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)

The model of sleep deprivation in rats by the platform method has been extensively studied in our laboratory as a possible animal model of mania. At the end of the period of sleep deprivation, the rat does not fall asleep as soon as it is returned to its home cage, but shows a period of wakefulness of about 30 min, during which the animal presents a cohort of symptoms that appear to mimic those present in idiopathic mania. In particular, during this period the animal displays insomnia, a high degree of hyperactivity, irritability, aggressiveness, hypersexuality and stereotypy. Haloperidol (0.2 mg/kg) was effective in reducing latency to sleep, while L-sulpiride was much weaker (< 50 mg/kg). The dopamine D1 receptor antagonist SCH 23390 exhibited an extremely high potency and efficacy in reducing sleep latency, a significant effect being observed with 3 micrograms/kg. The administration of the specific D1 receptor agonist SKF 38393 markedly prolonged the period of insomnia with the correlated behavioral syndrome. When lithium was added to the diet and consumed during the sleep deprivation period in adequate amounts to produce serum lithium levels of 0.7-1.0 mEq/l, sleep latency and locomotor activity were significantly reduced. The administration of naloxone (1-10 mg/kg) reduced the latency to sleep in a dose-related manner. By contrast, morphine (1 and 5 mg/kg, i.p.), beta-endorphin and [D-Ala2,D-Leu5]enkephalin (i.c.v., 2 and 1 micrograms, respectively) markedly prolonged the insomnia. The model not only represents a confirmation in the rat that sleep loss often precedes and may trigger a manic episode in man, but suggests that an opioid-dopamine interaction may play a pathogenetic role in mania.
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PMID:Sleep deprivation in the rat: an animal model of mania. 877 65

The authors describe the clinical course of a 10-year-old boy with bipolar disorder diagnosed at age 5 years. Lithium, carbamazepine, and valproic acid were ineffective or caused intolerable side effects. A trial of melatonin led to rapid relief of insomnia and aborted a manic episode. He has continued to take melatonin and adjunctive alprazolam for 15 months without recurrence of insomnia or mania. Affective disorders involving circadian dysregulation may respond to interventions that restore a normal sleep-wake cycle. Literature supporting this hypothesis is cited.
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PMID:Case study: the use of melatonin in a boy with refractory bipolar disorder. 918 38

This open study investigated the effects of sertraline in treating 13 adolescents, ages 12 to 18, who were hospitalized for treatment of a major depressive episode. The sample included 7 adolescents with nonendogenous depression and 6 with endogenous depression, as diagnosed by both Research Diagnostic Criteria (RDC) and Kiddie-SADS-P DSM-III-R endogenous subtype criteria. These patients were followed for an inpatient length of stay ranging from 9 to 38 days (mean 19 days), with later outpatient follow-up for a total of 12 weeks. Measures of depression were found to improve significantly, including suicidal ideation and most of the DSM-III-R symptoms of major depression. Sertraline (mean 110 mg or 1.96 mg/kg daily) significantly decreased scores on the 24-item Hamilton Depression Rating Scale and Montgomery-Asberg Depression Rating Scale from premedication baseline to treatment week 12, and also between weeks 1 (after a large week 1 improvement, presumably due to nondrug effects) and 12. There was a small but significant improvement on the Children's Global Assessment Scale between baseline and week 12, but the Family Global Assessment Scale showed no significant change; neither global assessment scale showed significant effects between weeks 1 and 12. Sleep disturbance was common (69%) after 12 weeks of treatment, but clinically significant improvements in sleep patterns were also observed. This open-label prospective study suggests that sertraline might be useful in treating adolescents with major depression. Adverse effects, mainly insomnia and drowsiness, were relatively common but usually manageable. One patient developed mania after 8 days of sertraline treatment at a dose of 100 mg daily.
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PMID:An open study of the effects of sertraline on adolescent major depression. 923 Dec 98

We assessed a consecutive series of 398 patients with probable Alzheimer's disease (AD) for the presence of Generalized Anxiety Disorder (GAD) using a standardized neuropsychiatric evaluation. Five percent of patients showed GAD during the 4 weeks preceding the psychiatric evaluation. AD patients with GAD showed significantly higher scores of depression, irritability, overt aggression, mania, and pathological crying than AD patients without GAD. The most severe symptoms of anxiety were those of tension, fears, insomnia, and physical complaints.
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PMID:Prevalence and correlates of anxiety in Alzheimer's disease. 970 53

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

Gabapentin is a new adjunctive medication to antiseizure therapies. Anecdotal evidence suggests that it may also help to alleviate mood symptoms in patients with bipolar illness. An open-label study examined the effects of adjunctive gabapentin in bipolar patients with mixed symptoms who had previously demonstrated only partial treatment responses. Mood ratings and side-effect profiles were followed weekly in 10 patients for 1 month. Decreases in Hamilton depression (P < 0.05) and Bech mania ratings (P < 0.01) were evident in the first week of treatment and were sustained. Potent early improvements were noted in early, middle, and late insomnia. The results suggest that gabapentin may be of benefit to bipolar patients who only partially respond to other mood stabilizers. A favorable side-effect profile and rapid action make this drug an attractive choice as an adjunctive therapy.
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PMID:Gabapentin as an adjunct to standard mood stabilizers in outpatients with mixed bipolar symptomatology. 1059 36

1. A profound alteration of circadian rhythm of sleep is often a central feature in manic syndrome. Melatonin (MLT) is a main synchronizer of the sleep/wake cycle, playing a role of transduction to brain functioning of informations about periodical environmental changes, i.e. the duration of daylength. 2. In several sleep phase disorders, MLT exerts a therapeutic effect, by normalizing the sleep/wake cycle. 3. Eleven patients, 8 males and 3 females, aged 22-43, meeting DSM IV diagnostic criteria for Bipolar Disorder, Manic Type, were selected for the presence of insomnia not responding to usual hypnotic therapies (benzodiazepine). 4. All the patients were on antimanic treatment. MLT 3 mg per os was administrated at 22.30 h for 1 month, without changing the previous antimanic and hypnotic treatments. All patients showed a significantly longer duration of sleep following MLT add-on. The severity of mania showed a parallel significant decrease. 5. The results of this pilot clinical study suggest that MLT add-on can be useful in antimanic therapy to treat resistant circadian sleep alterations as well as consequently exert a global therapeutic action on the manic state.
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PMID:Melatonin add-on in manic patients with treatment resistant insomnia. 1080 Jul 42

Interferon-alpha (IFN-alpha) is the only effective treatment for chronic hepatitis B and C. Over 2/3 of methadone-substituted patients suffer from chronic hepatitis C but a history of psychiatric disorders or drug addiction is still seen as a contraindication for IFN-alpha because of a possible increased risk of severe psychiatric side effects such as depression, suicide attempts or psychotic episodes. We report on the case of a 33-year-old patient with chronic hepatitis C and a positive psychiatric history (drug abuse, borderline personality and four suicide attempts). After 4 months of therapy with IFN-alpha he developed a psychosis with persecution mania, complex thought disorder, disturbance of sexual identity, sleeplessness, anxiety, depression and increased irritability with suicidal thoughts. Symptoms did not disappear after discontinuation of interferon treatment. To our knowledge, there are no other reports of persistent psychosis with a possible association to interferon treatment. Development of psychosis and other psychiatric side-effects may be an indication of possible neuromodulatory effects of IFN-alpha with long-term treatment. On the other hand, the treatment for hepatitis C was successful. Ideas for safer treatment in methadone patients with psychiatric co-morbidity and chronic hepatitis C are needed.
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PMID:Psychosis in a methadone-substituted patient during interferon-alpha treatment of hepatitis C. 1096 74

The antidepressant mirtazapine antagonizes central presynaptic alpha2-adrenergic auto- and heteroreceptors resulting in increased central norepinephrine and serotonin activity. Histamine H2 receptors are also antagonized, as are postsynaptic serotonin 5-HT2 and 5-HT3 receptors, leading to serotonergic activity primarily via 5-HT1A receptors. Based on the case report of a patient who developed mania with higher than recommended dosage of mirtazapine, we review the literature on the atypical nature of manic symptoms with mirtazapine. Eight subjects, including those in our study, were identified as having developed mirtazapine-induced mania with atypical features, consisting of dysphoria, irritability, insomnia, psychomotor agitation and abnormal gait. Predisposing features may have included the presence of underlying brain dysfunction and certain selective serotonin reuptake inhibitor-mirtazapine combinations. Dysphoric mania with atypical features may be induced by mirtazapine, providing support for a common hypothesis such as 'central norepinephrine hyperactivity' as the basis for development of mania with mirtazapine.
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PMID:Dysphoric mania induced by high-dose mirtazapine: a case for 'norepinephrine syndrome'? 1240 87

Moclobemide is a reversible inhibitor of monoamine-oxidase-A (RIMA) and has been extensively evaluated in the treatment of a wide spectrum of depressive disorders and less extensively studied in anxiety disorders. Nearly all meta-analyses and most comparative studies indicated that in the acute management of depression this drug is more efficacious than placebo and as efficacious as tricyclic (or some heterocyclic) antidepressants or selective serotonin reuptake inhibitors (SSRIs). There is a growing evidence that moclobemide is not inferior to other antidepressants in the treatment of subtypes of depression, such as dysthymia, endogenous (unipolar and bipolar), reactive, atypical, agitated, and retarded depression as with other antidepressants limited evidence suggests that moclobemide has consistent long-term efficacy. However, more controlled studies addressing this issue are needed. For patients with bipolar depression the risk of developing mania seems to be not higher with moclobemide than with other antidepressants. The effective therapeutic dose range for moclobemide in most acute phase trials was 300 to 600 mg, divided in 2 to 3 doses. While one controlled trial and one long-term open-label study found moclobemide to be efficacious in social phobia, three controlled trials subsequently revealed either no effect or less robust effects with the tendency of higher doses (600 - 900 mg/d) to be more efficacious. Two comparative trials demonstrated moclobemide to be as efficacious as fluoxetine or clomipramine in patients suffering from panic disorder. Placebo-controlled trials in this indication are, however, still lacking. A relationship between the plasma concentration of moclobemide and its therapeutic efficacy is not apparent but a positive correlation with adverse events has been found. Dizziness, nausea and insomnia occurred more frequently on moclobemide than on placebo. Due to negligible anticholinergic and antihistaminic actions, moclobemide has been better tolerated than tri- or heterocyclic antidepressants. Gastrointestinal side effects and, especially, sexual dysfunction were much less frequent with moclobemide than with SSRIs. Unlike irreversible MAO-inhibitors, moclobemide has a negligible propensity to induce hypertensive crisis after ingestion of tyramine-rich food ("cheese-reaction"). Therefore, dietary restrictions are not as strict. However, with moclobemide doses above 900 mg/d the risk of interaction with ingested tyramine might become clinically relevant. After multiple dosing the oral bioavailability of moclobemide reaches almost 100%. At therapeutic doses, moclobemide lacks significant negative effects on psychomotor performance, cognitive function or cardiovascular system. Due to the relative freedom from these side effects, moclobemide is particularly attractive in the treatment of elderly patients. Moclobemide is a substrate of CYP2C19. Although it acts as an inhibitor of CYP1A2, CYP2C19, and CYP2D6, relatively few clinically important drug interactions involving moclobemide have been reported. It is relatively safe even in overdose. The drug has a short plasma elimination half-life that allows switching to an alternative agent within 24 h. Since it is well tolerated, therapeutic doses can often be reached rapidly upon onset of treatment. Steady-state plasma levels are reached approximately at one week following dose adjustment. Patients with renal dysfunction require no dose reduction in contrast to patients with severe hepatic impairment. Cases of refractory depression might improve with a combination of moclobemide with other antidepressants, such as clomipramine or a SSRI. Since this combination has rarely been associated with a potentially lethal serotonin syndrome, it requires lower entry doses, a slower dose titration and a more careful monitoring of patients. Combination therapy with moclobemide and other serotonergic agents, or opioids, should be undertaken with caution, although no serious adverse events have been published with therapeutic doses of moclobemide to date. On the basis of animal data the combined use of moclobemide with pethidine or dextropropoxyphene should be avoided. There is no evidence that moclobemide would increase body weight or produce seizures. Some preclinical data suggest that moclobemide may have anticonvulsant property.
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PMID:Moclobemide: therapeutic use and clinical studies. 1504 13


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