Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This open-label clinical study was conducted for patients with schizophrenia in order to investigate the efficacy, safety and optimal dose of olanzapine. One hundred and fifty-six of the 159 enrolled patients were included in the analysis set. For the primary efficacy measure, the Final Global Improvement Rating (FGIR) score, 15.4% of patients had remarkable improvement, 58.3% of patients had moderate improvement or more, 79.5% of patients had slight improvement or more, and 10.3% of patients had increase in disease symptomatology (worsening). Results from the Brief Psychiatric Rating Scale (BPRS) in all individual items were improved from baseline. Olanzapine was effective not only against positive psychotic symptoms but also against negative symptoms. This was consistent with results from the Positive and Negative Syndrome Scale (PANSS). For the majority of patients, a dose range of 7.5-10.0mg/day, as a lower bound on the minimally effective dose, was suggested by the results of the dose to first response based on improvement in Global Improvement Rating (GIR) analyses. The ratio of olanzapine dose to equivalent haloperidol dose was estimated at 1.2 :1. The most commonly reported treatment-emergent signs and symptoms (TESS) occurring at a frequency of 10% or more were insomnia, weight increase, excitement, sleepiness, anxiety, malaise and dull headaches. There was a low incidence of extrapyramidal treatment-emergent signs and symptoms; the most commonly reported were akathisia (6.4%), tremor (5.8%) and muscle rigidity (2.6%).
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PMID:Olanzapine optimal dose: results of an open-label multicenter study in schizophrenic patients. Olanzapine Late-Phase II Study Group. 1099 65

The authors interviewed a consecutive series of medical inpatients (N = 241) using the Schedule for Affective Disorders and Schizophrenia to determine which depressive symptoms are associated with in-hospital mortality. Fifteen depressive symptoms, pain, and physical discomfort were assessed along with medical comorbidity. Twenty patients died in-hospital (8.3%). Logistic regression showed that anhedonia, hopelessness, worthlessness, indecisiveness, and insomnia predicted in-hospital death after adjusting for physical comorbidity and age. Clinicians should be aware that these depressive symptoms may predict mortality in medical inpatients. Future studies should address which treatment modalities lead to better outcomes.
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PMID:Association between depressive symptoms and mortality in medical inpatients. 1101 29

It is not uncommon for patients who are receiving antipsychotic medication to be given anticholinergic agents, such as biperiden, despite the relative absence of neurological side-effects. Two cases of schizophrenia are reported in which insomnia developed after biperiden withdrawal or reduction. The insomnia continued until biperiden treatment was reinstated, despite the fact that the patients did not exhibit signs or report symptoms indicative of antipsychotic drug-induced neurological side-effects. The occurrence of insomnia following the withdrawal of biperiden or reduction in the dose has not been previously reported. One potential explanation for the insomnia is cholinergic rebound following the withdrawal of biperiden.
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PMID:Insomnia related to biperiden withdrawal in two schizophrenic patients. 1111 12

Jet lag is a travel-induced circadian rhythm phenomenon that afflicts healthy individuals following long- distance flights through several time zones. The typical jet-lag manifestations - insomnia during local sleep time, day fatigue, reduced concentration, irritability, and exhaustion with mild depression - are attributed to transient desynchronization in the circadian rhythm until the internal biological clock is rephased to the new environmental conditions. There is strong evidence relating affective disorders with circadian rhythm abnormalities. Less convincing suggestions relate jet lag to psychosis. It can be hypothesized that in predisposed individuals jet lag may play a role in triggering exacerbation or even de novo affective disorders. Furthermore, we propose the possibility that psychosis and even schizophrenia can be elicited by jet lag. This outlook gains its support from case studies and some common underlying phase-advanced biological denominators involved in both jet lag sufferers and psychotic patients.
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PMID:Psychiatric aspects of jet lag: review and hypothesis. 1113 50

Subjective sleep quality has been identified as an important clinical construct in psychiatric disordered patients. The Pittsburgh Sleep Quality Index (PSQI), one of the most widely used standardized measures to assess subjective sleep quality, generates a global score and scores seven components. The present study psychometrically assessed clinical profiles of subjective sleep quality in 82 control and 92 psychiatric disordered subjects (primary insomnia, n=14; major depression, n=30; generalized anxiety disorder, n=24; and schizophrenia, n=24), using the Japanese version of the Pittsburgh Sleep Quality Index (PSQI-J). The overall reliability coefficient of the PSQI-J was high (Cronbach's alpha=0.77). Correlation coefficients between the PSQI-J global and component scores were statistically significant. The PSQI-J global and component mean scores were significantly higher in psychiatric disordered subjects than control subjects, except for the component of sleep duration. Using a cut-off point of 5.5 in the PSQI-J global score, estimations of sensitivity and specificity provided 85.7 and 86.6% for primary insomnia, 80.0 and 86.6% for major depression, 83.3 and 86.6% for generalized anxiety disorder, and 83.3 and 86.6% for schizophrenia, respectively. The present study supports the utility of the PSQI-J as a reliable and valid measure for subjective sleep quality in clinical practice and research.
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PMID:Psychometric assessment of subjective sleep quality using the Japanese version of the Pittsburgh Sleep Quality Index (PSQI-J) in psychiatric disordered and control subjects. 1116 88

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

Conventional antipsychotic agents can induce extrapyramidal symptoms (EPS) that may be alleviated by switching patients to novel agents such as olanzapine. Patients with schizophrenia and related disorders (ICD-10) who were taking haloperidol (N = 94; mean dose = 12.7 mg/day) and had EPS (Simpson-Angus Scale [SAS] > 3) were directly switched to 6 weeks of open-label olanzapine treatment (mean dose = 11.4 mg/day). There were significant mean improvements (p <0.001 for all measurements) from baseline to endpoint on the SAS (-9.69+/-5.33; percentage change, 87.2%), the Barnes Akathisia Scale (-1.00+/-1.19; percentage change, 82.5%), and the Abnormal Involuntary Movement Scale (-1.48+/-2.89; percentage change, 81.1%), and anticholinergic use decreased from 47.9% to 12.8% (mean baseline to endpoint change: -1.52+/-1.91-mg equivalents of benztropine; p < 0.001). Significant mean baseline to endpoint improvements (p < 0.001 for all measurements) were observed on the Positive and Negative Syndrome Scale (PANSS; -25.28+/-18.67; percentage change, 30.3%), the PANSS-extracted Brief Psychiatric Rating Scale (0-6 scale, -13.41+/-10.16; percentage change, 54.4%), and the Clinical Global Impressions Severity scale (-1.16+/-1.19; percentage change, 26.4%). Spontaneously reported treatment- emergent adverse events with a greater than 5% incidence were somnolence (16.0%), increased appetite (14.9%), weight gain (11.7%), headache (8.5%), anxiety (7.4%), dizziness (6.4%), and insomnia (5.3%). Criteria for a successful switch were met by 90.5% of patients. Psychotic symptom exacerbation was experienced by 30.9% of patients at any time during the study and by 11.7% of patients at endpoint. Results suggest that a direct switch to olanzapine is a therapeutic option when patients with haloperidol-induced EPS are unable to tolerate a more gradual switch.
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PMID:Olanzapine as alternative therapy for patients with haloperidol-induced extrapyramidal symptoms: results of a multicenter, collaborative trial in Latin America. 1147 21

Suicidal patients often report problems with their sleep. Although sleep-related complaints and EEG (electroencephalographic) changes have been seen widely across the spectrum of psychiatric disorders, sleep complaints such as insomnia, hypersomnia, nightmares, and sleep panic attacks are more common in suicidal patients. The subjective quality of sleep as measured by self-rated questionnaires also appears to be more disturbed in suicidal depressive patients. Sleep studies have reported various polysomnographic findings including increased REM (rapid eye movement) time and REM activity in suicidal patients with depression, schizoaffective disorder, and schizophrenia. One mechanism responsible for this possible association between suicide and sleep could be the role of serotonin (5HT). Serotonergic function has been found to be low in patients who attempted and/or completed suicide, particularly those who used violent methods. Aggression dyscontrol appears to be an intervening factor between serotonin and suicide. Additionally, agents that enhance serotonergic transmission decrease suicidal behavior. Serotonin has also been documented to play an important role in onset and maintenance of slow wave sleep and in REM sleep. CSF 5-HIAA levels have been correlated with slow wave sleep in patients with depression as well as schizophrenia. Moreover, 5HT2 receptor antagonists have improved slow wave sleep. Further studies are needed to investigate the possible role of sleep disturbance in suicidal behavior.
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PMID:Sleep and suicide in psychiatric patients. 1153 31

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


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