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

In the past 18 months, there has been considerable controversy regarding the benzodiazepine triazolam (Halcion). To review data supporting or not supporting the assertion that treatment with triazolam results in adverse reactions more frequently than with other benzodiazepines, the author used computerized literature searches (MEDLINE, English language articles from 1975 to the present) to identify reports of behavioral disinhibition, amnesia, delirium, rebound insomnia, and withdrawal reactions on benzodiazepines. Studies of disinhibitory reactions during benzodiazepine treatment do not substantiate the argument that they are more prevalent with triazolam than with other benzodiazepines. The behavioral disinhibition reactions during treatment with benzodiazepines are associated with higher dosages and pretreatment level of hostility. Anterograde amnesia occurs with many benzodiazepines, but usually without changes in a person's normal activities and behaviors. The reports of anterograde amnesia during benzodiazepine treatment describe people performing rather complex tasks during which outside observers could not detect any unusual behaviors. The prevalence of delirium during treatment with triazolam and other benzodiazepines is unclear, but delirium is more frequent at higher dosages and in the elderly. Controlled studies regarding the adverse effects of triazolam on sleep are lacking. The author concludes that despite the considerable adverse publicity in the lay press, there is little scientific evidence that triazolam is associated with disinhibitory or other adverse reactions at a greater frequency than other benzodiazepines.
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PMID:Disinhibition, amnestic reactions, and other adverse reactions secondary to triazolam: a review of the literature. 148 83

A case of psychosis occurring 13 days after 1st trimester abortion in a 17-year old primigravida without family history of mental illness of postpartum psychosis is described. The young woman denied any ambivalence or guilt concerning abortion. The abortion itself involved repeat hospitalization for evacuation of retained products, and a course of antibiotics (metronidazole). The illness was marked by insomnia, anorexia, labile mood, auditory hallucinations, inappropriate speech, flat affect, and withdrawal alternating with disinhibition. She was hospitalized 10 days after onset, and treated with neuroleptics (pimozide 4 mg/day). She improved rapidly, and was discharged, taking medication for a few more weeks. After stopping medication she became pregnant, and delivered without any further psychotic symptoms. It is unlikely that metronidazole caused the illness, although it has been associated with confusion, disorientation and hallucinations, because the symptoms occurred 2 days after discontinuing the drug. On the other hand, the patient's flat affect after recovery suggests she might have had incipient schizophrenia.
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PMID:Psychotic illness following termination of pregnancy. 259 Jul 89

Two benzodiazepine hypnotics, triazolam, 0.25 mg, with a short elimination t1/2, and quazepam, 15 mg, with a long t1/2, were evaluated in 22-night sleep laboratory studies. Quazepam improved sleep significantly during both short- and intermediate-term use. Daytime sleepiness, which decreased with continued use, was the side effect most often associated with quazepam dosing. In contrast, triazolam dosing did not significantly improve any of the major sleep efficiency parameters, and there was a rapid development of tolerance for the drug's slight initial effectiveness. In addition, there were a number of behavioral side effects including amnesia, confusion, and disinhibition. Withdrawal of triazolam was associated with sleep and mood disturbances (rebound insomnia and rebound anxiety), whereas quazepam exerted carryover effectiveness. Thus the data in this study show that the 0.25 mg dose of triazolam, which is being prescribed increasingly, has a profile of side effects that is similar to that of the 0.5 mg dose.
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PMID:Comparison of short and long half-life benzodiazepine hypnotics: triazolam and quazepam. 353 May 86

Alprazolam was evaluated in chronic insomniacs in a 1-mg bedtime dose. The 16-night sleep laboratory protocol included four placebo-baseline nights followed by seven nights of drug administration and five placebo-withdrawal nights. On the first three drug nights (nights 5 to 7), the drug was highly effective in inducing and maintaining sleep with this short-term use. By the end of the one week of administration (nights 9 to 11), however, the drug had lost about 40% of its efficacy. During drug use, one subject reported some difficulty in controlling expression of inappropriate emotions when interacting with others, which suggested the presence of disinhibition. On the third night following drug termination, there was a significant increase in sleep difficulty above baseline levels (rebound insomnia). This worsening was of comparable magnitude to the peak improvement of sleep with drug administration. Thus, the clinical utility of alprazolam when administered to insomniac patients appears to be limited because of a relatively rapid development of tolerance and possible disinhibitory reactions during drug use and the occurrence of rebound insomnia following withdrawal.
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PMID:Alprazolam: effects on sleep and withdrawal phenomena. 365 3

This is the first reported use of electroconvulsive treatment (ECT) in an adolescent with bipolar mania who had been treated with craniectomy for an intracranial neoplasm. The reported case is of a 16-year-old girl with a history of brain stem glioma (pontomesencephalic astrocytoma) diagnosed at 13 years of age. She presented in a psychiatric emergency room with suicidal ideation, depressed mood, irritability, olfactory hallucinations, early insomnia, grandiosity, and guilt. Her symptoms failed to respond to a trial of an antidepressant, mood stabilizer alone, and mood stabilizer in conjunction with a neuroleptic. The decision to use ECT was based on suicidal ideation, extreme disinhibition, and danger to self and others. Significant improvement in mood and remission in psychosis were noted after the eighth treatment. Comparison of 2-week pre-ECT and 3-month post-ECT cognitive testing revealed no change in IQ. This report highlights rapid response and the ability to tolerate ECT in an adolescent diagnosed with bipolar disorder, who had also been treated with radiation and craniotomy.
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PMID:Electroconvulsive treatment of a bipolar adolescent postcraniotomy for brain stem astrocytoma. 1035 19

To study the specific effects of central superior raphe nucleus (CeSR) lesions on the different sleep/wakefulness cycle states of the cat, nine animals with implanted electrodes for EOG, EMG and EEG recordings were used. Seven cats received diathermocoagulation lesions that destroyed between 13 and 100 percent of the CeSR; the remaining two cats, which suffered lesions in the paramedial region of the oral pontine reticular nucleus (RPO), were used to determine the effects on sleep/wakefulness states caused by damage to adjacent CeSR structures and/or passage fibres. Three prelesion and five postlesion weekly 24 h recordings were obtained from each cat. Recordings were scored according to the polygraphic criteria for wakefulness (W), drowsiness (D), slow wave sleep (SWS) and paradoxical sleep (PS). Results indicated that insomnia is not produced exclusively by CeSR lesions, since adjacent paramedial RPO lesions also decrease both SWS and PS; however, increased W occurred after the former while increased D occurred after the latter. Correlation coefficient analyses showed that W is the only state that correlates significantly with the volume of CeSR destroyed. The following correlations between different states of the sleep/wakefulness cycle were, however, significant: W-D, W-SWS and SWS-PS. Disinhibition of W, therefore, and not sleep loss seems to be the primary effect of CeSR lesions. Thus, the CeSR nucleus appears to be involved in arousal mechanisms rather than in direct sleep promotion.
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PMID:Re-examination of the effects of raphe lesions on the sleep/wakefulness cycle states in cats. 1060 78

A dopaminergic drug - lisuride exhibited increase in alpha, decrease in beta and slow activities on brain function measured by computerized EEG. It was postulated that reverse EEG changes might play role in the pathogenesis of RLS. During transition from wakefulness to sleep stage 1 changes in alpha activity initiate long-lasting alpha arousal responses and they continue increasingly at sleep stage 2. This dysfunction is probably due to a genetic vulnerability of EEG alpha rhythm and disinhibits the diencephalospinal dopamine system, mostly during sleep but also during wakefulness. The disinhibition produces background for activation of PLMs, disturbing sensations in brainstem and urge to move, motor restlessness at cerebral cortex, generally for legs. All lead to severe insomnia. In RLS patients, forced deviations from alpha to theta or beta activity are unsuitable and resting EEGs reflect a dopamine receptor-specific 'individual sensitivity.' This vulnerability is alleviated after lisuride with suitable CEEG changes.
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PMID:The primary restless legs syndrome pathogenesis depends on the dysfunction of EEG alpha activity. 1260 34

RLS cases may carry a genetic vulnerability called EEG alpha activity gate dyscontrols which appear during changes in vigilance and generally during sleep. It is triggered by forced EEG shifts either from alpha activity to delta or high alpha. Expressions of alpha activity gate dyscontrols may have a gate effect that trigger a second vulnerability-dopamine receptor specific individual sensitivity (DRSIS) and this leads to a deficiency in dopamine transmissions at diencephalospinal dopamine system (DSDS). Due to altered gene expressions in states of dopamine receptor function, DRSIS EEGs and RLS symptoms may be interpreted as follows: A. Disinhibition state is alpha activity gate dyscontrols induced inhibition of DSDS inhibitory dopamine modulations. Dopaminergic disinhibitions inhibit inhibitory interneurons of sensory and motor nuclei neurons that are involved in RLS. These sleep sensitive inhibitory interneurons possibly have GABA-ergic functions in sleep. (I) DSDS thalamic neurons' disinhibitory effects in thalamus on GABA-ergic interneurons of: (a) Intralaminar nuclei non-discriminative sensation neurons at thalamocortical premotor network leading to symptom of "a sense of urgency to move" generally referenced to legs.(b) Reticular thalamic nucleus (RTN) neurons. At polysomnography,during NREM sleep, disinhibited RTN neurons show alpha activity gate dyscontrol 1. These are recurrent subtypes of CAP in alpha band (7-12 Hz) pointing a difficulty in shifting to subtypes of CAP in low delta bands (0.25-2.5 Hz) and sleep fragmentations.(II) Supraspinal disinhibitory projections from DSDS thalamic neurons on GABA-ergic interneurons of: (a) Sensory neurons at posterior horns of spinal cord leading to dysesthesias, generally referenced to legs.(b) Medullary-reticulospinal neurons and by way of independent spinal rhythm generators on motoneurons leading to periodic limb movements in sleep.B. Activation state is an increase in symptoms. Sensory intralaminar and motor pontin nuclei neurons are in fact excitatory but are disinhibited in RLS. Due to altered gene expression, these neurons begin to perceive 'disinhibition' as reduced inhibition. Their glutamate receptors may activate deficient dopamine transmissions on RTN leading to alpha activity gate dyscontrol 2. This implies a failure in preventing shifts to frequent subtypes of CAP in high alpha and low beta bands (12-13 Hz) resulting in an increase of sensorimotor symptoms and appearance of motor restlessness, behavioral arousals and insomnia. C. Inhibition state is spontaneous relief from sensorimotor symptoms. Short or long-term synaptic plasticities of dopamine receptors towards activations initiate negative feedbacks from inhibitory interneurons. They are supported by inhibitory dopamine modulations- alertness and some awareness generally with regular high alpha EEGs, supraspinal inhibitions and a reverse movement pattern of PLMS during standing up and continuing to walk.
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PMID:In restless legs syndrome, during changes in vigilance, the forced EEG shifts from alpha activity to delta or high alpha may lead to the altered states of dopamine receptor function and the symptoms. 1732 Mar 7

Alcohol dependence and alcohol abuse or harmful use cause substantial morbidity and mortality. Alcohol-use disorders are associated with depressive episodes, severe anxiety, insomnia, suicide, and abuse of other drugs. Continued heavy alcohol use also shortens the onset of heart disease, stroke, cancers, and liver cirrhosis, by affecting the cardiovascular, gastrointestinal, and immune systems. Heavy drinking can also cause mild anterograde amnesias, temporary cognitive deficits, sleep problems, and peripheral neuropathy; cause gastrointestinal problems; decrease bone density and production of blood cells; and cause fetal alcohol syndrome. Alcohol-use disorders complicate assessment and treatment of other medical and psychiatric problems. Standard criteria for alcohol dependence-the more severe disorder-can be used to reliably identify people for whom drinking causes major physiological consequences and persistent impairment of quality of life and ability to function. Clinicians should routinely screen for alcohol disorders, using clinical interviews, questionnaires, blood tests, or a combination of these methods. Causes include environmental factors and specific genes that affect the risk of alcohol-use disorders, including genes for enzymes that metabolise alcohol, such as alcohol dehydrogenase and aldehyde dehydrogenase; those associated with disinhibition; and those that confer a low sensitivity to alcohol. Treatment can include motivational interviewing to help people to evaluate their situations, brief interventions to facilitate more healthy behaviours, detoxification to address withdrawal symptoms, cognitive-behavioural therapies to avoid relapses, and judicious use of drugs to diminish cravings or discourage relapses.
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PMID:Alcohol-use disorders. 1941 Jul 5

During the last decade, several studies have shown that insomnia, rather than a symptom of depression, could be a medical condition on its own, showing high comorbidity with depression. Epidemiological research indicates that insomnia could lead to depression and/or that common causalities underlie the two disorders. Neurobiological and sleep EEG studies suggest that a heightened level of arousal may play a common role in both conditions and that signs of REM sleep disinhibition may appear in individuals prone to depression. The effects of antidepressant drugs on non-REM and REM sleep are discussed in relation to their use in insomnia comorbid with depression. Empirical treatment approaches are behavioral management of sleep combined with prescription of a sedative antidepressant alone, co-prescription of two antidepressants, or of an antidepressant with a hypnotic drug.
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PMID:Comorbidity of insomnia and depression. 1993 13


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