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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

For a period of six months (april to october 1990) 361 manic-depressive in-patients or out-patients were examined and treated. 178 patients (119 females and 69 males) were suffering from depression at examination time. Among them, 34 women and 11 men had mixed mood disorders with a symptomatology near that of typical depression (major depression, according to the DSM III-R criteria) but not of mixed bipolar disorder. The main symptoms were: dysphoric mood with irritability; internal tension, psychic and sometimes physical agitation; emotional lability; head crowded with thoughouts or thoughts that vanish too quickly; sleep disorders with initial insomnia or with frequent night awakenings; suicidal thoughts or attempted suicide with impulsiveness. These patients sustained severe suffering. They were in no way slow-minded but rather talkative and expressive. Antidepressant drugs increased agitation and insomnia, and in some cases, suicidal impulses. BZDs had limited efficacy but neuroleptics given in small doses, anticonvulsants and lithium gave very effective results. A limited number of electroshocks provided rapid improvement. In many respects, depression with delirium seems a more severe form of the above-described combined depressive syndrome and responds to the same treatments. We think that this mood disorder includes excitement as an important component, although this was not clearly evident. However, it is not easy to conceive this syndrome as a mixture of depressive and manic symptoms; it should rather be regarded as another specific mood condition, either permanent or transient, situated between the two other conditions.
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PMID:[Mixed depressive syndrome]. 160 Aug 99

The physiological imbalances associated with organ insufficiency and the complexity of organ transplant surgery and postoperative care puts patients at risk for psychiatric disorders. The brain is susceptible to a variety of insults as a result of these complex processes, including those secondary to medications and infections. We review literature relevant to organ transplant patients and also include empirical knowledge based on clinical practice. We first describe the physiologic and psychiatric issues for each major organ that is commonly transplanted, including liver, kidney, heart, bone marrow, and pancreas, as well as multiple organ transplantation. We then discuss the pharmacologic treatment and neuropsychiatric side effects of rejection with various immunosuppressants, including cyclosporine, azathioprine, OKT3, FK506, and corticosteroids. Certain bacterial, fungal, viral, and protozoal infections occur more frequently in the transplant population; their relationship to neuropsychiatric dysfunction is discussed. We then present details of psychopharmacotherapy of delirium, other organic mental disorders, depression, mania, anxiety, and insomnia, with attention to drug interactions and differential diagnosis. Particularly cautious monitoring of medication doses and serum levels is recommended in these patients.
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PMID:Psychopharmacology and neuropsychiatric syndromes in organ transplantation. 187 24

1. The authors review the literature describing acute symptomatology produced by the gradual or abrupt withdrawal of heterocyclic antidepressants, monoamine oxidase inhibitors (MAOI) and neuroleptics. 2. Withdrawal of heterocyclic antidepressants and antipsychotic agents causes similar symptomatology. Symptoms produced by the discontinuation of these drugs include nausea, emesis, anorexia, diarrhea, rhinorrhea, diaphoresis, myalgias, paresthesias, anxiety, agitation, restlessness, and insomnia. 3. Psychotic relapse is often presaged by anxiety, agitation, restlessness, and insomnia. Prodromal symptoms are distinguished from the effects of neuroleptic withdrawal by a temporal relationship of the latter to reductions in the dosage or discontinuation of antipsychotic agents. 4. Withdrawal of MAOIs can result in severe anxiety, agitation, pressured speech, sleeplessness or drowsiness, hallucinations, delirium, and paranoid psychosis. 5. MAOI withdrawal phenomena resemble the symptoms produced by the discontinuation of chronically administered psychostimulants. 6. The capacity of MAOIs to exert amphetamine-like effects presynaptically and the propensity of somatic treatments for depression to subsensitize presynaptic receptors regulating the release of catecholamines provide a basis for the development of psychotic symptoms upon the withdrawal of MAOI. Evidence for this hypothesis is reviewed.
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PMID:Heterocyclic antidepressant, monoamine oxidase inhibitor and neuroleptic withdrawal phenomena. 196 71

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

An 80-year-old retired teacher developed impairment of memory and suffered from delusions of theft. Four years later, she became disoriented as to person, time and situation, restless, began mutter to herself, and displayed night delirium and insomnia. She was subsequently diagnosed as having senile dementia of the Alzheimer type (SDAT). She died of bronchopneumonia and multiple metastases from breast cancer at the age of 85 years. Family history was non-contributory. The brain weighed 1,020 g and showed diffuse atrophy. Histologically, there was moderate loss of neurons in the cerebral cortex, which was accentuated in the frontal and temporal lobes. In addition, numerous senile plaques were observed in the neocortex and hippocampus. Several senile plaques were also found in the amygdala, innominate substance, neostriatum, claustrum, thalamus, hypothalamus and tegmentum of the mesencephalon. Neurofibrillary tangles (NFTs) were mostly restricted to the hippocampus and parahippocampal gyrus, their number being compatible with the patient's age. No obvious neuronal loss was noted in the nucleus basalis of Meynert, neostriatum, substantia nigra or locus ceruleus, which are well known to be involved in Alzheimer's disease and SDAT. Recently, Terry et al proposed a new disease concept, "SDAT without neocortical NFTs". The histopathology of the cerebral cortex in our patient was very similar, if not identical, to those observed in their patients. However, the above authors did not mention any subcortical changes, leaving the detailed neuropathological picture unclear. Tentatively, we classified the present case as senile dementia with numerous neocortical senile plaques and preserved subcortical nuclei.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[An autopsy case of senile dementia with numerous neocortical senile plaques and preserved subcortical nuclei]. 259 44

The author reviews the literature reporting the untoward effects of withdrawing monoamine oxidase inhibitors (MAOIs). The withdrawal of these agents can result in severe anxiety, agitation, pressured speech, sleeplessness or drowsiness, hallucinations, delirium and paranoid psychosis. MAOI withdrawal phenomena resemble the symptoms produced by the discontinuation of chronically administered psychostimulants. The capacity of MAOI to exert amphetamine-like effects presynaptically, and the propensity of somatic treatments for depression to subsensitize presynaptic receptors regulating the release of catecholamines, can provide a basis for the development of psychotic syndromes upon the withdrawal of MAOIs. Evidence for this hypothesis is reviewed.
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PMID:Monoamine oxidase inhibitor withdrawal phenomena: symptoms and pathophysiology. 284 11

We report two cases of severe withdrawal symptoms after abrupt discontinuation of a long-term normal-dose benzodiazepines (BZD) administration. Case 1, a 61-year-old man, suffered from delirium on the 7th day after abrupt discontinuation of nitrazepam, 10 mg/day. Case 2, a 49-year-old woman, suffered from auditory hallucination on the 4th day and visual cognitive disorder on the 5th day after abrupt discontinuation of nitrazepam, 5 mg/day, and triazolam, 0.5 mg/day. A withdrawal syndrome after discontinuation of normal-dose BZD is uncommon, and a psychotic withdrawal reaction is even more uncommon. We show how a continuous administration of BZD for a period of longer than 6 months and the presence of severe insomnia are risk factors predictive of a psychotic reaction. We also explain the predictive method used to determine the onset time of such a severe state. In the case of a psychotic state, we recommend intravenous diazepam injection. To prevent withdrawal reaction, we also recommend a gradual reduction after administration of normal-dose BZD.
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PMID:[Two cases of psychotic state following normal-dose benzodiazepine withdrawal]. 290 78

On the basis of sleep-polygraphic examinations of twelve alcoholics over a period of six days is given on the sleep behaviour during alcohol withdrawal. The study showed the withdrawal symptoms described in the literature, such as withdrawal insomnia, REM rebound and persisting shortening of the deep sleep time, in ten patients whereas in two cases the examinations had to be interrupted in the third night because of a withdrawal delirium. In these cases, however, an almost 100 per cent REM occurrence was seen from the first night. The significance of these findings with respect to an early prediction of the outbreak of the delirium and for the pathogenesis of the delirium in general is discussed.
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PMID:[Sleep polygraphic studies in the preliminary stages of delirium tremens]. 372 69

Though recovery of consciousness after drug overdose may occur within a day or two, the drug itself may not finally leave the brain for another one to three weeks, and at this late time a withdrawal syndrome can occur, with insomnia, restlessness, raised paradoxical (R.E.M.) sleep, epileptic phenomena, and even delirium. It is proposed that a high degree of drug-tolerance and dependence can be rapidly acquired after overdose.Abnormal sleep features of 10 patients resolved only slowly over a period of up to two months after overdose. The data support the view that R.E.M. sleep is concerned with processes of brain repair.
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PMID:Late brain recovery processes after drug overdose. 431 51


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