Effects Of Antipsychotic Therapy Research Articles

Clinical and Therapeutic Factors Affecting the Social Adaptation of Patients with Schizophrenia

Background: сurrently, the question remains open about the factors that affect the social functioning of patients with schizophrenia, including the role of negative symptoms and neurocognitive deficits. The aim: to study factors that affect the social functioning of patients with schizophrenia. Patients and methods: 64 in-patient with schizophrenia (mean age 35.9 ± 10.9 years) were examined at the stage of remission. The disease duration was 9.71 ± 6.0 years. The majority of patients suffered from paranoid and hallucinatory-paranoid attacs (43 and 23%, respectively). The study used follow-up, clinical and psychopathological methods as well as psychometric scales: PANSS, SANS, ВАСS, Calgary scales and UKU scales. An integrative indicator was introduced to assess the social adaptation of patients. Results: it is shown that as the duration of the disease increases, the indicator of social adaptation decreases. The presence of side effects of antipsychotic therapy is associated with restrictions on the social functioning of patients, but the use of second-generation antipsychotics contributes to an increase in the level of social functioning of patients. Patients with more pronounced apathetic-abulic disorders, flattened affect, anhedonia-asociality and social isolation are characterized by a lower level of social functioning. Adapted patients differ from maladapted patients by better indicators of auditory-speech memory, motor skills, information processing speed, ability to plan and problem solving behavior. Conclusion: the integrative indicator of social adaptation of patients with schizophrenia is associated with a number of cognitive and negative symptoms, features of antipsychotic therapy and the duration of the disease.

Aberrant alternative splicing of HTR2A exon II in peripheral blood lymphocytes of drug-naïve schizophrenic patients

The aim of the study was to characterize the pattern of transcript isoforms of HTR2A exon II in lymphocytes of the blood as peripheral biomarkers of schizophrenia development and the effectiveness of antipsychotic therapy. We primarily observed an increase in mRNA levels and elevation of alternative variants in a sample of drug-naïve schizophrenic patients compared to the control group. There was no association of the expression level of HTR2A transcript isoforms with the effectiveness of the antipsychotic therapy. Antipsychotic-induced akathisia was associated with a significant reduction in the mRNA levels of the studied isoforms. In summary, our results suggest that levels of HTR2A exon II transcript isoforms are upregulated in patients with schizophrenia, but at the same time, elevated expression level of the studied HTR2A transcripts is associated with fewer side effects of the therapy.

Neuroleptic Malignant Syndrome: A Potential Etiology of Multisystem Organ Failure in a Burn Patient

Neuroleptic malignant syndrome (NMS) is described in the medical literature but rarely seen among acutely ill trauma patients. A 44-year-old man with burns to the hands and back after a chemical explosion was transported to an outside facility where he received treatment for presumed acute coronary syndrome after developing ventricular tachycardia and elevated serum troponins after the exposure. His cardiac catheterization was unremarkable, but an echocardiogram revealed severe cardiomyopathy, and he was also in multisystem organ failure. He was transferred to our facility after hospital day 2 for treatment of his multisystem organ failure and 2% total body surface area burns. His laboratory results were remarkable for a creatine kinase of >100 000 units/L, and he required 14 g of intravenous calcium. Upon further investigation, the patient reported taking ziprasidone for his bipolar disorder, and he had a core temperature of 103.5 °F on his initial presentation to the outside facility. As he convalesced, the unifying diagnosis was NMS. NMS is a side effect of antipsychotic therapy and is manifested by hyperpyrexia, rigidity, autonomic instability, and altered consciousness. An elevated creatine kinase >100 000 units/L is almost pathognomonic for NMS. Patients can also present with leukocytosis, organ failure, and electrolyte disturbances including hypocalcemia. We hypothesized that dehydration, the warm environmental conditions at our patient's job, and immense stress resulting in a catecholamine surge following his trauma were inciting triggers to this event. This case highlights the importance of considering alternate diagnoses in patients whose clinical presentation does not fit the most "obvious cause."

Pharmacogenetics of antipsychotics in adolescents with acute psychotic episode during first 14days after admission: effectiveness and safety evaluation.

Prediction of the antipsychotic's effectivenessis a relevant topic in the field of personalized medicine. The research design of this study is a prospective observation with posthoc analysis of associations of genetic polymorphisms with safety parameters and effectiveness of antipsychotic therapy. We observed 53 adolescents with an acute psychotic episode which were prescribed antipsychotics for 14days. We evaluated the effectiveness of antipsychotics with the Positive and Negative Symptoms Scale and the safety with the UKU Side Effects Rating Scale, Simpson-Angus Scale, and Barnes Akathisia rating scale. We genotyped CYP3A4*22 (rs2740574), CYP3A5*3 (6986A>G, rs7767746), CYP2D6*4, *9, *10 (rs3892097, rs1065852), ABCB1 1236C>T (rs1128503), 2677G>T/A (rs2032582), 3435C>T (rs1045642), DRD2 (rs1800497), DRD4 (rs1800955), HTR2A (rs6313) by the real-time polymerase chain reaction method. We found significantly more frequent "increased dream activity" between CYP2D6 intermediate metabolizers and normal metabolizers (54 vs. 22%; p=0.043). The «increased duration of sleep» was more often observed in homozygotes TT of ABCB1 2677G>T/A (50 vs. 15.8%, p=0.006) and TT of 3435C>T (41.7 vs. 8.2%, p=0.007). We found that CYP2D6 and ABCB1 polymorphisms were associated with the safety of antipsychotics in adolescents with an acute psychotic episode.

Прогностическая модель риска развития гиперпролактинемии у пациентов с шизофренией на фоне антипсихотической терапии

Использование антипсихотических средств ассоциировано с повышенным уровнем пролактина. Лекарственно-индуцированная гиперпролактинемия (ГП) имеет не только краткосрочные, но и долгосрочные последствия, которые могут серьезно повлиять на качество жизни пациента. Клинические проявления ГП включают гинекомастию, галакторею, нарушения менструального цикла, сексуальные дисфункции, бесплодие, а также значимый рост вероятности развития остеопороза и онкологических заболеваний. В развитии данного побочного эффекта антипсихотической терапии участвуют не только экзогенные, но и генетические факторы. Целью данной работы было исследование клинических и молекулярно-генетических факторов развития лекарственно-индуцированной ГП и создание прогностической модели риска развития ГП, которая в перспективе может быть использована для оптимизации и персонализации назначаемой терапии при лечении шизофрении. Исследование проведено в выборке русских, проживающих в Западно-Сибирском регионе России, больных шизофренией (n=446). Средний возраст пациентов составил 41,5 ± 13,4 года (возрастной диапазон - от 18 до 65 лет). Клиническая симптоматика оценивалась по шкалам позитивных и негативных синдромов (Positive and Negative Syndrome Scale - PANSS), общего клинического впечатления (Clinical Global Impression - CGI), оценки побочного действия (Udvalg for Kliniske Undersogelser Scale - UKU), на всех пациентов заполнялся модифицированный вариант карты стандартизированного описания больного шизофренией. На основании содержания гормона пролактина в сыворотке крови были выделены подгруппы пациентов с ГП (n=227) и с нормальным уровнем пролактина (n=219). Выполнен молекулярно-генетический анализ 88 полиморфных вариантов генов серотониновых (HTR2C, HTR3A, HTR3B, HTR6, HTR2A, HTR1A, HTR1B) и дофаминовых (DRD1, DRD2, DRD2/ANKK1, DRD3, DRD4) рецепторов, дофаминового транспортера SLC6A3, переносчика норадреналина SLC6A2, системы ферментов цитохромов P450 (CYP1A2*1F, CYP2D6*3, CYP2D6*4, CYP2C19*3, CYP2C19*17, CYP2C19*2), катехол-О-метилтрансферазы СОМТ, p-глутатион S-трансферазы GSTP1, ATXN1, KREMEN1 и пролактина PRL. Получена прогностическая модель с включением генетических маркеров «rs1176744» (HTR3B), «rs10042486» (HTR1A), «rs936461» (DRD4), «rs179997» (ATXN1), «rs1076562» (DRD2), «rs3773678» (DRD3), «rs167771» (DRD3), «rs1587756» (DRD3), «rs134655» (KREMEN1),»rs3892097» (CYP2D6*4), «rs1341239» (PRL), «rs4975646» (SLC6A3), «rs13333066» (SLC6A2), а также негенетических факторов, таких как пол, возраст и доза антипсихотика в хлорпромазиновом эквиваленте (CPZeq). Разработанную фармакогенетическую панель можно рассматривать в качестве биологического предиктора развития антипсихотик-индуцированной ГП при шизофрении до назначения фармакотерапии. The use of antipsychotics is associated with elevated prolactin levels. Drug-induced hyperprolactinemia (HP) has not only short-term, but also long-term consequences, which can seriously affect the patient’s quality of life. Clinical manifestations of HP include gynecomastia, galactorrhea, menstrual irregularities, sexual dysfunctions, infertility, as well as a significant increase in the likelihood of developing osteoporosis and cancer. Not only exogenous, but also genetic factors are involved in the development of this side effect of antipsychotic therapy. The aim of this work was to study the clinical and molecular genetic factors of the development of drug-induced HP and the creation of a prognostic model of the risk of developing HP, which in the future can be used to optimize and personalize the prescribed therapy in the treatment of schizophrenia. The study was conducted in populations of russians with schizophrenia (n = 446), living in the West Siberian region of Russia. The average age of patients was 41,5 ± 13,4 years (18 - 65 age range). Clinical symptoms were assessed using the Positive and Negative Syndrome Scale (PANSS), the Clinical Global Impression scale (CGI), the side effect rating scale (Udvalg for Kliniske Undersogelser Scale - UKU), and a modified version of the card of a standardized description of patient with schizophrenia. Based on the results on the serum prolactin level patients were divided into subgroups: with HP (n = 227) and with normal prolactin levels (n = 219). Molecular genetic analysis of 88 polymorphic variants of serotonin receptors genes (HTR2C, HTR3A, HTR3B, HTR6, HTR2A, HTR1A, HTR1B) and dopamine receptors genes (DRD1, DRD2, DRD2 / ANKK1, DRD3, DRD4), dopamine transporter gene SLC6A3, noradrenaline transporter gene SLC6A2, genes of the cytochrome P450 enzymes (CYP1A2*1F, CYP2D6*3, CYP2D6*4, CYP2C19*3, CYP2C19*17, CYP2C19*2), gene of catechol-O-methyltransferase COMT, gene of glutathione S-transferase P (GSTP1), genes ATXN1, KREMEN1 and prolactin gene PRL was performed. A prognostic model was obtained with the inclusion of the genetic markers “rs1176744” (HTR3B), “rs10042486” (HTR1A), “rs936461” (DRD4), “rs179997” (ATXN1), “rs1076562” (DRD2), “rs3773678” (DRD3), “rs167771” (DRD3), “rs1587756” (DRD3), “rs134655” (KREMEN1), “rs3892097” (CYP2D6*4), “rs1341239” (PRL),”rs4975646” (SLC6A3),”rs1333302” (SLC6A2), as well as non-genetic factors such as gender, age and dose of antipsychotic in chlorpromazine equivalent (CPZeq). The developed pharmacogenetic panel can be considered as biological predictors of the development of antipsychotic-induced HP in schizophrenia before the appointment of pharmacotherapy.

Effects of antipsychotic therapy on lipid and carbohydrate metabolism of schizophrenic patients

Atypical antipsychotic drugs such as Olanzapine (Ola) induce weight gain and metabolic changes associated with the development of type 2 diabetes. The mechanisms underlying these undesired side-effects are currently unknown. Chagnon et al. showed that the common allele rs7973796 of the prepro-melanin-concentrating hormone (PMCH) gene is associated with a greater body mass index in Ola-treated schizophrenic patients. As PMCH encodes for the orexigenic neuropeptide melanin-concentrating hormone (MCH), it was hypothesized that MCH is involved in Ola-induced metabolic changes. We have recently reported that the intragastric infusion of Ola results in hyperglycaemia and insulin resistance in male rats. In order to test in vivo the possible involvement of the PMCH gene in the pathogenesis of Ola side-effects, we administered Ola intragastrically in wild-type (WT) and PMCH knock-out (KO) rats. Our results show that glucose and corticosterone levels, as well as endogenous glucose production, are elevated by the infusion of Ola in both WT and KO animals. Thus, the lack of MCH does not seem to affect the acute effects of Ola on glucose metabolism. On the other hand, these effects might be obliterated by compensatory changes in other hypothalamic systems. In addition, possible modulatory effects of the MCH KO on the long term effects of Ola, i.e. increased adiposity, body weight gain, have not been investigated yet.

Amenorrhea and benign intracranial hypertension as an effect of antipsychotic therapy in a patient with schizophrenia

Amenorrhea and benign intracranial hypertension as an effect of antipsychotic therapy in a patient with schizophrenia

Role of Serotonin from Thought and Anxiety to Weight Gain and Metabolic Syndrome

Studies indicated that targeting localized serotonin 5-HT2C receptors can treat obesity which is consistent with the role in regulating pathways of food intake and body weight that could lead to obesity. The association of diminished serotonergic activity with metabolic syndrome may have implications for the prevention and treatment of the metabolic syndrome. Antipsychotics are 5-HT2C receptors antagonists that can knock down the satiety centers located in ventromedial nucleus in hypothalamus leading to increased weight gain. The potential for weight gain differs among atypical antipsychotics. While ziprasidone and aripiprazole care thought to be weight neutral, dibenzodiazepines like clozapine and olanzapine are implicated in lot of weight gain that can cause obesity and metabolic syndrome. The amount of body weight gain varies with each drug. The difference in weight gains between quetiapine and each of the other atypical medication was significant in our studies (Mean weight gain was least with quetiapine 9.31b and greatest for olanzapine 20.89 lb). Weight gain was also greater with olanzapine than with clozapine. In the literature survey we observed clozapine has been associated with some of the largest bodyweight gains of olanzapine in the long term use and higher weight gain with clozapine seems to be on shorter duration. For many of the metabolic disorders related to weight gain and obesity, scientists have implicated abdominal visceral fat. An increase in visceral fat, in turn, leads to an increased concentration of free fatty acids in the portal vein. An increased free fatty acid concentration may lead to a decrease in hepatic insulin clearance, insulin resistance, hyperinsulinemia, and hypertension. This sequence of events may lead to diabetes, assorted dyslipidemia, and ultimately to coronary artery disease. The purpose of the study was to evaluate the impact of intervention on improving overall cardiovascular adverse effects of antipsychotic therapy. Long-term metabolic complications such as obesity, diabetes, dyslipidemia, hypertension, and ECG changes were of particular interest but the results from our study has not shown any significant change in clinical practice that lead to reduction in cardiovascular risk. During the study period (8/2009 – 11/2009), 118 treatment recommendations were made by pharmacy students and clinical pharmacist preceptor and most were for new lipid and FBG/HgA1C panel for missing lab values or more accurate assessment of patient’s recent status and 82 recommendations were accepted. As appreciated by the result from this study period, the key limiting factor in accurately assessing effectiveness of consultant intervention is that the treatment decision is ultimately made by the patient’s psychiatrist who reviews the recommendation. However the clinical recommendation from the psychopharmacy consultant may still help to increase overall awareness on part of psychiatrists regarding patients’ current cardiovascular risk. Whether it will lead to active intervention will be dependent on other factors. For example, most of the psychopharmacy recommendations are for lipid and A1C/FBG labs as seen during this study period, but even when the recommendation is accepted, the patient may not necessarily require therapeutic intervention as the lab values often do not show any significant changes or are stable-normal. Or in case the recommendation is not accepted, it may be influenced by the therapy/lab cost or availability of other nonpharmacological interventions (e.g. diet/lifestyle modification) more so than the clinical competency of the recommending pharmacist. Other limiting factors of the study include lack of control group for comparison and need for objective monitoring tool for evaluating overall cardiovascular risk of the patients. For this study period, there was significant cardiovascular reduction seen through clinical pharmacy intervention in high-risk patients receiving antipsychotic. More studies are needed to support clinical pharmacist’s role in improving overall cardiovascular risk associated with antipsychotic therapy but in the meanwhile, interdisciplinary monitoring and careplan in regards to high- risk patients should be continued and American diabetic association recommends serum glucose and serum lipids on quarterly basis for the patients who receive atypical antipsychotics (dibenzodiazepine more so) and that is the standard of care. In the future, there may be several changes that can be made to the study protocol for better assessment of effectiveness of clinical pharmacy intervention. First, one may consider increasing the sample size by increasing the duration and thus more patients to increase the power of the study. Second, recommending pharmacist should leave a written progress note for which other psychiatrist/physicians may be able to refer back to rather than verbal recommendations to one attending psychiatrist as done so far. And lastly, one may consider

Extrapyramidal syndromes caused by antipsychotics

Extrapyramidal syndromes are significant side effects of antipsychotic therapy due to their severity, frequent occurrence and complications. This paper gives a brief summary of the literature with the emphasis on epidemiology, etiology, diagnosis and differential diagnosis, as well as the treatment of extrapyramidal disorders induced by antipsychotics. Sustained muscle contractions cause twisting and repetitive movements or abnormal postures. It may appear either as an acute or delayed, i.e. tardive sign. The incidence of dystonia is 2-3% among the patients treated with antipsychotics, and 50% among the ones cured with conventional antipsychotics. AKATHISIA: The main feature of this curious adverse effect is the psychomotor restlessness and the inability to remain motionless. Although akathisia is not very frequent, its incidence and prevalence ranges from 5 to 50% among the treated patients. It is most probably a result of the blockage ofdopaminergic receptors. The most frequent secondary Parkinsonism is the one caused by drugs. The characteristic parkinsonian signs regress 4 to 16 weeks after the discontinuation of antipsychotic therapy. In the era of atypical antipsychotics this adverse effect appears less frequently. Involuntary choreatic movements may appear days and months after the introduction of continuous use of antipsychotics. The individual susceptibility may play the major role in the development of this side effect. Numerous studies have compared conventional and atypical antipsychotics as well as atypical ones with one another in order to decrease the risk of development of extrapyramical side effects as well as to prevent their occurrence and improve their treatment.

S28-03 - Pharmacogenetics of therapy response in schizophrenia

Pharmacogenetics in schizophrenia comprises pharmacokinetical and pharmacodynamical aspects as well as an approach to identify candidate genes associated with therapy response or side effects. Firstly focussing on classical drug targets like dopaminergic or serotonergic receptors, currently also developmental and regulatory genes presumably associated with effects of antipsychotic therapy are identified. The aim of this study was to investigate associations between therapy response in schizophrenic patients and different polymorphisms previously been identified within a genome wide array in rodents treated with MK-801 and/or haloperidol combined with some well-known schizophrenia candidate genes. We genotyped for 200 different polymorphisms in 285 schizophrenic patients, who were treated with different antipsychotics within randomized controlled trials. Psychopathology was measured weekly using the PANSS scale. Correlations between psychopathology and genotypes were calculated by using a linear model (ANCOVA).We found significant associations between some well-known candidate genes (e.g. D2-, 5HT1A-, and α1A-receptors) and different PANSS subscales at baseline and after four weeks of antipsychotic treatment considered as therapy response. Furthermore we also identified several significant associations between some genes introduced from the animal model and psychopathology at baseline and towards therapy response. Some of them were formerly described in the literature (e.g. Homer1, Phospholipase C and Transthyretin), but most of them have not been related to schizophrenia or antipsychotic treatment by now (e.g. PLEKHA6, CLIC6 and SOSTDC1).This indicates an involvement of genes in the pathophysiology of schizophrenia apart from yet known candidate genes and might further help in detecting differential therapy response in individuals with schizophrenia.

Antihistaminerge Antipsychotika verursachen Gewichtszunahme

In recent years, weight gain has increasingly gained attention as a side effect of antipsychotic therapy due to its metabolic and cardiovascular health risks and its negative effect on therapy compliance. The various antipsychotics show clear differences concerning their influence on body weight. These differences seem to be mainly due to the affinity of these substances to the histaminergic H1 receptors and due to serotonergic mechanisms. In the hypothalamus, the antihistaminergic effect of those antipsychotics which are associated with a high amount of weight gain leads to an increase of the activity of the adenosine monophosphate-activated protein kinase (AMPK). Hypothalamic AMPK activity has an integrative function regarding orexigenic and anorexigenic signals.

Serum nitric oxide metabolite levels and the effect of antipsychotic therapy in schizophrenia

Recently it was proposed that nitric oxide metabolites (NO) may have a role in the pathophysiology of schizophrenia and major depressive disorders. The present study was performed to assess changes in serum nitric oxide metabolite levels in schizophrenic patients compared with healthy controls. Our secondary aim was to further evaluate the impact of psychopharmacologic treatment on circulating NO levels not assessed previously. Serum NO levels of patients with schizophrenia (n=20) before and after 6 weeks of treatment were compared with those of healthy controls (n=20). Severity of schizophrenia and response to treatment were assessed with positive and negative symptoms of schizophrenia. NO levels were estimated by Griess method in serum samples. In patients with schizophrenia, pre-treatment serum NO levels were higher than those of control subjects (39.15 +/- 18.24 vs. 25.40 +/- 5.83 micromol/L, p=0.036) and also of post-treatment values (34.41 +/- 16.35 vs. 25.40 +/- 5.83 micromol/L, p=0.049), respectively. However, no significant difference was found between serum NO levels in pre- and post-treatment values. Our findings of increased serum NO levels in schizophrenic patients confirmed the role of NO in the pathophysiology of schizophrenia. However, we found that antipsychotic drugs do not reveal significant effects on serum levels of NO in schizophrenia in a 6-week treatment regimen. Further studies with longer therapy periods may suggest some new clues for novel treatment strategies employing antioxidants and NOS inhibitors in schizophrenia.

The effects of antipsychotic therapy on serum lipids: a comprehensive review

Objectives: The purpose of this paper is to review the literature since 1970 documenting the effects of antipsychotic agents on serum lipids, including a discussion of possible mechanisms for the observed phenomena, the clinical significance and recommendations for monitoring hyperlipidemia during antipsychotic therapy. Results: High-potency conventional antipsychotics (e.g., haloperidol) and the atypical antipsychotics, ziprasidone, risperidone and aripiprazole, appear to be associated with lower risk of hyperlipidemia. Low-potency conventional antipsychotics (e.g., chlorpormazine, thioridazine) and the atypical antipsychotics, quetiapine, olanzapine and clozapine, are associated with higher risk of hyperlipidemia. Possible hypotheses for lipid dysregulation include weight gain, dietary changes and the development of glucose intolerance. Conclusions: Given the multiple cardiovascular risk factors seen in patients with schizophrenia, great care must be exercised in the choice of antipsychotic therapy to minimize the medical burden of additional risk imposed by hyperlipidemia. It is recommended that a lipid panel be obtained at baseline in all patients with schizophrenia, annually thereafter for patients on agents associated with lower risk of hyperlipidemia and quarterly in patients on agents associated with higher risk for hyperlipidemia. All patients with persistent dyslipidemia should be referred for lipid-lowering therapy or switched to a less lipid-offending antipsychotic agent.

Decreased levels of soluble intercellular adhesion Molecule-1 (sICAM-1) in unmedicated and medicated schizophrenic patients

Background: The soluble intercellular adhesion molecule-1 (sICAM-1) is a marker for the activation of the cellular immune system. Since an activation of the immune system has been observed in a part of the schizophrenic patients, we measured the serum levels of soluble ICAM-1 (sICAM-1) in schizophrenic patients and correlated them to the patient’s psychopathology. Methods: To monitor a possible effect of antipsychotic therapy, 36 schizophrenic patients were examined twice: first without antipsychotic medication immediately after admission to the hospital and then, after clinical improvement before discharge. The results were compared with those of 36 age- and gender-related healthy individuals. Results: The schizophrenic patients showed significantly decreased serum levels of sICAM-1 at the first examination (248 ± 95 ng/mL) and at re-examination (266 ± 95 ng/mL) compared with the comparison group (323 ± 74 ng/mL). Patients with more pronounced negative symptoms showed higher levels of sICAM-1 at the first examination. Conclusions: We conclude that reduced sICAM-1 levels in schizophrenia indicate a reduced activity of the cellular immune system in at least a subgroup of schizophrenic patients.

Effectiveness of Antipsychotic Therapy in a Naturalistic Setting

Therapeutic ineffectiveness and noncompliance with antipsychotic agents are major contributors to rehospitalization in patients with psychotic disorders. It is unknown whether risperidone's favorable side effect profile compared with that of the conventional antipsychotics results in improved compliance and reduced hospitalizations in a naturalistic setting. The purpose of this study was to test the hypothesis that treatment with risperidone reduces readmission rates and associated costs when compared with treatment with perphenazine or haloperidol. Inpatients prescribed either risperidone, perphenazine, or haloperidol between January 1, 1995, and December 31, 1995, as a single oral antipsychotic at discharge were retrospectively identified. Data were collected for that index hospitalization and for a 1-year follow-up period. Primary outcome measures included re-admission rates, changes in antipsychotic therapy, anticholinergic drug use, and costs. There were 202 evaluable patients (81 treated with risperidone, 78 with perphenazine, and 43 with haloperidol). Baseline demographics were similar between groups except that more patients in the risperidone group had a primary diagnosis of psychotic disorder or had been hospitalized in the year prior to study. The percentage of patients readmitted during the 1-year follow-up period was similar among drug groups (41% risperidone, 26% perphenazine, and 35% haloperidol) when controlled for baseline differences in diagnosis and hospitalization history (p = .32). Anticholinergic drug use was more common in the haloperidol group (p = .004). Mean yearly cost (drug + hospitalization) in the risperidone group was $20,317, nearly double that in the other treatment groups (p < .001). The results from this naturalistic study indicate that the high cost of risperidone is not offset by a reduction in readmission rates when compared with conventional antipsychotics.

Antipsychotic tolerability: The attitudes and perceptions of medical professionals, patients and caregivers towards the side effects of antipsychotic therapy

Antipsychotic tolerability: The attitudes and perceptions of medical professionals, patients and caregivers towards the side effects of antipsychotic therapy