Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0917801 (insomnia)
 10,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
 ...
PMID:Heterocyclic antidepressant, monoamine oxidase inhibitor and neuroleptic withdrawal phenomena. 196 71

An analysis from the Finnish East and West Cohort of the Seven Countries Study tested the hypothesis that front line service during modern warfare is associated with depression later in life. World War Two-era Finnish combat veterans were compared to Finnish veterans who were non-combatants. Both groups were followed from 1959 to 1984. Dependent variables were the Zung depression scale and other measures of psychosocial adaptation and mental health. Analysis of variance of Zung scores by combat exposure was close to statistical significance (p = 0.0501). Even if statistical significance had been reached, it is felt that the absolute magnitude of the differences between the populations appear quite trivial. A significant association was found for those who had participated in over nine battles and when grouping depression, sleeplessness, paranoia, hallucinations, schizophrenia, and other mental illness into the general category of any mental illness (O.R. = 4.414; 95% C.I. = 1.113, 17.503). This seems to support the residual stress hypothesis pertaining to modern combat exposure.
 ...
PMID:Depression late after combat: a follow-up of Finnish World War Two veterans from the seven countries east-west cohort. 205 71

This study evaluates the reverse first night effect (FNE) in insomniacs. All insomniacs evaluated at the Dartmouth Sleep Disorders Center between 1975 and 1980 were studied if they met specific criteria (n = 89). First night effects were assessed using the following four variables: sleep efficiency, sleep latency, percentage of rapid eye movement (REM) sleep, and REM latency. The 20 subjects who showed the strongest normal FNE were compared with the 20 showing the strongest reverse FNE. The two groups were similar in age, sex, and most aspects of reported home sleep. They differed in their sleep on night 1, but on nights 2 and 3 their sleep was quite similar. Both groups overestimated their sleep latencies on night 1 (by subjective reports) but unlike the normal FNE group, the reverse FNE patients very accurately assessed their sleep latency on nights 2 and 3. Reverse FNE patients had significantly higher scores than normal FNE patients on the Minnesota Multiphasic Personality Inventory (MMPI) K (defensiveness, guardedness) and Pa (paranoia) scales, and they were less depressed, marginally less anxious, and somewhat more sensation-seeking and more susceptible to boredom. This study concluded that evaluations using only 1 night in the laboratory may be missing the larger picture of a patient's insomnia. When data from only 1 laboratory night are available for an insomniac, care should be taken with the label of "subjective complaint without objective findings" in patients who are defensive, guarded, and sensation-seeking.
 ...
PMID:Reverse first night effect in insomnia. 271 Oct 96

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.
 ...
PMID:Monoamine oxidase inhibitor withdrawal phenomena: symptoms and pathophysiology. 284 11

Twenty patients, diagnosed as suffering from treatment-resistant major depression, were treated with one or more drugs that decrease corticosteroid biosynthesis. Nine were psychotic, 11 nonpsychotic. Seventeen completed the treatment (8 psychotic, 9 nonpsychotic); 13 responded (5 psychotic, 8 nonpsychotic; 11 responded completely (i.e., a drop in the Hamilton Depression Scale of at least 50%, to < or = 15), and 2 responded partially. The mean age of the responders (45.2 +/- 12.6 years) did not differ significantly from that of the nonresponders (48.7 +/- 12/3). Data were analyzed in the following categories; (1) the presence or absence of psychosis, (2) response or nonresponse to treatment, and (3) the drug(s) used (aminoglutethimide, ketoconazole, or a combination of either of these with metyrapone). The patients improved over time on the Hamilton Depression Scale independent of the medication used. Responders demonstrated improvement in mood, insomnia, anxiety, diurnal variation, paranoia and obsessive compulsiveness. Nonpsychotics responded better than psychotics.
 ...
PMID:The psychotropic effects of inhibitors of steroid biosynthesis in depressed patients refractory to treatment. 777 45

Agitation is one of the diagnostic features of catatonia in the DSM IV classification, but permanent forms of agitated catatonia have occasionally been described. We report the case of a 43-year-old man who had already suffered from undifferentiated schizophrenia for 7 years, and in whom we diagnosed agitated catatonia. While our patient was being treated with a neuroleptic during a second episode of paranoia, a state of agitation was observed which persisted for a further 8 months. During this period, he was treated with several different neuroleptics and benzodiazepines, either alone or in association, without any improvement. No organic cause was found. He was then transferred to our electroconvulsive therapy (ECT) unit, with a diagnosis of schizophrenic agitation resistant to drug therapy. ECT was begun, and he was only given droperidol in case of agitation and alimemazine for insomnia, neither of which had any effect. In view of his persistent agitation without any purpose, echolalia and echopraxia, stereotyped movements with mannerisms and marked mimicking and grimacing, we diagnosed him as having agitated catatonia. After the fourth session of ECT, we decided to stop all treatment and gave him lorazepam at a dose of 12.5 mg daily. Twenty-four hours later, all symptoms of agitation had disappeared. In our opinion, permanent catatonic agitation is not rare. In our case, the neuroleptic treatment maintained and may even have worsened the symptomatology. Lorazepam can be used as a therapeutic test for this type of agitation, especially if it does not respond to neuroleptics. This also allows the patient to be sedated rapidly and effectively, thus preventing him from injuring himself further.
 ...
PMID:A case of agitated catatonia. 1007 Nov 81

Methamphetamine, called meth, crystal, or speed, is a central nervous system stimulant that can be injected, smoked, snorted, or ingested orally; prolonged use at high levels results in dependence. Methamphetamine (MA) is a derivative of amphetamine, which was widely prescribed in the 1950s and 1960s as a medication for depression and obesity, reaching a peak of 31 million prescriptions in the United States in 1967. Until the late 1980s, illicit use and manufacture of MA was endemic to California, but the MA user population has recently broadened in nature and in regional distribution, with increased use occurring in midwestern states. An estimated 4.7 million Americans (2.1% of the U.S. population) have tried MA at some time in their lives. Short- and long-term health effects of MA use include stroke, cardiac arrhythmia, stomach cramps, shaking, anxiety, insomnia, paranoia, hallucinations, and structural changes to the brain. Children of MA abusers are at risk of neglect and abuse, and the use of MA by pregnant women can cause growth retardation, premature birth, and developmental disorders in neonates and enduring cognitive deficits in children. MA-related deaths and admissions to hospital emergency rooms are increasing. Although inpatient hospitalization may be indicated to treat severe cases of long-term MA dependence, optimum treatment for MA abusers relies on an intensive outpatient setting with three to five visits per week of comprehensive counseling for at least the first three months. The burgeoning problems of increased MA use must be addressed by adequate treatment programs suitable for a variety of user types.
 ...
PMID:History of the methamphetamine problem. 1090

The neuropsychiatry of Parkinson's disease (PD) and its correlates are reviewed. Dementia occurs in up to 30% and can be treated with cholinesterase inhibitors. Cognitive impairments involve executive, visuospatial, attentional, and memory dysfunctions. Apathy may respond to dopamine agonists or cholines-terase inhibitors. Cognitive impairment, psychosis, and depression predict quality of life. Visual hallucinations and paranoia are common, and respond to low dose clozapine. Depression is common and predicts caregiver burden and depression. The best data suggest the efficacy of nortriptyline and the safety of SSRIs. Anxiety disorders occur in 40% of patients, especially off-period panic attacks and specific phobias. Bromazepam has proven useful for anxiety in PD, but buspirone has only diminished drug-induced dyskinesias to date. Sleep disorders occur in up to 94% of patients. Insomnia is common and is treated by dopaminergic agent dose reduction, nocturnal dosing, treatment of depression, or use of short half-lived hypnotics, depending on etiology. Parasomnias include REM behavior disorder and vivid dreams and nightmares. Excessive daytime somnolence occurs in at least 15% of patients. Sleep attacks are common and patients should be warned about driving when taking dopamine agonists. Sexual disorders occur in most patients. Paraphilias are associated with dopamine agonists, and clozapine may be useful in their treatment. Surgical therapies are associated with a wide variety of neuropsychiatric features, and vigilance for suicide attempts with subthalamic nucleus stimulation seems warranted. Neuropsychiatric disorders are important determinants of quality of life and caregiver burden in PD. More clinical research is needed to establish effective treatments.
 ...
PMID:The neuropsychiatry of Parkinson's disease. 1617 59

Insomnia is a potential cause of anxiety, depression, and anomalies of experience; separate research has shown that anxiety, depression and anomalies of experience are predictors of paranoia. Thus insomnia may contribute to the formation and maintenance of persecutory ideation. The aim was to examine for the first time the association of insomnia symptoms and paranoia in the general population and the extent of insomnia in individuals with persecutory delusions attending psychiatric services. Assessments of insomnia, persecutory ideation, anxiety, and depression were completed by 300 individuals from the general population and 30 individuals with persecutory delusions and a diagnosis of non-affective psychosis. Insomnia symptoms were clearly associated with higher levels of persecutory ideation. Consistent with the theoretical understanding of paranoia, the association was partly explained by the presence of anxiety and depression. Moderate or severe insomnia was present in more than 50% of the delusions group. The study provides the first direct evidence that insomnia is common in individuals with high levels of paranoia. It is plausible that sleep difficulties contribute to the development of persecutory ideation. The intriguing implication is that insomnia interventions for this group could have the added benefit of lessening paranoia.
 ...
PMID:Insomnia and paranoia. 1909 52

The function and dysfunction of the central noradrenergic system were reviewed together with the implications for the pathophysiological understanding of functional psychosis. Like the peripheral noradrenergic system, the central noradrenergic system plays a pivotal role in fight/flight reactions and stress. Overactivity of the system induces not only a sympathotonic state but also hyperarousal accompanied by insomnia, anxiety, irritability, emotional instability, paranoia, and excitation. On the other hand, its underactivity lowers the sympathetic tone and arousal level, resulting in hypersomnia, blunted responsiveness, or apathy. It has been confirmed in animal experiments that excess stress causes dysfunctions of the central noradrenergic system as a result of compensation, such as the overutilization-induced oversynthesis of noradrenaline. Dysfunction of the system, particularly its overactivity, plays an important role in various functional psychoses such as anxiety disorder, schizophrenia, and mood disorder, as well as behavioral and psychological symptoms of dementia (BPSD). Pharmacologically, the sedative effect of minor and major tranquilizers on hyperarousal is mediated by their action as noradrenaline antagonists. Some antidepressants potentiate noradrenergic activity, and should be used carefully in hyperaroused depressive patients. Thus, clinical evaluation of the central noradrenergic pathophysiology will provide us with information related to arousal to advance our understanding and treatment of functional psychoses.
 ...
PMID:[Central noradrenergic system in psychiatry]. 1982 61


1 2 3 4 Next >>