Zyprexa scientific update |
|
 |
|
Synapse 2010 Jun 3.
Chen S. Seeman P, Liu F.
Department of Neuroscience,Centre for Addiction and Mental Health, Clarke Division, 250 College Street, Toronto, Ontario, Canada M5T 1R8.
Antipsychotic drug binding in the substantia nigra: An examination of high metoclopramide binding in the brains of normal, Alzheimer's Disease, Huntington's Disease, and Multiple Sclerosis patients, and its relation to tardive dyskinesia.
This project was done in order to determine why the annual incidence of metoclopramide-associated tardive dyskinesia is much higher than that for the commonly used antipsychotics. In order to test the hypothesis that metoclopramide tardive dyskinesia may be associated with high concentrations of metoclopramide in the substantia nigra under clinical conditions, the nonspecific binding of tritiated antipsychotics to the dissected melaninized regions of post-mortem human substantia nigra was measured. The nonspecific binding at 1 nM [(3)H]ligand was 7.3, 4.2, 2.6, 0.91 and 0.66 fmoles/mg for [(3)H]haloperidol, [(3)H]clozapine, [(3)H]raclopride, [(3)H]metoclopramide, and [(3)H]olanzapine, respectively. After adjusting these values for the known free concentrations of these drugs in plasma or spinal fluid, the amounts that would be bound under clinical conditions would be 231, 113, 15, 11, and 3.4 fmoles/mg for metoclopramide, clozapine, raclopride, haloperidol and olanzapine,respectively. Using rat striatum as baseline to define antipsychotic binding to non-nigral tissue, the excess amount of binding to the Alzheimer nigral tissue under clinical conditions would be 209, 19, 0, 3.4 and 0.8 fmole/mg for metoclopramide, clozapine, raclopride, haloperidol, and olanzapine, respectively, with a similar pattern for nigral tissues from Huntington and Multiple Sclerosis patients. The high accumulation of metoclopramide is sufficiently high to cause nigral nerve cell membrane damage by metoclopramide's detergent-like action, possibly explaining metoclopramide's toxic ability to elicit early tardive dyskinesia. In addition, the nonspecific binding of metoclopramide was much higher in Alzheimer-diseased substantia nigra, consistent with the fact that older individuals are relatively more vulnerable to metoclopramide tardive dyskinesia. Synapse,2010.
Schizophr Bull 2010 May 31
Rummel-Kluge C, Komossa K, Schwarz S, Hunger H, Schmid F, Kissling W, Davis JM, Leucht S.
1Klinik und Poliklinik für Psychiatrie und Psychotherapie der Technischen Universität München, Klinikum rechts der Isar, Möhlstrasse 26, 81675 München,Germany.
Second-Generation Antipsychotic Drugs and Extrapyramidal Side Effects: A Systematic Review and Meta-analysis of Head-to-Head Comparisons.
Objective: While all second-generation antipsychotics (SGAs) are promoted for having a low risk of extrapyramidal side effects (EPS), clinical observations suggest differences between the various agents. Nevertheless, this question has never been examined in a systematic review and meta-analysis of head-to-head comparisons.
Methods: We searched the register of the Cochrane schizophrenia group (last search May 2007), supplemented by MEDLINE (last search July 2009) for randomized, blinded studies comparing the following SGAs in the treatment of schizophrenia or related disorders: amisulpride, aripiprazole, clozapine, olanzapine, quetiapine, risperidone, sertindole, ziprasidone, and zotepine. At least 3 reviewers extracted the data independently. The primary outcome was "use of antiparkinson medication." The results were combined in a meta-analysis.
Results: We included 54 studies with 116 arms. Risperidone was associated with more use of antiparkinson medication than clozapine, olanzapine, quetiapine, and ziprasidone. Ziprasidone showed more use of antiparkinson medication than olanzapine and quetiapine and zotepine more than clozapine. There was no significant difference between amisulpride and its comparators (olanzapine, risperidone, or ziprasidone). Quetiapine showed significantly less use of antiparkinson medication than the 3 other SGAs it was compared with (olanzapine, risperidone, and ziprasidone). Scale-derived data (Barnes Akathisia Scale and Simpson Angus Scale) were limited.
Conclusions: Our meta-analysis demonstrates that there are differences between the SGAs in their ability to induce EPS that clinicians consider warrant treatment with antimuscarinic drugs. Even though the differences were relatively small, they might be important for individual patients and should be taken into account in drug choice.
J Psychopharmacol 2010 May 24.
Osuntokun OO, Millen B, Xu WL, Kryzhanovskaya LA, Robertson-Plouch C, Carlson JL, Acharya N, Corya SA.
Lilly Research Laboratories,Eli Lilly and Company.
Metabolic parameters in patients treated with olanzapine or other atypical antipsychotics.
The relative risk of changes in metabolic parameters during treatment with atypical antipsychotics has not been fully investigated. Baseline-to-endpoint mean and anytime-categorical changes in metabolic parameters were evaluated in Lilly active comparator-controlled clinical trials. Olanzapine-treated patients gained significantly more baseline-to-endpoint weight versus risperidone- (3.3 kg [N = 713; median exposure [ME, days] = 68] versus 1.8 kg [N = 697; ME = 65], p < 0.001), ziprasidone- (2.8 kg [N = 463; ME = 168] versus -1.3 kg [N = 443; ME = 89], p < 0.001), and aripiprazole-treated patients (3.7 kg [N = 273; ME = 104] versus 0.5 kg [N = 275; ME = 187], p < 0.001). Significantly more olanzapine-treated patients gained >/=7% of their baseline weight versus risperidone- (30.6% [N = 713; ME = 169] versus 20.2% [N = 697; ME = 140], p < 0.001), ziprasidone- (30.0% [N = 463; ME = 147] versus 6.5% [N = 443; ME = 165], p < 0.001), and aripiprazole-treated patients (40.3% [N = 273; ME = 170] versus 16.4% [N = 275; ME = 154], p < 0.001). Olanzapine-treated patients had significantly greater baseline-to-endpoint changes in fasting triglycerides compared with ziprasidone- (0.24 mmol/L [N = 365; ME = 168] versus -0.24 mmol/L [N = 316; ME = 140], p < 0.001) and aripiprazole-treated patients (0.28 mmol/L [N = 215; ME = 195] versus -0.19 mmol/L [N = 210; ME = 194], p < 0.001). Olanzapine-treated patients had significantly greater baseline-to-endpoint changes in fasting glucose than ziprasidone- (0.25 mmol/L [N = 379; ME = 168] versus -0.04 mmol/L [N = 333; ME = 133], p = 0.016) and aripiprazole-treated patients (0.27 mmol/L [N = 227; ME = 195] versus 0.04 mmol/L [N = 220; ME = 194], p = 0.048). The study concluded that there are changes with varying frequencies and magnitude in some metabolic parameters in patients treated with olanzapine compared with other atypical antipsychotics.
J Clin Psychopharmacol 2010 Jun; 30(3):286-9.
Kinon BJ, Chen L, Stauffer VL, Sniadecki J, Ascher-Svanum H, Kollack-Walker S, Jacob J, Kapur S
Lilly Research Laboratories,Eli Lilly and Company, Lilly Corporate Center, Indianapolis, IN 46285, USA.
Early onset of antipsychotic action in schizophrenia: evaluating the possibility of shorter acute efficacy trials.
Extended placebo-controlled clinical trials in schizophrenia research pose an ethical challenge. This study examines factors that have implications for the design and duration of placebo-controlled acute efficacy trials: Does early response discriminate active drug (AD) from placebo, and are the early differences sustained over time? A post hoc pooled analysis of 2 randomized 6-week double-blind clinical trials was performed comparing patients with schizophrenia treated with placebo or low-dose olanzapine (1 mg/d; placebo/low dose [PBO] group, n = 170) to patients treated with a 10- to 20-mg/d dose of haloperidol or medium- to high-dose olanzapine (7.5 to 17.5 mg/d; AD group, n = 252). Mixed-model repeated-measure analysis tested for group differences. Power analysis was undertaken to compare study designs with shorter durations. At 2 weeks, the mean reduction in the Brief Psychiatric Rating Scale total score was significantly greater for the AD group (-10.1) compared with the PBO group (-4.1; P < 0.001); this difference was sustained until the study ended (6 weeks). A higher proportion of early treatment responders were observed for the AD group (52%) compared with the PBO group (29%; P < 0.001). Early nonresponse to placebo or drug was predictive of subsequent nonresponse (negative predictive value: PBO = 95%, AD = 84%). Power analysis indicates that the placebo-drug differences are robust at 2 weeks. Treatment responders from the AD and the PBO groups followed a similar response path. Early response to antipsychotic treatment discriminated AD from placebo. Reducing placebo-controlled clinical trials from 6 weeks to 2 to 4 weeks was found to be a viable option for efficacy identification in acutely ill patients.
Drugs Today (Barc ) 2010 Mar ;46(3):173-81.
Owen RT.
Crewe,Cheshire, UK.
Olanzapine: a review of rapid and long-acting parenteral formulations.
Olanzapine, an atypical antipsychotic was first introduced in 1996 as an oral formulation and is used in the treatment of schizophrenia and bipolar disorder. Recent developments have included parenteral formulations to improve compliance in the treatment of schizophrenia and to treat agitation in patients with schizophrenia and bipolar mania. Olanzapine pamoate long acting injection (depot) is a novel formulation of the atypical antipsychotic olanzapine, which is licensed for the maintenance treatment of schizophrenia. When administered as the pamoate salt, olanzapine has an elimination half-life of approximately 30 days, allowing it to be given at 2- or 4-weekly intervals. An 8-week, randomized, double-blind study in 404 patients acutely ill with schizophrenia demonstrated significant antipsychotic efficacy (versus placebo). A 24-week, randomized, double-blind, active-controlled study in 1,065 schizophrenia patients stabilized with oral olanzapine demonstrated the depot formulation could delay exacerbation of positive symptoms or hospitalization. Apart from local injection reactions and a postinjection delirium/sedation syndrome, no new adverse events additional to those seen with oral olanzapine have been notedto date. The pivotal clinical trials of olanzapine rapid-acting intramuscular injection are reviewed in addition to post-hoc analyses, controlled and naturalistic studies since its launch.
J ClinPsychiatry 2010 Apr 20.
Van Ameringen M, Mancini C, Patterson B, Benett M, Oakman J.
Anxiety Disorders Clinic, 1F Clinic, McMaster University Medical Centre, Hamilton Health Sciences, Box 2000, Hamilton, Ontario, L8N 3Z5, Canada
A randomized,double-blind, placebo-controlled trial of olanzapine in the treatment of trichotillomania.
BACKGROUND: Trichotillomania has been considered as part of the obsessive-compulsive disorder spectrum; however, trichotillomania treatment with obsessive-compulsive disorder medications has largely been unsuccessful.
OBJECTIVE: To determine whether a dopaminergic treatment as used in tics and Tourette's syndrome would be effective in trichotillomania.
METHOD: Twenty-five participants with DSM-IV trichotillomania participated in a 12-week, randomized, double-blind, placebo-controlled trial of flexible-dose olanzapine for trichotillomania. Recruitment occurred between August 2001 and December 2005, and follow-up was completed in February 2006. The primary outcome measure was the Clinical Global Impressions-Improvement (CGI-I) scale, and secondary measures of efficacy included the Yale-Brown Obsessive Compulsive Scale for Trichotillomania (TTM-YBOCS) and the Clinical Global Impressions-Severity of Illness (CGI-S) scale. RESULTS: Eleven of 13 participants (85%) in the olanzapine group and 2 of 12 (17%) in the placebo group were considered responders according to the CGI-I (P = .001). There was a significant change from baseline to end point in the TTM-YBOCS (P < .01) and the CGI-S (P < .001). The mean +/- SD dose of olanzapine at end point was 10.8 +/- 5.7 mg/d. Twenty-one of 25 patients (84%) reported at least 1 adverse event, but no adverse events resulted in early withdrawal from the study.
CONCLUSION: Olanzapine seems to be a safe and effective treatment for primary DSM-IV trichotillomania.
Clin Exp Rheumatol 2009 Sep-Oct; 27(5 Suppl 56):S86-91.
Malemud CJ.
ospitals Case Medical Center, Cleveland, Ohio 44106-5076, USA.
Focus on pain mechanisms and pharmacotherapy in the treatment of fibromyalgia syndrome.
OBJECTIVE: To critically evaluate the role of several notable 'pain pathways' in the fibromyalgia syndrome (FMS).
METHODS: PubMed provided the data base for peer-reviewed basic and clinical science studies on musculoskele-tal and neuropathic pain mechanisms with a principal emphasis on critically appraising papers from 2002 to the present. RESULTS: FMS pharmacotherapy is more prevalent in clinical practice as our understanding of the cellular, molecular and pathophysiologic mechanisms contributing to widespread musculoskeletal and neuropathic pain has emerged. Thus, several 'pain pathways' including high-voltage activated Ca2+ channels and the K(v)1 family of K+ channels ion channels appear related to the efficacy of pregabalin and amitryptyline, respectively, in FMS. Additionally, serotonergic and serotonergic/norepinephrine receptor-mediated mechanisms may explain the reported pharmacologic efficacy in FMS of mirtazapine, duloxetine and milnacipran. By contrast, the decreased level of micro-opioid receptors in the CNS of FMS patients suggests a mechanism as to why opioid therapy should be avoided. However, increased peripheral benzodiazepine receptors on monocytes from FMS patients suggested an explanation for the reported efficacy of olanzapine in FMS.
CONCLUSION: Pregabalin was the first drug approved by the FDA for the treatment of FMS-related pain. Drugs that have been assessed for their potential use in FMS pharmacotherapy include gabapentin and tricylic antidepressants. These drugs appear to target specific Ca2+ or K+ ion channels notable for their involvement in mediating neuropathic pain. Serotonin and norepinephrine reuptake inhibitors including, mirtazapine, duloxetine and milnacipran appear to be more efficacious in FMS than selective serotonin reuptake inhibitors. Milnacipran became the second FDA-approved drug for FMS.
Iran J Allergy Asthma Immunol 2009 Sep;8(3):135-9.
Shariati GR, Ahangari G, Hossein-nezhad A, Asadi SM, Pooyafard F, Ahmadkhaniha HR.
Department of Medical Genetic,National Institute for Genetic Engineering and Biotechnology (NIGEB), Tehran, Iran.
Expression changes of serotonin receptor gene subtype 5HT3a in peripheral blood mononuclear cells from schizophrenic patients treated with haloperidol and Olanzapin.
Serotonin receptors are involved in pathophysiology of schizophrenia and may mediate other neurotransmitter effects. We investigated serotonin receptors gene expression in peripheral blood mononuclear cells (PBMC) of naïve schizophrenic patients, before and after treatment. Also serotonin receptor gene expression was compared in two treatment groups including Haloperidol and Olanzapine. The PBMC was separated from whole blood by Ficoll-hypaque. The total cellular RNA was extracted and the cDNA was synthesized. This process was followed by real-time PCR using primer pairs specific for 5HT(3a) serotonin receptor mRNA and beta-actin as internal control. The results showed the presence of subtype of serotonin receptor in lymphocytes. Serotonin gene expression showed significant changes in Olanzapine treatment group which correlated with Clinical Global Impression (CGI) score improvement. In conclusion, the present study has shown that human PBMC express serotonin receptors 5HT(3a). Moreover, clinical symptom improvement of Olanzapin may be demonstrated by a change in serotonin receptor gene expression.
Isr J Psychiatry relat Sci. 2009; 46(3):213-20.
Poyurovsky M, Faragian S, Fuchs C, Pashinian A.
Tirat Carmel Mental Health Center, Tirat Carmel,Israel.
Effect of the selective norepinephrine reuptake inhibitor reboxetine on cognitive dysfunction in schizophrenia patients: an add-on, double-blind placebo-controlled study.
The noradrenergic (NE) system mediates cognitive dysfunction in schizophrenia patients, and the NE transporter represents a putative target for cognitive enhancing therapy. In a double-blind placebo-controlled study we evaluated the effect of add-on reboxetine (4 mg/day), a selective norepinephrine reuptake inhibitor (NRI), co-administered with atypical antipsychotic olanzapine (10 mg/day) on cognitive functioning in DSM-IV schizophrenia patients. The Automated Neuropsychological Assessment Metrics battery and Wisconsin Card Sorting Test were used to assess selective cognitive functions at baseline and endpoint (6 weeks). Clinical assessment was also performed. No between-group differences were found in neurocognitive tests, suggesting that reboxetine did not significantly change patients' cognitive performance compared to placebo. Reboxetine was well-tolerated and did not interfere with the therapeutic effect of olanzapine. Long-term studies using higher reboxetine dosages and alternative NRIs (e.g., atomoxetine) are needed to determine the role of NRIs as cognitive enhancers in patients with schizophrenia and other disorders associated with cognitive impairments.
Ther Drug Monit 2009 Dec; 31(6):758-63.
Spina E, D'Arrigo C, Santoro V, Muscatello MR, Pandolfo G, Zoccali R, Diaz FJ, de Leon J.
Section of Pharmacology, Department of Clinical and Experimental Medicine and Pharmacology, University of Messina and IRCCS Centro Neurolesi Bonino-Pulejo, Messina, Italy.
Effect of valproate on olanzapine plasma concentrations in patients with bipolar or schizoaffective disorder.
The effect of valproate on the steady-state plasma concentrations of olanzapine was investigated in 18 patients with bipolar or schizoaffective disorder. Additional valproate, at a dose ranging from 600 to 2000 mg/d, was administered for 4 weeks to patients stabilized on olanzapine (5-20 mg/d). During valproate coadministration, mean plasma olanzapine concentrations decreased significantly from 32.9 +/- 9.7 ng/mL at baseline to 27.4 +/- 9.8 ng/mL at week 2 (P = 0.02), and to 26.9 +/- 9.2 ng/mL at week 4 (P = 0.001). Smoking also decreased plasma olanzapine concentrations. Valproate coadministration with olanzapine was well tolerated and no patient showed a worsening of his or her psychopathological condition. These findings indicate that valproate, at doses of up to 2000 mg/d, is associated with a minimal, presumably not clinically significant, decrease in plasma olanzapine concentrations, possibly as a result of induction of olanzapine metabolism. New studies are needed to confirm that valproate could have mild inductive effects.
J Psychopharmacol 2009 Oct 14.
Cipriani A, Rendell J, Geddes JR.
Department of Medicine and Public Health, Section of Psychiatry and Clinical Psychology, University of Verona.
Olanzapine in the long-term treatment of bipolar disorder: A systematic review and meta-analysis.
Olanzapine was licensed in the USA by the Food and Drug Administration in 2003 for the prevention of relapse in patients with bipolar disorder when the acute manic episode had responded to treatment with olanzapine. However, olanzapine is commonly used in clinical practice for preventing relapse in patients with bipolar disorder even when acute response has not been demonstrated. The aim of this systematic review and meta-analysis is to determine the effectiveness and acceptability of olanzapine in preventing recurrent mood episodes in bipolar disorder. MEDLINE, EMBASE, the Cochrane Collaboration Depression, Anxiety and Neurosis Controlled Trials Register and the Cochrane Central Register of Controlled up to July 2008 were accessed. Only randomised controlled trials comparing olanzapine with placebo or other active drugs for long-term treatment were included. Two reviewers independently extracted data. Authors were contacted to provide additional data. Of the five trials included in this review, four were conducted by Eli Lilly, the manufacturer of olanzapine. Olanzapine was more effective than placebo at preventing manic relapse, but there was no difference between olanzapine (alone or in combination with lithium or valproate) and placebo (alone or in combination with lithium or valproate) in terms of relapse into any mood episode, as defined as primary outcome by authors in each of the primary studies. We conclude that olanzapine may prevent further manic episodes only in patients who have responded to olanzapine in an acute manic or mixed episode and who have not previously had a satisfactory response to lithium or valproate.
Psychiatr Danub 2009 Sep; 21(3):371-5.
Sagud M, Mihaljević-Peles A, Mück-Seler D, Pivac N, Vuksan-Cusa B, Brataljenović T, Jakovljević M.
University Department, Clinical Hospital Zagreb,10000 Zagreb, Croatia.
Smoking and schizophrenia.
Smoking prevalence for schizophrenic patients is higher than this for general population. More than 60% of schizophrenic patients are current smokers, which contributes to excessive mortality in these patients. The reasons for high frequency of both smoking prevalence and heavy smoking in schizophrenic patients is thought to be at least partially related to enhancement of brain dopaminergic activity, which, in turn, results in behavioral reinforcement due to stimulant effects. Smoking stimulates dopaminergic activity in the brain by inducing its release and inhibiting its degradation. There is also evidence that cigarette smoking can reduce deficits relative to dopamine hypofunction in prefrontal cortex. Recent neuroimaging studies have further contributed the evidence of complex influences of cigarette smoking on brain dopaminergic function. It has been suggested that smoking may be an attempt by schizophrenic patients to alleviate cognitive deficits and to reduce extrapyramidal side-effects induced by antipsychotic medication. Cigarette smoke also increases the activity of CYP 1A2 enzymes, thus decreasing the concentration of many drugs, including clozapine and olanzapine. There is also evidence that smoking is associated with increased clearance of tiotixene, fluphenazine and haloperidol. Given the high frequency of smoking in schizophrenic patients, clinicians need to check smoking status in each patient. Schizophrenic patients who smoke may require higher dosages of antipsychotics than nonsmokers. Conversely, upon smoking cessation, smokers may require a reduction in the dosage of antipsychotics.
Vertex. 2008 Sep-Oct; 19(81):254-60.
Adrianzen C, Sanchez M, Cordova J, Castillo I.
Gerente Médico de Investigación Clínica en Neurociencias, Eli Lilly & Co. Afiliada LACMASS Lima, Perú.
[Olanzapine versus haloperidol: effectiveness in functionality and health state in a sample of Venezuelan patients with schizophrenia]
OBJECTIVE: To compare olanzapine versus haloperidol effectiveness, in terms of relapse rates in Venezuelan patients with schizophrenia.
METHODS: A randomized, open label, follow-up study of 9-months after clinical stabilization or hospital discharged was conducted. The Medical Outcomes Study Form Health Survey (SF-36) and the Quality of Life Index from Mezzic & Cohen were used to evaluate the health state and quality of life. Safety parameters were collected.
RESULTS: Thirty-one patients in olanzapine and 40 in haloperidol were enrolled and discontinuation rates were 65% and 68% respectively. Only one patient in haloperidol relapsed. Health status improved more with olanzapine showing statistically significant improvement in five of the eight items of the SF-36. Olanzapine was slightly superior improving quality of life. More adverse events were registered with haloperidol (p = 0.036). More extrapyramidal symptoms, akathisia and insomnia were reported with haloperidol and more weight gain with olanzapine but the differences were not significant.
CONCLUSIONS: Both medications were similar preventing relapses. Health status and functionality improved more with olanzapine versus haloperidol. Safety results are consistent with the known profile of the drug. Study limitations on design and conduction of this study restrict its generalization.
Psychiatr Pol 2008 Nov-Dec; 42(6):841-58.
Jarema M, Meder J, Araszkiewicz A, Tyszkowska M.
III Klinika Psychiatryczna IPiN w Warszawie.
[Antipsychotics in clinical practice. Treatment of the first schizophrenic episode]
AIM: The aim was to obtain the information regarding the choice of antipsychotic drugs in the treatment of first episode schizophrenia. In particular, the factors influencing doctors' preferences and their opinion about several antipsychotics and the availability of these drugs were evaluated.
METHODS: The anonymous questionnaire was presented to 100 psychiatrists; 50 of them were in hospital and 50 were in the out-patient practice. The questionnaire consisted of 17 questions regarding the pharmacological treatment of the first schizophrenic episode.
RESULTS: The most frequently prescribed drug was olanzapine (33%), then risperidone (26%), and perazine (25%). In hospitals, risperidone was more frequently administered than perazine (29% and 24% respectively) while in out-patient clinics perazine slightly outnumbered risperidone (25% vs 23%). Fluoxetine was prescribed to 18% of out-patients, but not to hospitalized ones. Doctors performed treatment verification mainly (in 39% of patients) after 4 weeks of therapy. The change of antipsychotics was made more frequently in 28% of those hospitalized than the out-patients (16%) and mainly due to the lack of efficacy. More psychiatrists considered the most important attribute of the drug to be the efficacy toward the negative symptoms (77%) than the positive symptoms (59% of doctors).
CONCLUSIONS: Prescription practice of psychiatrists shows the popularity of olanzapine and risperidone in the treatment of the first psychotic episode, but also indicates the strong position of perazine, which results from the current administrative regulations. Three times more psychiatrists think that patients should have an unrestricted (by the law) access to olanzapine or risperidone than to perazine. The most important attribute of an antipsychotic in the first episode schizophrenia turned out to be its efficacy toward the negative symptoms. Psychiatrists admitted that they chose an antipsychotic much more frequently on the basis of their own knowledge than on the basis of experts' opinion or the administrative regulations.
Drug Mettab Lett.2008 Apr;2(2):100-14.
Cashman JR, Zhang J, Nelson MR, Braun A
Human BioMolecular Research Institute, 5310 Eastgate Mall, San Diego, CA 92121, USA.
Analysis of flavin-containing monooxygenase 3 genotype data in populations administered the anti-schizophrenia agent olanzapine.
Flavin-containing monooxygenase 3 (FMO3) genotype data for European-, Latin-, African- and Asian-American schizophrenia patients administered olanzapine were compared to age-, gender-, and race/ethnicity-matched controls. Single nucleotide polymorphisms and haplotypes associated with case-control status was undertaken to determine the potential role of FMO3 in olanzapine therapeutic response. The relationship between side effects and FMO3 genotype and allele frequencies was also studied. For European Americans, significant differences in individual cases versus controls were observed between FMO3 158 and 257 alleles and genotype frequencies and schizophrenia delusions, hallucinations, and weight gain/increased appetite but this was not observed in a replicated population. For Latin Americans, a significant difference in individual cases versus controls was observed for FMO3 158 and 257 for schizophrenia delusions as well as hallucinations and delusions. Sleepiness and weight gain was associated with allele 308. In African Americans, a comparison of allele frequency and diagnosis showed a significant dependence on allele 158 in individual cases versus controls. FMO3 genotype and allele frequency was not significantly associated with auditory hallucinations or delusions. For Asian Americans, no significant difference in allele or genotype frequency and auditory hallucination and delusions was observed in individual cases versus controls. In female Asian American, allele frequency for FMO3 257 was significantly associated with diagnosis and in males, genotype frequency for FMO3 257 and diagnosis was significantly associated.
Acad Emerg Cal.2008 Sep; 15(9):806-11.
Hill CH, Miner JR, Martel ML.
Department of Emergency Medicine,Hennepin County Medical Center, Minneapolis, MN, USA.
Olanzapine versus droperidol for the treatment of primary headache in the emergency department.
OBJECTIVES: The objective was to determine if there is a difference in pain relief or frequency and severity of side effects in emergency department (ED) patients with primary headache treated with either intramuscular (IM) olanzapine or IM droperidol.
METHODS: This was a prospective, randomized nonblinded clinical trial of adult ED patients undergoing treatment for suspected primary headache. Consenting patients were randomized to receive either droperidol 5 mg IM or olanzapine 10 mg IM. Prior to receiving treatment, patients were asked to complete a 100-mm visual analog scale (VAS) describing their pain and a 4-point verbal rating scale (VRS) describing their pain as none, mild, moderate, or severe. Patients also completed a 100-mm VAS describing their level of nausea. Pain and nausea measurements were repeated 30 and 60 minutes after medication administration. Patients also completed the Barnes Akathisia Scale (BAS) 30 and 60 minutes after medication administration. Descriptive statistics were used as appropriate. Pain relief was compared both in terms of the decrease in VAS scores and in the proportion of patients who reported moderate or severe pain whose report later changed to mild or no pain.
RESULTS: One-hundred patients were enrolled; 13 were withdrawn before administration of the study medication, 8 in the droperidol group and 5 in the olanzapine group, leaving 87 patients for analysis. Forty-two patients received droperidol and 45 received olanzapine. In the droperidol group, 35/40 (87.5%) patients who had reported moderate or severe pain at baseline reported mild or no pain at 60 minutes. In the olanzapine group, 38/44 (86.4%) reported this change (p = 0.89). The mean percent change from baseline VAS pain score at 60 minutes was -37% (95% CI = -84% to 11%) for droperidol and -37% (95% CI = -64% to 10%) for olanzapine (p = 0.30). The mean percent change from baseline for the VAS nausea score was -59% (95% CI = -70% to -47%) for droperidol and -64% (95% CI = -77% to -51%) for olanzapine (p = 0.83). There was no difference in any report of akathisia by the BAS between the groups (p = 0.63).
CONCLUSIONS: Both olanzapine and droperidol are effective treatments for primary headaches in the ED. No significant differences were found between the medications in terms of pain relief, antiemetic effect, or akathisia. Olanzapine may be used to treat primary headache and it is an effective alternative to droperidol.
J Clin Psychiatry 2008 Sep; 69(9):1416-22.
Ujike H, Nomura A, Morita Y, Morio A, Okahisa Y, Kotaka T, Kodama M, Ishihara T, Kuroda s
Department of Neuropsychiatry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-cho,Okayama 700-8558, Japan.
Multiple genetic factors in olanzapine-induced weight gain in schizophrenia patients: a cohort study.
OBJECTIVE: One of the clinically significant adverse effects of olanzapine treatment is weight gain, which shows substantial inter-individual differences and may be influenced by genetic variation. The aim of this investigation was identification of genetic risk factors associated with olanzapine-induced weight gain.
METHOD: Inpatients with DSM-IV-TR schizophrenia (N = 164) were administered olanzapine for 8 to 24 (mean +/- SD = 17.9 +/- 9.4) weeks. The clinical background, body mass index (BMI), and clinical response to olanzapine were investigated. Twenty-one loci of diverse candidate genes encoding dopamine, serotonin (5-HT), histamine, and adrenergic receptors, tumor necrosis factor-alpha, ghrelin, adiponectin, and peroxisome proliferator-activated receptor gamma-2, were analyzed. The study was conducted from June 2001 to June 2003 at 4 psychiatric hospitals in Japan.
RESULTS: BMI increased by a mean +/- SD 4.3 +/- 10.7% after treatment with olanzapine (mean +/- SD dose = 15.5 +/- 5.8 mg/day). Olanzapine-induced weight gain correlated negatively with baseline BMI and positively with clinical global improvement and the length of olanzapine treatment (p < .0001), but it did not correlate with the daily dose of olanzapine, concomitant antipsychotics, sex, age, or smoking. Four genetic variants, the 102T allele of HTR2A, the 825T allele of GNB3, the 23Cys allele of HTR2C, and the 64Arg/Arg genotype of ADRB3, were significantly associated with olanzapine-induced weight gain. Stepwise regression analysis revealed that the baseline BMI predicted 12.5% of the weight gain, and the 2 latter genetic factors added 6.8%. The patients with double and triple genetic risk factors showed 5.1% and 8.8% BMI increases, respectively, during olanzapine treatment, whereas the patients with a single or no risk factor showed approximately a 1% BMI increase.
CONCLUSIONS: We identified genetic variants of 5-HT(2A) and 5-HT(2C) receptors, the G-protein beta-3 subunit, and the adrenergic receptor beta-3, as genetic risk factors for olanzapine-induced weight gain, and they showed additive genetic effects on weight gain.
Neuropsychopharmacol Hung 2007 Oct;9(3):115-24.
István S, Agoston T, Tamás T, Zoltán J.
SZTE Pszichiátriai Klinika, Szeged, Hungary.
[A naturalistic, observational study of outpatients with schizophrenia: efficacy and safety results after 6 months. The International Schizophrenia Outpatient Health Outcomes study, IC-SOHO]
The International Schizophrenia Outpatient Health Outcomes study, IC-SOHO is a three-year international observational study that investigates clinical and health outcomes of antipsychotic treatments. 7658 outpatients treated for schizophrenia were enrolled in the study, who needed an antipsychotic therapy to initiate or switch. The primary analysis compared the group taking olanzapine with the group taking any other antipsychotics, while the secondary comparison was performed between those treated with olanzapine and those with risperidone. Efficacy analysis was carried out based on changes in Clinical Global Impression of Severity scale (CGI-S), which was performed at a global symptom level, as well as with respect to the patients' positive, negative, cognitive and depressive symptoms. In addition, adverse events were also evaluated. Results of the analysis of the 3- and 6-month data from Hungary are disclosed in this publication. 200 patients were enrolled in the country. Demographics of the treatment groups were not significantly different. At 3 and 6 months after treatment initiation, there were no significant between-group differences in improvement of global symptomatology, however, cognitive symptoms improved more in the Olanzapine-group compared to those taking other antipsychotics (p<0.05). In patients showing Extrapyramidal Symptoms (EPS) at baseline, these symptoms finished to a greater extent among those receiving olanzapine than in those receiving other antipsychotics (after 6 months D<0.0001). Half a year later, significantly less patients showed extrapyramidal adverse events (p=0,0007), and the previous EPS terminated to a greater extent (p=0.0016) in the olanzapine group, as compared to those taking risperidone. No between-group differences were found in changes of sexual functions, as well as of weight and Body Mass Index measures. Switching antipsychotic initiated at study baseline, and adding-on one or more other antipsychotic to the initial one, were significantly less frequent in the Olanzapine-group compared to those initiated other antipsychotics. In the first 3 months, treatment compliance was significantly higher with olanzapine therapy than with other antipsychotic treatments, and with risperidone respectively. Results from the Hungarian sample correspond with results from higher analysis levels of wider patient populations of IC-SOHO study. Olanzapine showed outstanding efficacy in lessening cognitive disturbances and global clinical symptomatology associated with schizophrenia. Extrapyramidal symptoms of patients treated with olanzapine improved significantly better compared with those patients who received other antipsychotics and risperidone respectively.
J Can Acad Child Adolesc Psychiatry. 2007 Nov; 16(4):167-172.
Norris ML, Spettigue W, Buchholz A, Henderson KA.
Regional Eating Disorders Program, Children’s Hospital of Eastern Ontario,Ottawa, Ontario.
Challenges Associated with Controlled Psychopharmacological Research Trials in Adolescents with Eating Disorders
INTRODUCTION: Eating disordered populations present many unique challenges both to clinicians and researchers. Adolescents with eating disorders can be difficult to treat, and the challenges associated with research in this area can be significant.
OBJECTIVES: THIS PAPER WAS WRITTEN WITH THREE MAIN OBJECTIVES IN MIND: to comment on some of the barriers impeding mental health research in general, to highlight challenges faced in the design and implementation of ED-specific studies, and to integrate personal insight into some of the many challenges that we have encountered during our experience with a randomized clinical trial examining the efficacy of olanzapine for the adjunctive treatment of youth with Anorexia Nervosa.
DISCUSSION: It is hoped that providing information in this context will allow researchers greater insight into some of the many challenges that accompany study of this cohort.
Int J Clin Pharmacol Ther. 2007 Dec;45(12):631-42.
Habil MH, Gondoyoewono H, Chaudhry HR, Samanwongthai U, Hamid AR, Hashmi IT, Budiman R, Knowles AG, Buenaventura R.
Department of Psychological Medicine, University of Malaya, Kuala Lumpur, Malaysia
Effectiveness and safety of olanzapine in the treatment of Asian outpatients with schizophrenia.
OBJECTIVE: The objective of this study was to assess the effectiveness and safety of olanzapine in the treatment of schizophrenia among Asian patients in an outpatient setting.
METHODS: This was an open-label, prospective, observational study involving 339 patients from Indonesia, Pakistan, Malaysia, Thailand, and Singapore. Brief Psychiatric Rating Scale (BPRS), Clinical Global Impression Severity scale (CGI-S), and safety parameters were assessed.
RESULTS: 62% of patients responded to olanzapine treatment, defined a priori as a reduction in BPRS of > 40% from baseline. Following the 8-week treatment period, the BPRS total, BPRS positive, BPRS negative, and CGI-S scores decreased by 18.7 (95% CI: 17.4, 20.2), 6.1 (5.6, 6.6), 2.9 (2.6, 3.2), and 1.5 points (median 1.0), respectively (p < 0.0001). In total, 31 of the 339 patients (9.1%) failed to complete the study according to the study description. Loss to follow-up and personal conflict were the most common reasons for discontinuation. There were 30 treatment-emergent adverse events with six serious cases, assessed as unrelated to study drug, reported.
CONCLUSION: This study further demonstrates the effectiveness and safety of olanzapine in actual clinical practice settings, in reducing the severity of psychopathological symptoms in Asian patients with schizophrenia.
J Clin Psychiatry. 2007 Dec;68(12):1828-33.
Khan A, Schwartz K, Stern C, Redding N, Kolts RL, Brown WA, Robinson DS.
Northwest Clinical Research Center, Bellevue, Wash., USA
Mortality risk in patients with schizophrenia participating in premarketing atypical antipsychotic clinical trials.
OBJECTIVE: Given the concern that mortality rates may be increased in geriatric patients exposed to atypical antipsychotic agents, we assessed mortality rates for adult patients with schizophrenia assigned to an investigational antipsychotic (olanzapine, quetiapine, risperidone, or ziprasidone), a control antipsychotic (haloperidol or chlorpromazine), or placebo in preapproval clinical development programs to assess relative risk with atypical antipsychotics as compared to typical antipsychotics or placebo.
METHOD: We reviewed safety data (from clinical trials conducted from approximately 1982 to 2002) for 16,791 adult patients with schizophrenia (DSM-III or DSM-IV criteria) in U.S. Food and Drug Administration (FDA) Summary Basis of Approval (SBA) reports for 6 antipsychotic drugs. Mortality rates were calculated for each treatment group (investigational agent, active control, or placebo) on the basis of patient exposure years (PEY) and gross mortality. We compared the differences in mortality rates between placebo and investigational agents, active controls, and all antipsychotic drugs combined using odds ratios. RESULTS: By PEY analysis, the mortality rate for patients assigned to placebo treatment was significantly higher (p < .05) than for either the investigational antipsychotic (OR = 0.23, 95% CI = 0.13 to 0.45) or the active control group (OR = 0.19, 95% CI = 0.08 to 0.45). Although rates based on gross mortality were also higher with placebo treatment, statistical significance was only seen when comparing patients assigned to placebo with those assigned to the active control antipsychotic group (OR = 0.35, 95% CI = 0.15 to 0.82).
CONCLUSIONS: Despite reported excess mortality with antipsychotic use in elderly patients with dementia, SBA data did not reveal a similar increased risk of antipsychotics in adult patients with schizophrenia. However, methodological limitations of the FDA SBA reports may affect the generalizability of these findings.
Neuro Endocrinol Lett. 2007 Dec;28(6):881-8.
Svestka J, Synek O, Tomanová J, Rodáková I, Cejpková A.
Department of Psychiatry, University Hospital, Brno, Czech Republic
Differences in the effect of second-generation antipsychotics on prolactinaemia: six weeks open-label trial in female in-patients.
OBJECTIVES: The main objective was to evaluate the effect of five second-generation antipsychotics (amisulpride, quetiapine, olanzapine, risperidone, and zotepine) on prolactinaemia during 6 week therapy in 433 female in-patients with mainly schizophrenic disorders. Secondary objectives included identification of dynamics of change in serum prolactin levels and correlations of changes of prolactinaemia with some demographic and clinical parameters. METHODS: The trial was a prospective, open-label, single-center one with a flexible dosing of SGAs. The therapeutic effect of SGAs was assessed by a change of scores of CGI-S and CGI-I scales from a baseline to the endpoint. Blood samples were taken in the morning under fasting condition.
RESULTS: Amisulpride and risperidone increased prolactinaemia significantly in 100% of patients, as early as after week 1 of the therapy. Quetiapine and zotepine relatively reduced prolactinaemia significantly, as early as from week 1 of the quetiapine treatment. Olanzapine led to a transient mild prolactin elevation. The much lower prevalence of hyperprolactinaemia over 2 000 mIU/l differentiates olanzapine from amisulpride and risperidone. Prolactin elevation did not correlate with age, menopausal condition, therapeutic efficacy, antipsychotic daily dose, serum levels of lipids and glucose. There was significant correlation with first vs. subsequent psychotic episodes, weight, EPS and serum levels of thyroid hormones.
CONCLUSION: Amisulpride and risperidone had marked and early prolactin elevating effects, requiring, therefore, more frequent monitoring of prolactinaemia and associated undesirable effects and risks than olanzapine, quetiapine and zotepine.
University of Pennsylvania School of Medicine 2006,Nov 22
By Jeff Minerd, Reviewed by Zalman S. Agus
Zyprexa is effective drug but may have metabolic effect
It is reported that Zyprexa is an effective drug for the treatment of Schizophrenia. This antipsychotic medication is the most effective drug for schizophrenia. Continuous use of Zyprexa may some times cause metabolic issues.
The newer atypical antipsychotic drugs may not always outperform the old ones in managing schizophrenia, investigators said here. That's what the results of the Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) study suggested, said Rajiv Tandon, M.D., of the University of Florida in Tallahassee.
Dr. Tandon discussed the CATIE trial and its results at a symposium held in conjunction with the U.S. Psychiatric & Mental Health Congress here. The symposium was sponsored by Janssen pharmaceuticals of Titusville, N.J. In CATIE, nearly 1,500 patients with schizophrenia (ages 18 to 65) were recruited at 57 sites in the U.S. Participants were randomly assigned to Zyprexa (olanzapine) at 7.5 to 30 mg per day, Triavil (perphenazine) at 8 to 32 mg per day, Seroquel (quetiapine) at 200 to 800 mg per day, Risperdal (risperidone) at 1.5 to 6 mg per day, or Geodon (ziprasidone) at 40 to 160 mg per day.
Triavil is an older, typical antipsychotic developed in the mid-1950s. This class of drugs is associated with extrapyramidal side effects, Dr. Tandon noted. Follow-up in CATIE was 18 months. Endpoints included time to discontinuation of a particular drug as well as efficacy measures. Discontinuation of antipsychotic medications is common because they don't work in all patients and because of adverse effects, including metabolic side effects, extrapyramidal side effects, and weight gain, Dr. Tandon said. Overall, 74% of patients discontinued their study medication and switched to a new medication before 18 months, including:
• 49% of those assigned to Zyprexa.
• 55% of those assigned to Risperdal.
• 65% of those assigned to Seroquel.
• 70% of those assigned to Geodon and Triavil.
The time to discontinuation of treatment for any cause was significantly longer in the Zyprexa group than in the Seroquel (P<0.001) or Risperdal (P=0.002) group, but not in the Triavil (P=0.021) or Geodon (P=0.028) group. The times to discontinuation because of intolerable side effects were similar among the groups. However, Zyprexa was associated with more discontinuation for weight gain or metabolic effects, and Triavil was associated with more discontinuation for extrapyramidal effects. Zyprexa was the most effective drug in terms of the rates of discontinuation, but it was the "worst offender" in terms of metabolic side effects, Dr. Tandon said.
Furthermore, the efficacy of the typical antipsychotic Triavil appeared similar to that of Seroquel, Risperdal, and Geodon in patients at low risk for extrapyramidal side effects, he said. The CATIE study suggests that in schizophrenic patients with a low risk for extrapyramidal side effects, typical antipsychotics may work as well as the atypical "if you can get the dosing just right," Dr. Tandon said. Individual dosing is the key because there is considerable variation in how patients respond to differing doses of antipsychotic drugs and in patients' susceptibility to their side effects, Dr. Tandon said.
Successfully managing schizophrenia is crucial because the disease is such a heavy burden not only on individuals but on the healthcare system, said Jacqueline M. Feldman, M.D., of the University of Alabama at Birmingham, a second speaker at the symposium. Half of all mental hospital beds are filled by patients with schizophrenia, Dr. Feldman said. And about 16% of all patients getting healthcare services have schizophrenia, she added. Half of schizophrenia patients attempt suicide at some point during their lives, and 10% of them succeed. Finally, one-third to two-thirds of the homeless in the United States have schizophrenia, Dr. Feldman said.
New York State Psychiatric Institute, Columbia University Medical Center 2005,July 15
Jeffrey Lieberman, M.D.
published in NY
Zyprexa in schizophrenia proved to prevent brain loss
A recent study proved that Zyprexa has the capability to prevent brain loss. Zyprexa is more effective than any other conventional antipsychotic drug. It can prevent the loss of gray matter which contains brains cell's and billions of connections among the cells.
A new brain imaging study of recently diagnosed schizophrenia patients has found, for the first time, that the loss of gray matter typically experienced by patients can be prevented by one of the new atypical antipsychotic drugs, Zyprexa (olanzapine), but not by haloperidol, an older, conventional drug. The study also confirmed previous studies that show patients who experience less brain loss do better clinically.
"This is a really big breakthrough," says the study's leader, Jeffrey Lieberman, M.D., director of the New York State Psychiatric Institute and chairman of psychiatry at Columbia University Medical Center. "The drugs we have for schizophrenia can't cure people who've been sick for years, but this study shows that the newer atypical drugs, if started early, can prevent the illness from progressing. If our findings are confirmed, one could argue that we should treat new patients with atypical drugs like Zyprexa (olanzapine) rather than older conventional medications such as haloperidol and chlorpromazine." Gray matter contains the bulk of the brains cell's and the billions of connections among the cells. Loss of gray matter in patients with schizophrenia has been linked to social withdrawal and progressive deterioration in cognition and emotion-which are among the least responsive symptoms to medications.
To see if antipsychotic drugs could slow the initial brain changes in new patients, Dr. Lieberman and colleagues at 14 sites in North America and Europe measured brain volume and cognitive changes in 263 first-episode schizophrenia patients and 58 non-schizophrenic volunteers over a two-year period. Half of the patients received the atypical antipsychotic Zyprexa (olanzapine) and the other half took the conventional antipsychotic haloperidol. Dr. Lieberman initiated the study when he was professor of psychiatry at the University of North Carolina, which also coordinated the research.
The study found that, on average, haloperidol-treated patients lost about two percent of their gray matter, or about 12 cubic centimeters. No changes were detected in the olanzapine-treated patients and the normal volunteers. Patients who lost gray matter, particularly in the frontal lobe of the brain, also had greater problems with cognitive functioning, as measured by tests of verbal fluency, verbal learning and memory.
Schizophrenia has always been known as a disease that causes progressive worsening of symptoms and deterioration in function, but only in the last 10 years have researchers found that the brains of schizophrenics are also progressively deteriorating.
"People used to think that the deterioration was inevitable, but now we're thinking that if you can prevent the acute episodes of psychosis in schizophrenia you can actually stop the loss of gray matter," Dr. Lieberman says.
"It also gives us hope that we will be able to completely forestall the disease in the future by intervening before psychosis even begins," Dr. Lieberman adds. "In three to five years, we should have ways to identify which adolescents will become schizophrenic, and we can then begin to test the preventative power of treatments."
Am J Health Syst Pharm. 2005 Mar 15;62(6):610-5.
Russo PA, Smith MW, Namjoshi M.
Outcomes Research and Econometrics, The Medstat Group, Washington, DC.
Health care costs for schizophrenia patients started on olanzapine versus risperidone.
Author summarizes the difference in cost of treatment for schizophrenia using olanzapine or risperidone. From the study conducted, it is clear that Olanzapine initiators are more expensive than risperidone initiators. But in total, there is no significant difference in the treatment using Olanzapine initiators or risperidone initiators.
PURPOSE: The change in direct medical costs for schizophrenia patients who were started on olanzapine or risperidone and who were privately insured was studied. METHODS: A retrospective analysis of 1996-1999 data from the databases representing the health care experiences of individuals employed by large organizations and their dependents was performed. The sample included all individuals with a drug claim for olanzapine or risperidone, a claim with a schizophrenia diagnosis within 90 days of the drug claim, no claim for the same drug in the prior six months, and continuous health-plan enrollment for 12 months before and after the prescription. RESULTS: The sample included 162 patients initiated on olanzapine and 119 patients initiated on risperidone. Demographic and clinical profiles were not significantly different between groups. Annual schizophrenia-related prescription and outpatient costs increased following initiation on olanzapine or risperidone compared with the preinitiation period. This was partially offset by a decrease in inpatient expenditures. Olanzapine initiators had higher outpatient drug expenditures than risperidone initiators in the 12 months following initiation (adjusted means, $2105 versus $1934) (p < 0.05), but there was no significant difference between groups in total schizophrenia-related payments ($5251 versus $4950). CONCLUSION: The total health care expenditure related to treating schizophrenia was similar between privately insured patients who were initiated on olanzapine and patients who were started on risperidone.
Arch Phys Med Rehabil. 2005 Mar;86(3):587-90.
Mukand JA, Fitzsimmons C, Wennemer HK, Carrillo A, Cai C, Bailey KM.
Olanzapine for the treatment of hemiballismus: A case report.
A research report on the treatment of hemiballismus using Olanzapine. Zyprexa is effective in the treatment of hemiballismus than haloperidol. This drug has the power to reduce the effect of agitation in hemiballismus patients.
Olanzapine for the treatment of hemiballismus: a case report.
Hemiballismus is a rare movement disorder characterized by involuntary, large amplitude movements of the limbs of 1 side of the body. We describe the case of a man in his late sixties with slurred speech, agitation, and right-sided hemiballismus resulting from a left thalamic hemorrhagic stroke. Treatment with haloperidol was unsuccessful, but both the hemiballismus and agitation diminished significantly after initiation of olanzapine (Zyprexa). The improvement in the hemiballismus was quantified by recording the number of hemiballistic movements that occurred while the patient performed standardized 30-minute sessions (daily for 5d). With the first task (reaching within the base of support while seated), the average number of hemiballismic movements per session decreased from a baseline of 23.5 to 3.0 in the upper extremity and from 20.5 to 7.0 in the lower extremity. With the second task (catching a ball while seated), the abnormal movements decreased from 52 to 6.3 in the upper extremity and from 34.5 to 2.7 in the lower extremity. This case suggests that olanzapine may be a valuable pharmacologic alternative for patients with hemiballismus.
Zyprexa description...
|
|
Drug category:Schizophrenia, Psychosis
 Zyprexa scientific update
Buy here
|
|
My Basket