-maintenance insomnia to 34 insomniacs--ranging in age from 35 to 78 years--in small groups. Twenty-two subjects received immediate and 12 received delayed treatment. Three self-report measures of sleep disruption were collected on daily sleep diaries at baseline, termination of treatment, 1-month follow-up, and 12-month follow-up. Although amount of time awake at night was correlated with age (r = .50), response to treatment was not. Even though older people experienced more time awake after sleep onset prior to treatment, they were able to profit from therapy as well as the younger insomniacs. Countercontrol therapy reduced the sleep complaint for the total group by about 30% at the end of treatment, with gradual improvement continuing through a 4-week follow-up. Nevertheless, it appears that sleep-maintenance insomnia may be more difficult to treat than sleep-onset problems.
Psychol Aging 1986 Sep
PMID:Countercontrol treatment of sleep-maintenance insomnia in relation to age. 326 3

We evaluated a behavioral treatment package consisting of sleep period restriction, sleep education, and modified stimulus control in the treatment of sleep-maintenance insomnia in older adults. A multiple baseline design was used with 4 chronic insomniac subjects, ages 59, 65, 65, and 72. Sleep diaries and an objective behavioral measure of sleep were used to monitor improvement. Results revealed clinically significant reductions in time awake after sleep onset in 3 subjects, coincident with the initiation of treatment. These improvements were maintained at 2- and 6-month follow-ups. The 4th subject showed little improvement; however, a polysomnogram conducted on this subject at the end of the study revealed a fragmented sleep pattern secondary to periodic movements of sleep (nocturnal myoclonus). These encouraging but preliminary results call for further controlled evaluations of the efficacy of this behavioral treatment package for sleep-maintenance insomnia. The importance of conducting polysomnographic studies on elderly insomniacs is discussed.
Psychol Aging 1988 Sep
PMID:Treatment of sleep-maintenance insomnia in older adults: sleep period reduction, sleep education, and modified stimulus control. 326 67

Sixty volunteers with insomnia participated in a randomized, double-blind, controlled clinical trial. After an initial six nights of placebo, 30 subjects (the abrupt-withdrawal group) received 0.5 mg of triazolam nightly for 7 to 10 nights, after which they received placebo. The other 30 subjects (the tapered-dosage group) received the same initial placebo treatment, then triazolam at 0.5 mg for seven nights, at 0.25 mg for two nights, and at 0.125 mg for two nights, and then placebo. As compared with the initial placebo period, the triazolam period significantly reduced the interval before the onset of sleep (sleep latency), and it prolonged sleep duration, reduced the number of awakenings, and improved the self-rated soundness of sleep in all cohorts. In the abrupt-withdrawal group, plasma levels of triazolam were undetectable the morning after the first night of placebo substitution, and subjects reported prolongation of sleep latency (57 minutes longer than base line), reduction in sleep duration (1.4 hours less than base line), and increased awakenings (1.2 per night above base line). The symptoms of rebound sleep disorder lasted one or possibly two nights, and there was a reversion toward base line on subsequent placebo nights. In the tapered-dosage group, however, plasma triazolam levels fell gradually to zero, and rebound symptoms were decreased or eliminated. Thus, rebound sleep disorder following abrupt discontinuation of triazolam can be attenuated by a regimen of tapering.
N Engl J Med 1987 Sep 17
PMID:Effect of gradual withdrawal on the rebound sleep disorder after discontinuation of triazolam. 330 80

The effects of fenfluramine on 21 maladaptive behaviors in 20 autistic individuals were examined over a 9-month period utilizing a double-blind, cross-over, placebo-controlled design. Raters carried out time-sampled observations in the school and residence. In addition, videotaped data were collected in controlled settings and assessed by the raters at the conclusion of the study. Some individuals displayed negative side effects such as tension, agitation, insomnia, and sweating during the 16-week period they received fenfluramine. The results demonstrated that fenfluramine caused no significant reductions in maladaptive behaviors. The lack of any significant positive results from this medication and the side effects observed strongly indicate the need for caution in the use of fenfluramine with autistic persons.
J Autism Dev Disord 1987 Sep
PMID:Effects of fenfluramine on autistic individuals residing in a state developmental center. 330 29

Although the initial sleep disorders classifications provided a framework for categorizing diagnoses, these early instruments had a number of limitations. Among their shortcomings were a lack of specific diagnostic criteria, limited clinical validation, and an overreliance on sleep laboratory findings. As a result, many of the diagnoses were not only poorly substantiated, but they lacked clinical relevance. Also, because of a fusing of diagnoses, a causal relationship was implied that may have been nonexistent and could misdirect the treatment focus. The ICD-10 represents a clinically based diagnostic classification. Furthermore, this classification system includes diagnostic criteria and encourages multiple diagnoses for a more complete description of the patient's clinical presentation. In addition, the ICD-10 allows for differentiation of psychogenic, developmental, and organic factors. Finally, it can be fully applied in the office setting, which allows physicians to maximize their interviewing and assessment skills to complete the diagnoses and subsequent treatment plans. Thus, this classification system strongly reinforces the doctor-patient relationship. It also facilitates consideration of the entire scope of the patient's problems in a truly biopsychosocial perspective. The prevalence of insomnia ranges across studies from 20 to 30% of the adult population. Before adulthood, its prevalence is below 2%. About 5% of adults complain of excessive daytime sleepiness. Among the conditions of excessive daytime sleepiness, narcolepsy has a prevalence of 0.1% and sleep apnea not more than 1% in the general adult population. Nightmares have a prevalence of about 5% in adulthood and 20% in childhood. Sleepwalking and night terrors have a prevalence of less than 1% in adulthood and 15 and 5%, respectively, in childhood.(ABSTRACT TRUNCATED AT 250 WORDS)
Semin Neurol 1987 Sep
PMID:Nosology and prevalence of sleep disorders. 333 58

Within the context of the comprehensive treatment of sleep disorders, which includes medical, neurologic, psychiatric, and social interventions, use of medication is often indicated. Among the three benzodiazepine hypnotics that are available in the United States for the treatment of insomnia, flurazepam is effective for both sleep induction and maintenance, and it retains most of its efficacy over a 4-week period of nightly administration; temazepam is effective only for sleep maintenance, and triazolam improves both sleep induction and maintenance with initial but not with continued administration. Rebound phenomena are more frequent and intense with the more rapidly eliminated drug, triazolam, and to a lesser degree with temazepam. Also, with triazolam, certain behavioral side effects, such as amnesia and psychotic-like symptoms, have been reported. With flurazepam, which is a slowly eliminated benzodiazepine, daytime sedation is more frequent than with the other two drugs. When insomnia is secondary to major depression, antidepressant medication should be administered. Methylphenidate, amphetamines, or other stimulant medications are used for the symptomatic treatment of the sleepiness and sleep attacks of narcolepsy and hypersomnia. For cataplexy and the other two auxiliary symptoms of narcolepsy, imipramine or other tricyclics are the drugs of choice. Protriptyline and medroxyprogesterone have been used in treating mild cases of obstructive sleep apnea, but their efficacy is limited. Similarly, for the treatment of central sleep apnea, medroxyprogesterone and acetazolamide have shown only limited effects. Medication for patients with sleepwalking, night terrors, or nightmares should be prescribed judiciously, and primarily when treatment of an underlying psychiatric condition is desired. The neuropharmacology of sleep should also consider drugs that may cause sleep disorders. Medications with sleep disturbing effects include various antihypertensives, bronchodilators, and the energizing antidepressants. Withdrawal of REM-suppressant drugs, such as the barbiturates, may cause nightmares in association with a REM rebound. Occasionally, a drug or a combination of drugs may produce somnambulistic-like activity in some patients.
Semin Neurol 1987 Sep
PMID:Clinical neuropharmacology of sleep disorders. 333 64

Sixty-three outpatients with chronic insomnia were treated for 3 weeks under double-blind conditions with either brotizolam (n = 29) at a dose of 0.25 mg or 0.5 mg or placebo (n = 34). A 3-day placebo period preceded and followed the double-blind treatment phase. Brotizolam consistently produced significantly more sleep improvement than placebo but also more adverse effects. In those patients switched abruptly from brotizolam to placebo, rebound insomnia was observed, being most marked at the first post-brotizolam placebo night.
Clin Pharmacol Ther 1986 Sep
PMID:Brotizolam, a triazolothienodiazepine, in insomnia. 352 13


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