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

This first clinical study of olanzapine in Japanese patients with schizophrenia was conducted to investigate the efficacy and safety of olanzapine. Eighty-one patients were included in the analysis set. Mean modal dose for those patients were 9.4 +/- 3.6 mg/day. For the primary efficacy measure (Final Global Improvement Rating score), 14.8% of patients had remarkable improvement, 59.3% of patients had moderate improvement or better, and 86.4% of patients had slight improvement or better. Results from the Brief Psychiatric Rating Scale showed improvement from baseline in all clusters including positive psychotic symptoms (thought disturbance) but also against negative symptoms (anergia). The most commonly reported treatment-emergent signs and symptoms with > or =10% incidence, were insomnia, weight increase, excitement, sleepiness, and anxiety. There was a low incidence of extrapyramidal treatment-emergent signs and symptoms, and events reported were tremor (6.2%), muscle rigidity (3.7%), and akathisia (2.5%). The most commonly reported treatment-emergent laboratory changes, with > or = 20% of incidence, were prolactin elevations (24.3%) followed by increases in triglycerides (20.4%). However, mean prolactin values tended to be normalized during the study. This study result suggests that olanzapine is an "atypical" antipsychotic.
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PMID:Efficacy and safety of olanzapine, an atypical antipsychotic, in patients with schizophrenia: results of an open-label multicenter study in Japan. 1144 86

Patients with Parkinson's disease can experience a number of sleep disorders, including insomnia, parasomnias and daytime somnolence [specifically, excessive daytime sleepiness (EDS) and sleep attacks]. Insomnia is a frequent and important complaint of patients with the disease. Both the pathology of Parkinson's disease and dopaminergic drugs may contribute to the much higher than expected frequency of sleep fragmentation and disrupted sleep among these patients. In addition, coexisting depression seems to be a major and frequent risk factor for insomnia in Parkinson's disease. After recognising a sleep problem, the first step in management is to examine and diagnose the type of insomnia and possible medical or psychological factors that may disturb nocturnal sleep. The next step is to give the patient appropriate advice on sleep hygiene. Increasing the dosage of dopaminergic drug treatment will often increase sleep disruption and should be avoided unless the patient's sleep is primarily disturbed by the motor manifestations of parkinsonism during the night. Depression should be looked for and if appropriate be treated in any patients with insomnia. If it becomes necessary to treat the patient with an hypnosedative agent, it is important to use a drug with a short half-life and that manifests as few adverse effects as possible the next morning. Up-to-date guidelines for the use of hypnosedatives should be followed. Patients with Parkinson's disease experience a wide range of parasomnias. The majority of behaviours may be related to rapid eye movement (REM) sleep behaviour disorder (RBD) or to a spectrum of symptoms ranging from vivid dreaming to psychosis. RBD is effectively treated with clonazepam. In addition, the atypical antipsychotics have given physicians new and better treatment options for psychotic symptoms in individuals with Parkinson's disease. EDS is common in Parkinson's disease, while sleep attacks seem to be rare manifestations of the disease or its treatment. Significant EDS is found in 15% of patients with Parkinson's disease compared with in 1% of healthy elderly people. Sleep attacks are observed in patients treated with all dopaminergic medications but have recently been brought to prominence because of their association with the newer dopamine agonists ropinirole and pramipexole. Patients with Parkinson's disease should be informed about the possibility of developing sleep problems during the day when prescribed new drugs. Appropriate actions with regard to driving must be taken if significant and persistent daytime somnolence or sleep attacks appear.
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PMID:Sleep disorders in patients with Parkinson's disease: epidemiology and management. 1146 32

The side-effect profile of levofloxacin was compared with that of other fluoroquinolones based on European and international data from approximately 130 million prescriptions. Levofloxacin was found to be very safe with a low rate of hepatic abnormalities (1/650,000). In contrast, 140 trovafloxacin-treated patients developed hepatic problems, 14 of which were severe, and 8 required transplantation. The main CNS problems associated with fluoroquinolones include dizziness, convulsions, psychosis, and insomnia. Levofloxacin, ofloxacin, and moxifloxacin reportedly have the lowest potential of inducing central nervous system (CNS) adverse events among the fluoroquinolones currently available. Cardiovascular problems were seen in 1/15 million levofloxacin prescriptions compared to 1-3% of sparfloxacin patients having QTc prolongation of greater than 500 msec. Moxifloxacin was also associated with QTc prolongation when compared to non-fluoroquinolone comparators. Nausea, vomiting, and diarrhoea remain the main adverse drug reactions (ADRs) associated with levofloxacin. However, the ADR rate for levofloxacin is still one of the lowest of any fluoroquinolone at 2% (compared to 2-10% for other fluoroquinolones). Ofloxacin and levofloxacin have a very low phototoxic potential, whereas this is a problem for sparfloxacin, enoxacin, and pefloxacin. The tolerance profile of levofloxacin can be considered to be very good, and better than most, if not all of the fluoroquinolones available.
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PMID:Comparison of side effects of levofloxacin versus other fluoroquinolones. 1154 84

Mood disturbances are common sequelae of traumatic brain injury (TBI), but the scientific database for such disorders is very limited in descriptive, prognostic, and treatment data. Post-TBI symptoms often cross diagnostic boundaries and include cognitive loss, amotivation, psychosis, mood, changes, or other domains. The treating physician must be mindful that clear diagnostic boundaries may not exist. Premorbid level of functioning commonly affects post-TBI level of functioning. When setting treatment goals, this must be considered. Patients who had lower levels of psychosocial functioning before the injury may not fare as well afterwards. Treatment of post-TBI mood symptoms should proceed after a full diagnostic work-up including imaging and electroencephalographic (EEG) studies, neuropsychologic testing, and physical and laboratory examinations. Once the diagnostic picture is established, treatment should then proceed with a multidisciplinary team (physician, social worker, neuropsychologist, and others). For the medications, consider both target symptoms and side effects; start medications with low doses and raise slowly, give full therapeutic trials before switching or adding second agents, avoid benzodiazepines if possible, limit anticholinergic or antidopaminergic agents, and avoid providing large quantities of lethal medications. When starting medications for the treatment of mood disorders following TBI, several general principles of treatment in this population should be considered, including: balancing treatment of target symptoms with the potential for adverse effects; making use of side effects to treat comorbid problems when present (ie, relatively antidepressant for depression and marked insomnia); using a "start low, go slow" approach; continuing dose escalation to full therapeutic levels (ie, completing therapeutic trials) before switching or adding augmenting agents; avoiding agents with predictable and functionally important adverse effects (ie, benzodiazepines, strongly anticholinergic or antidopaminergic agents); and avoiding prescription of large and potentially lethal quantities of medications.
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PMID:Emotional Disturbances Following Traumatic Brain Injury. 1173 4

Well-known adverse effects of amisulpride include nausea, insomnia or tiredness, gastrointestinal, extrapyramidal and endocrine symptoms. Cardiac disorders, however, appear to be an extremely rare complication of the drug. Only a few case reports on this complication have been published so far, which deal with QT prolongation, hypotension, hypertension and palpitations. Bradycardia has not yet been mentioned. Here, we will report on a case of asymptomatic bradycardia that developed subsequent to therapeutic doses of amisulpride in a 25-year-old male patient with chronic paranoid-hallucinatory schizophrenia. The patient had been rehospitalized for an acute exacerbation of the psychosis. When the patient failed to respond at the beginning of hospitalization, the treatment was changed from clozapine to amisulpride. After a complete switchover to amisulpride, the patient's ECG showed sinus bradycardia and QT prolongation. When the daily dose of amisulpride was reduced from 800 mg/d to 600 mg/d, the patient's ECG quickly normalized (including blood pressure and pulse rate) within a few days. The patient did not report any cardiovascular-related complaints. Since the cardiovascular-specific diagnostics did not yield any indicative results, bradycardia may be a rare complication of amisulpride treatment.
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PMID:Asymptomatic bradycardia associated with amisulpride. 1177 48

The effects of haloperidol, risperidone, and thioridazine on the pharmacokinetics and side-effect profile of quetiapine were investigated in 36 patients with schizophrenia, schizoaffective disorder, or bipolar disorder in a single-center, two-period, multiple-dose, open-label, randomized trial. Over a one-to two-week period, quetiapine doses were escalated to 300 mg twice daily (bid). Patients were then treated for at least 7 days at the target quetiapine dose and subsequently entered into the combination therapy period, receiving haloperidol (7.5 mg, bid), risperidone (3 mg, bid), or thioridazine (200 mg, bid) for 8.5 days (after 3 days of dose escalation). Key assessments included the pharmacokinetics of quetiapine at steady state (area under the curve within a dosing interval [AUCtSS], maximum [CmaxSS], and minimum [CminSS] observed plasma concentrations, and oral clearance [Cl/f]), as well as the UKU Side Effect Rating Scale scores and safety evaluations. Neither risperidone nor haloperidol had significant effects on quetiapine pharmacokinetics. However, thioridazine produced statistically significant changes, decreasing the least squares means values of the AUCtSS, CmaxSS, and CminSS by 40%, 47%, and 31%, respectively, and increasing Cl/f by 68%. Increases in the following adverse events were noted during coadministration: somnolence (risperidone), insomnia and dry mouth (all three coadministered therapies), and dizziness (thioridazine). UKU side effect items that became worse in >or= 25% of patients during each coadministration period included sedation and increased sleep duration. Results of laboratory tests, electrocardiograms, and vital sign measurements revealed few clinically important changes. Clinical stability can be maintained with good tolerability during the transition from quetiapine monotherapy to periods of coadministration with haloperidol, risperidone, or thioridazine. Coadministration of either haloperidol or risperidone did not have any important effects on the steady-state pharmacokinetics of quetiapine. Thioridazine significantly increased the oral clearance of quetiapine. Increased doses of quetiapine may be necessary to control psychotic symptoms when thioridazine is coadministered with quetiapine.
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PMID:The safety and pharmacokinetics of quetiapine when coadministered with haloperidol, risperidone, or thioridazine. 1191 Feb 56

The therapeutic use of methylphenidate for the management of attention-deficit hyperactivity disorder in children is increasing. As therapeutic use increases, the risk increases of unintentional overdoses, medication errors, and intentional overdoses caused by abuse, misuse, or suicide gestures and attempts. Side effects during therapy, which include nervousness, headache, insomnia, anorexia, and tachycardia, increase linearly with dose. Clinical manifestations of overdoses include agitation, hallucinations, psychosis, lethargy, seizures, tachycardia, dysrhythmias, hypertension, and hyperthermia. Methylphenidate tablets can be abused orally, or they can be crushed and the powder injected or snorted. Despite its abuse potential, there is disagreement regarding the extent to which methylphenidate is being diverted from legitimate use to abuse in preteens and adolescents.
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PMID:Abuse and toxicity of methylphenidate. 1198 Dec 94

Insomnia in children is a nonspecific impairing symptom that may be the result of normal developmental changes, psychosocial duress, a sleep disorder, a psychiatric disorder, other medical disorders, substance misuse, or an adverse effect of medication. Careful clinical assessment of insomnia in children may include the use of symptom rating scales, laboratory testing, or other medical assessment. Short- and long-term treatment of insomnia in children involves management of etiological factors and associated syndromes. Controlled treatment studies of pediatric insomnia are limited to <10 published studies of psychosocial and/or psychopharmacological treatment in young children. Directive parent education and behavior modification techniques have been effective in short-term treatment of insomnia in young children, and may be the preferred treatment of extrinsic insomnia, as well as an important adjunctive treatment of any insomnia symptoms. Two benzodiazepines [flurazepam and delorazepam (chlordesmethyldiazepam)], one antihistamine (niaprazine) and one phenothiazine [alimemazine (trimeprazine)] have been shown to be effective in the short-term treatment of insomnia in young children, although none of these agents have US Food and Drug Administration approval for pediatric insomnia. Short-acting benzodiazepines may have a role in the brief treatment of pediatric insomnia associated with an anxiety or mood disorder, psychosis, aggression, medication- induced activation, or anticipatory anxiety associated with a medical procedure. However, tachyphylaxis and risk of misuse preclude the long-term use of benzodiazepines for the treatment of insomnia in children. Newer hypnotics, which appear better tolerated than the benzodiazepines in studies of adults, may have a role when combined with psychosocial treatments of pediatric insomnia. Treatment of intrinsic pediatric insomnia may additionally involve chronotherapy or medical management.
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PMID:Insomnia in children: when are hypnotics indicated? 1203 75

Carbamoyl phosphate synthetase I deficiency (CPSID) is a rare metabolic disorder affecting the first enzymatic step of urea cycle. We report clinical manifestations of a female case of late-onset CPSID in Japan. An 18-year-old girl was admitted to emergency room due to acute comatose state. Her parents had no apparent consanguineous history. She had suffered from intermittent psychotic episodes (excitation, aggressive behavior and insomnia) with nausea and vomiting from the age of 13, mostly coinciding with menstrual period. She had minor learning disability without major neurological deficits and convulsions. Her mental status was estimated as normal in her intermenstrual period. She had been diagnosed as having hysteria and premenstrual syndrome. Her neurological findings on admission showed deep coma and hypotonic tetraparesis. Plasma ammonia level was markedly elevated (684 micrograms/dl) without significant liver dysfunction. Blood urea nitrogen decreased to 6 mg/dl. Continuous venovenous filtration with subsequential administration of sodium benzoate and l-arginine was started to eliminate blood ammonia. Although the plasma ammonia level decreased to 300 mu/dl in next 10 hours, severe cerebral edema was observed in head computed tomography subsequently, followed by marked cerebral atrophy. Finally, her consciousness status became almost alert a month after the onset, but her mental status was severely retarded. CPSI activity of her biopsied liver markedly decreased and she was diagnosed as having CPS ID. CPSI cDNA analysis of her biopsied liver demonstrated a V1149G mutation. Genomic DNA analysis showed that she was heterozygous in V1149G mutation. The mutation allele was derived from her father. The causative factor for absence or very low level of maternal CPSI mRNA will require further analysis.
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PMID:[A case of late-onset carbamoyl phosphate synthetase I deficiency, presenting periodic psychotic episodes coinciding with menstrual periods]. 1208 Jun 9

Ephedrine is a sympathicomimetic agent that stimulates the central nervous and cardiovascular systems and causes bronchodilatation. It is one of the alkaloids in the herb Ephedra which is the basis of several over-the-counter herbal products, among which a number of popular weight-loss products. The Dutch Inspectorate for Health Care has received reports of adverse reactions presumably associated with Ephedra-containing weight-loss products. These adverse reactions comprised mainly palpitations, stress, headache and insomnia. The Ministry of Health in Canada has recently requested a market recall of some ephedrine-containing herbal products in response to a large number of adverse reactions reported in association with these products. The adverse reactions included stroke, heart attacks, cardiac arrhythmias, seizures and psychotic disorders. The voluntary recall concerns especially products that were marketed without approval and contain Ephedra in combination with caffeine or other stimulants. In the Netherlands, the status of Ephedra-containing products is currently reconsidered.
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PMID:[Ephedrine and ephedra in weight loss products and other preparations]. 1214 23


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