Wen-Ho Chang

China Medical University Hospital, 臺中市, Taiwan, Taiwan

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Publications (25)93.18 Total impact

  • Psychopharmacology 07/2008; 200(2):301-3. · 4.06 Impact Factor
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    ABSTRACT: The Val158Met polymorphism of the catechol-O-methyltransferase gene has been demonstrated to be associated with prefrontal executive function explaining 4% of variance in perseverative errors on the Wisconsin Card Sorting Test (WCST). Studies suggest that dopamine D(1) and D(3) and serotonin 5-HT(2A) and 5-HT(6) receptors may also be involved in prefrontal cognitive function and that genetic polymorphisms (D(1) A-48G, D(3) Ser9Gly, 5-HT(2A) T102C, and 5-HT(6) T267C) of these receptors may be associated with brain glucose metabolism or neurophysiological function. The current study's objective was to investigate whether executive function varies with these genetic variations. A sample of 216 healthy Han Chinese adults were measured with the WCST and genotyped for the 4 genetic polymorphisms. Kruskal-Wallis tests showed a significant difference in WCST perseverative errors among the genotypes D(3) Ser9Gly (p = 0.009), 5-HT(2A) T102C (p = 0.038) and 5-HT(6) T267C (p = 0.010), but not in the genotype D(1) A-48G. Multiple regression analysis for the WCST natural logarithm values (i.e., for fulfilling the normal distribution requirement) showed that subjects' perseverative errors were significantly influenced by D(1) A-48G, D(3) Ser9Gly, 5-HT(2A) T102C and 5-HT(6) T267C polymorphisms after adjustment of other variables. The preliminary data suggest that D(1), D(3), 5-HT(2A) and 5-HT(6) genetic mutations may influence prefrontal executive cognition in healthy adults. Further studies in larger samples with other ethnicities or in mentally ill patients are warranted.
    Journal of psychiatry & neuroscience: JPN 02/2008; 33(1):47-53. · 6.24 Impact Factor
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    ABSTRACT: A serious side effect of atypical antipsychotics is increased body weight, which leads to further morbidity and nonadherence to medication. It has been suggested that both genetic and nongenetic variables may influence antipsychotics-related weight gain. This study aimed to simultaneously explore the effects of multiple candidate genes and environment factors on body weight of schizophrenia patients who received risperidone, a commonly used atypical antipsychotic agent. One hundred twenty-three ethnically Han Chinese inpatients with acutely exacerbated schizophrenia were given risperidone monotherapy for up to 42 days. Body weight and clinical manifestations were assessed biweekly. Drug efficacy was measured by the Positive and Negative Syndrome Scale (PANSS), and safety was evaluated by the Extrapyramidal Symptom Rating Scale (ESRS) and the UKU Side Effect Rating Scale. We collected body weight as the response value. Potential prognostic factors were baseline body weight, age, sex, diagnosis subtypes, risperidone dosage, PANSS total scores, treatment duration (weeks 0-6), and 15 genetic variants [across 10 candidate genes: 5-HT1A, 5-HT2A, 5-HT2C, 5-HT6, D1, D2, D3, and alpha1-adrenergic receptors, brain-derived neurotrophic factor (BDNF), and cytochrome P450 2D6 (CYP2D6)]. Because there were repeated assessments, multiple linear regression with the generalized estimating equation (GEE) method was used to adjust the within-subject dependence. Of 15 genetic polymorphisms examined, 5-HT2A 102-T/C, 5-HT2C -759-C/T, 5-HT6 267-C/T, BDNF 66-Val/Met, and CYP2D6 188-C/T significantly influenced body weight, and so did baseline body weight, age, gender, schizophrenia subtype, and treatment duration and efficacy. These results suggest that numerous genetic and nongenetic factors affect antipsychotics-related weight gain.
    Journal of Clinical Psychopharmacology 05/2006; 26(2):128-34. · 3.51 Impact Factor
  • Journal of Clinical Psychopharmacology 09/2005; 25(4):391-3. · 3.51 Impact Factor
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    ABSTRACT: Risperidone and other newer atypical antipsychotics are becoming the mainstay for schizophrenia treatment. Recent studies suggest that the 5-hydroxytryptamine receptor 2A (5-HT2A) gene (HTR2A) T102C and G-1438A polymorphisms may influence treatment response of risperidone or olanzapine for schizophrenia's negative symptoms (e.g., blunted affect and social withdrawal). In addition, the HTR6 T267C polymorphism has been linked to risperidone response for positive symptoms (delusions and hallucinations). The dopamine D2 receptor (DRD2) Ser311Cys polymorphism may also play a role in determining risperidone efficacy for positive, negative and cognitive symptoms, the DRD2 Ins-A2/Del-A1 diplotype may predict better risperidone response, and the DRD3 Ser311Cys variant may affect general treatment response of several atypical agents. Although investigators have started to explore genetic effects on cognitions of schizophrenia patients receiving antipsychotics, future larger sized pharmacogenetic studies on both psychotic symptoms and cognitive functions are warranted.
    Pharmacogenomics 04/2005; 6(2):139-49. · 3.86 Impact Factor
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    ABSTRACT: Risperidone is an atypical antipsychotic agent with efficacy for both positive and negative symptoms of schizophrenia. Risperidone is a potent dopamine D3 antagonist and agonism at D3 sites induces behavioral suppression in rodents. We thus hypothesized that D3 antagonism may contribute to response to risperidone in negative symptoms. This study aimed to explore the influence of the Ser9Gly polymorphism of the dopamine D3 receptor (DRD3) gene on response to risperidone after controlling for nongenetic factors. One hundred twenty-three Han Chinese patients with acutely exacerbated schizophrenia were given risperidone monotherapy for up to 42 days. Clinical manifestations were measured biweekly with Positive and Negative Syndrome Scale and Nurses' Observation Scale for Inpatients Evaluation (for assessment of social functioning). For adjusting the within-subject dependence over repeated assessments, multiple linear regression with generalized estimating equation methods was used to analyze the effects of Ser9Gly polymorphism and other covariates on clinical performance. Compared with patients with the Gly9Gly genotype, those with either Ser9Ser or Ser9Gly had better performance on negative symptoms after control for other prognostic factors (P = 0.0002 and 0.0092, respectively). Patients with the Ser9Ser genotype had better social functioning than those with Gly9Gly (P = 0.0029). The Ser9Gly polymorphism, however, did not significantly affect positive symptoms. Male gender, fewer previous hospitalizations, and higher risperidone dose also predicted better treatment response. These data suggest that the DRD3 Ser9Gly polymorphism or, alternatively, another genetic variation that is in linkage disequilibrium, may influence response to risperidone in negative symptoms and social functioning.
    Journal of Clinical Psychopharmacology 03/2005; 25(1):6-11. · 3.51 Impact Factor
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    ABSTRACT: Risperidone is an atypical antipsychotic agent with efficacy for both positive and negative symptoms of schizophrenia. However, what makes an antipsychotic 'atypical' remains unclear. We recently found that the T102C polymorphism in the 5-HT2A receptor gene could affect risperidone's efficacy for negative symptoms. The present study investigated the effect of the Ser311Cys polymorphism in the dopamine D2 receptor (DRD2) gene on risperidone treatment response. A total of 123 Han Chinese patients with acutely exacerbated schizophrenia were given risperidone for up to 42 days. Clinical manifestations were measured bi-weekly with Positive and Negative Syndrome Scale (PANSS) and Nurses' Observation Scale for Inpatients Evaluation (NOSIE, for assessment of social function). For adjusting the within-subject dependence over repeated assessments, multiple linear regression with generalized estimating equation methods was utilized to analyse the effects of Ser311Cys polymorphism and other covariates on clinical performance. Compared with patients who had the Ser311Ser genotype, patients with the Ser311Cys genotype had lower scores on PANSS Positive, Negative, General Psychopathology and Cognitive subscales and NOSIE, after adjustment for 5-HT2A T102C polymorphisms and other confounders. The 5-HT2A T102C polymorphism had marginal influences on PANSS Total and Negative subscale scores. Male gender, fewer previous hospitalizations, and higher risperidone dose predicted better treatment response after control for other variables. The preliminary results suggest that variations in the DRD2 gene influence risperidone treatment response for positive, negative, and cognitive symptoms, general psychopathology, and social functioning. Several clinical factors may also contribute to inter-individual differences in risperidone treatment response.
    The International Journal of Neuropsychopharmacology 01/2005; 7(4):461-70. · 5.64 Impact Factor
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    ABSTRACT: Olanzapine, an atypical antipsychotic agent, is a substrate of the cytochrome P4501A2 (CYP1A2) enzyme. Administration of a potent CYP1A2 inhibitor (eg, fluvoxamine) may alter the pharmacokinetics of olanzapine. This study investigated the pharmacokinetic interactions between olanzapine and fluvoxamine in patients with schizophrenia. Ten male smokers were administrated a single dose of olanzapine 10 mg at baseline, followed by 2 weeks of fluvoxamine 50 mg/day and another 2 weeks of fluvoxamine 100 mg/day. Olanzapine 10 mg was given at day 10 during each fluvoxamine treatment. After pretreatment with fluvoxamine, the area under the curve, maximal plasma concentration, and half-time of olanzapine were significantly increased by 30% to 55%, 12% to 64%, and 25% to 32%, respectively. Volume of distribution and apparent clearance were significantly reduced by 4% to 26% and 26% t O 38%, respectively, after administration of fluvoxamine. Increases in area under the plasma concentration-time curve from time 0 to infinity appear to be dose dependent. Presumably, altered olanzapine pharmacokinetics are attributed to the inhibition of CYP1A2. Patients treated with the combination of olanzapine and fluvoxamine should be monitored carefully.
    The Journal of Clinical Pharmacology 01/2005; 44(12):1385-90. · 2.84 Impact Factor
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    ABSTRACT: A single dose of haloperidol decanoate 100 mg was administered to 15 schizophrenic patients. Blood samples were obtained prior to injection, 1 h, 3 h, 6 h, 8 h, 1 day, 2 days, 3 days, 4 days, 5 days, 6 days, one week, two weeks, three weeks and four weeks post-injection. Haloperidol and its reduced metabolite, reduced haloperidol, plasma levels were assayed by HPLC with electrochemical detection. The pharmacokinetic parameters of haloperidol were determined. The mean time of maximal (Tmax) plasma levels for haloperidol was 5·73 ± 0·80 days. The haloperidol plasma levels showed a biexponential decline with an elimination half-life of 15·78 ± 5·90 days. Reduced haloperidol was rapidly formed from the haloperidol. The Tmax of reduced haloperidol was 7·00 ± 2·35 days. The mean ratio reduced haloperidol/haloperidol was 0·155 ± 0·111. Since the Tmax occurs at approximately six days, a weekly loading dose of haloperidol decanoate is feasible during the transition from oral to depot therapy.
    Human Psychopharmacology Clinical and Experimental 10/2004; 10(1):47 - 51. · 2.10 Impact Factor
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    ABSTRACT: Adjunctive fluvoxamine inhibits clozapine metabolism and decreases plasma norclozapine (a toxic metabolite of clozapine) to clozapine ratios. This study aimed to demonstrate the effects of fluvoxamine on clozapine-related weight gain, hyperglycemia, and lipid abnormalities. Sixty-eight treatment-resistant inpatients with a DSM-IV diagnosis of schizophrenia were randomly assigned to 2 treatment groups for 12 weeks. The monotherapy group (N = 34) received clozapine (< or = 600 mg/day). The coadministration group (N = 34) received fluvoxamine (50 mg/day) plus low-dose clozapine (< or = 250 mg/day). The study was conducted from August 1999 to October 2002. The 2 groups were similar in demographic data; baseline body weight and body mass index (BMI); baseline serum glucose, triglyceride, and cholesterol levels; and steady-state plasma clozapine concentration. The monotherapy patients (but not the coadministration patients) had significantly higher (p < .05) body weight, BMI, and serum glucose and triglyceride levels after treatment than at baseline. At week 12, the monotherapy patients also had significantly higher glucose (p = .035), triglyceride (p = .041), and norclozapine (p = .009) (and numerically higher cholesterol) levels than the cotreatment patients. The changes in weight and serum glucose and triglyceride levels were significantly correlated (p = .026, p = .005, and p = .028, respectively) with the plasma concentration of norclozapine but not with plasma levels of clozapine. These results suggest that fluvoxamine cotreatment can attenuate weight gain and metabolic disturbances in clozapine-treated patients. Plasma levels of norclozapine, but not clozapine, are associated with increases in weight and serum glucose and triglyceride levels. Of note, coadministration of fluvoxamine could increase plasma clozapine levels markedly and carry the risk of adverse events. If this combined treatment is applied, conservative introduction with reduced clozapine dosage and careful therapeutic drug monitoring of clozapine concentration is recommended.
    The Journal of Clinical Psychiatry 07/2004; 65(6):766-71. · 5.81 Impact Factor
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    ABSTRACT: Risperidone doses for acute schizophrenia were rather high in most recent studies. We tested a hypothesis that fine-tuning risperidone dosage to relieve side effects still yields efficacy. Clinical factors influencing the dosing were also determined. One hundred and forty-six schizophrenia inpatients with acute exacerbation entered a prospective, 6-week, repeated measures study. Risperidone doses were titrated to 6 mg/day (if tolerable) within 7 days, but were lowered thereafter if adverse reactions appeared. Efficacy and safety were measured biweekly. Forty-eight patients tolerated the 6-mg/day target dose well, while the other 98 received lower final doses (mean+/-SD=3.4+/-0.9 mg/day) to curtail adverse effects. At endpoint, 64.3% of the low-dose patients and 43.8% of the high-dose subjects responded to treatment [>/=20% reduction in the Positive and Negative Syndrome Scale (PANSS) total score] ( P=0.018). In detail, the low-dose individuals were significantly superior in percentage changes in the PANSS total and general-subscale scores at endpoint. The low-dose group also tended to improve more (albeit statistically insignificantly) in the PANSS positive and negative subscales and other efficacy measures. Compared to the patients with undifferentiated subtype, those with disorganized subtype received higher dosage by 0.90 mg/day, after controlling for other variables ( P=0.008). Paranoid subtype was similar to undifferentiated subtype in drug doses. Patients with longer illness duration also showed a trend to use higher dosage ( P=0.078). These findings suggest that dosage adjustment to diminish side effects does not compromise risperidone response and that disorganized patients and perhaps patients with longer illness duration are prone to receive larger doses.
    Psychopharmacology 05/2004; 172(4):393-9. · 4.06 Impact Factor
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    ABSTRACT: Previous genetic-response studies, usually without considering environmental factors, encountered great difficulties in replication of results. Although atypical antipsychotics are becoming the mainstay for schizophrenia treatment which makes an antipsychotic "atypical" remains unclear. Risperidone (a widely used atypical antipsychotic agent) and several other atypicals have high affinities for 5-HT6 and 5-HT7 receptors. This study investigated the effects of the T-->C 267 polymorphism in the 5HT6 receptor gene and two rare Pro279Leu and Thr92Lys substitutions in the 5HT7 receptor gene on risperidone efficacy after rigorous control for nongenetic confounders. We found an association between the T-->C 267 polymorphism of the 5HT6 receptor gene and response to risperidone in 123 acutely ill schizophrenia inpatients after adjustment for confounders. Compared to patients with the T/C 267 genotype, those with T/T 267 showed less severe positive symptoms (p=0.006) and general psychopathology (including anxiety, depression, and cognitive dysfunctions) (p=0.005). The T-->C 267 polymorphism had no influences on negative symptoms. The two rare polymorphisms in the 5HT7 receptor gene were not observed in our sample. In conclusion, the 5HT6 receptor gene variant can affect risperidone response to positive symptoms and general psychopathology (but not negative symptoms) after control for nongenetic factors.
    Schizophrenia Research 04/2004; 67(1):63-70. · 4.59 Impact Factor
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    ABSTRACT: There is strong evidence to suggest that genetic variation plays an important role in inter-individual differences in medication response and toxicity. Most of the previous pharmacogenetic studies, however, cannot be reconfirmed. Of note, drug efficacy or side effects depend not only on genetic factors but also on nongenetic factors, such as illness duration, past treatment history, and drug dosage or blood concentration. However, most pharmacogeneticists did not consider or control the possible impact of the nongenetic factors. Schizophrenia is a severe neuropsychiatric disorder with a polygenic mode of inheritance that is also governed by nongenetic factors. Schizophrenia's symptoms are principally subdivided into two subtypes, positive and negative. The positive symptoms include delusions and hallucinations; the negative symptoms, blunted affect and social withdrawal. Atypical antipsychotics are usually superior in the treatment of negative symptoms than typical agents. Although atypical agents are becoming the mainstay for schizophrenia treatment, what makes an antipsychotic “atypical” remains unclear. One of our recent studies have simultaneously evaluated the effects of genetic and nongenetic determinants on the efficacy of risperidone (a widely used atypical antipsychotic agent). We found that 5-HT2A receptor 102-T/C polymorphism could predict clinical response (mainly for negative symptoms rather than positive symptoms) in schizophrenia. Among nongenetic factors, fewer previous hospitalizations and higher risperidone dosage also predicted better treatment response after control for the 102-T/C polymorphism and other confounders. It is hoped that this novel study model could revolutionize future research in pharmacogenetics or other fields of genetics. Drug Dev. Res. 60:164–171, 2003. © 2003 Wiley-Liss, Inc.
    Drug Development Research 09/2003; 60(2):164 - 171. · 0.87 Impact Factor
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    ABSTRACT: Predictors for risperidone-related weight gain remain unclear. This study aimed to identify clinical factors influencing body weight in risperidone-treated patients. One hundred forty-six newly hospitalized DSM-IV schizophrenia patients with acute exacerbation entered this prospective, 6-week, repeated-measures trial. The mean +/- SD risperidone dose was 4.3 +/- 1.4 mg/day at week 6. Efficacy, body weight, and tolerability were measured biweekly. Efficacy was assessed with the Positive and Negative Syndrome Scale (PANSS) and the Nurses' Observation Scale for Inpatient Evaluation (NOSIE). For determining the impacts of possible prognostic factors on body weight, we utilized generalized estimating equation methods to control for other variables and the within-subject dependence over repeated assessments. After the effects of other factors (including baseline body weight) were adjusted, every 1-week increase in treatment duration raised body weight by 0.442 kg (p <.0001). Increasing baseline body weight by 1 kg reduced weight gain by 0.022 kg (p <.0001). Every 1-year increment in age decreased body weight by 0.052 kg (p <.001). Undifferentiated subtype predicted higher weight by around 0.9 kg than other sub-types (p <.05). Each 1-mg/day increment in risperidone dosage heightened body weight by 0.084 kg (p =.015). Responders (those with PANSS total-score reduction > or = 20%) also had higher weight by 0.513 kg on average (p =.007). Specifically, every 1-point diminution in score in PANSS total, PANSS positive, PANSS negative, PANSS cognitive, and NOSIE increased body weight, on average, by 0.029 kg, 0.057 kg, 0.079 kg, 0.079 kg, and 0.035 kg, respectively (p < or =.009). Other variables did not have significant influences. The results suggest that lower initial body weight, younger age, undifferentiated subtype, higher dosage, and treatment response (for positive, negative, and cognitive symptoms and social functioning) are associated with greater weight gain in acutely ill patients treated with risperidone. Further studies with longer observation and in other populations are needed.
    The Journal of Clinical Psychiatry 03/2003; 64(3):316-20. · 5.81 Impact Factor
  • Journal of Clinical Psychopharmacology 01/2003; 22(6):626-8. · 3.51 Impact Factor
  • Journal of Clinical Psychopharmacology 11/2002; 22(5):530-2. · 3.51 Impact Factor
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    ABSTRACT: This study investigated the effect of the 102-T/C polymorphism in the 5-HT(2A) receptor gene on risperidone efficacy. One hundred Han Chinese patients with acutely exacerbated schizophrenia were given risperidone for up to 42 days. The patients were genotyped for 5-HT(2A) polymorphisms. Psychopathology was measured biweekly with the Positive and Negative Syndrome Scale while the patients were taking risperidone. Generalized estimating equation methods were used to analyze the effects of treatment duration, T/C genotypes, and other prognostic factors on Positive and Negative Syndrome Scale performance. Patients with the C/C genotype had lower total scores, negative subscale scores, and general psychopathology scores but not positive subscale scores on the Positive and Negative Syndrome Scale than patients with the 102-T/C genotype. Patients with the T/C and T/T genotypes had comparable total and subscale scores. The number of previous hospitalizations and the dose of risperidone also affected Positive and Negative Syndrome Scale total scores. These results suggest that variations in the 5-HT(2A) receptor gene may influence individual responses to risperidone.
    American Journal of Psychiatry 10/2002; 159(9):1593-5. · 14.72 Impact Factor
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    ABSTRACT: Response predictors of risperidone or other newer atypical antipsychotics for schizophrenia treatment remain unclear. This study aimed to investigate the influence of patient demographics on risperidone efficacy for schizophrenia. One hundred twenty-one newly hospitalized patients who had schizophrenia with acute exacerbation entered this prospective, 6-week risperidone trial. The target dose was 6 mg/day, or lower in case of side effects. Consequently, the mean +/- SD dose remained quite stable after week 2 and reached 4.4 +/- 1.3 mg/day at week 6. Efficacy and side effect assessments were conducted biweekly. The mean total score of the Positive and Negative Syndrome Scale (PANSS) declined during the trial, particularly within the first 4 weeks. Further, of the various efficacy scores (and their natural logarithm values) collected, only the logarithm of the PANSS total score was selected to serve as the response value, because it was normally distributed and thus suitable for regression analyses. After adjusting the effects of treatment duration (weeks 0-6) and other patient-related variables with the generalized estimating equation method, each 1-week increase in duration of prior hospitalizations raised the PANSS total by 0.04% (p = 0.002) and each 1-year increment in the education duration decreased the PANSS by 0.94% (p = 0.04). Gender, age, age at illness onset, duration of illness, diagnosis subtype, or number of prior hospitalizations, however, did not significantly impact the response value. These preliminary results suggest that longer hospitalization duration and shorter education predict higher symptomatology. Further studies with longer observation and larger samples in not only acutely ill patients but also other populations (e.g., first-episode patients) are warranted.
    Journal of Clinical Psychopharmacology 09/2002; 22(4):353-8. · 3.51 Impact Factor
  • Journal of Clinical Psychopharmacology 09/2002; 22(4):439-40. · 3.51 Impact Factor
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    ABSTRACT: For agitated dementia showing insufficient response to conventional antipsychotics, the feasibility of transition to atypical agents remains unknown. Sixty-two Chinese inpatients with dementia and disruptive behaviors were recruited into an 8-week screening trial of haloperidol. Thirty-five (56%) of them responded insufficiently. They then entered a prospective, 16-week, open-labeled study. Haloperidol was abruptly shifted to risperidone 0.5 mg/day at weeks 1 to 4 and then 1 mg/day at weeks 5 to 12. At weeks 13 to 16, the regimen was shifted back to haloperidol at previous doses, mostly 1 mg/day. Safety, efficacy, cognition, and moods were evaluated at least every 4 weeks. Generalized estimating equation methods were used for determining the effects of the prognostic variables on the outcome values. Risperidone, particularly at 0.5 mg/day, was generally tolerable. The Brief Psychiatric Rating Scale (BPRS) score decreased progressively under risperidone treatment; at week 12, 16 (46%) patients showed response (>or=25% reduction in the BPRS). Patients with vascular dementia were more likely to respond than those with Alzheimer's disease ( p = 0.02). Haloperidol reinstitution resulted in no further improvement, except trend increments in motor symptoms. Risperidone also tended to benefit the performance on the Behavioral Pathology in Alzheimer's Disease Rating Scale. Six (17%) patients improved on moods and self-care with risperidone. These preliminary results suggest that crossover from haloperidol to risperidone is generally safe and effective and may produce favorable moods in agitated dementia patients. Vascular dementia is a predictor of treatment response. In contrast to the dose (1 mg/day) recommended for most white individuals, 0.5 mg/day could be tried at first in Chinese patients. Because of the design's limitations, further controlled studies are warranted.
    Journal of Clinical Psychopharmacology 02/2002; 22(1):4-10. · 3.51 Impact Factor

Publication Stats

414 Citations
93.18 Total Impact Points

Institutions

  • 2003–2008
    • China Medical University Hospital
      • Department of Psychiatry
      臺中市, Taiwan, Taiwan
  • 2002–2008
    • Buddhist Tzu Chi General Hospital
      T’ai-pei, Taipei, Taiwan
  • 2005
    • China Medical University (ROC)
      臺中市, Taiwan, Taiwan
  • 2004
    • Wan Fang Hospital
      T’ai-pei, Taipei, Taiwan
  • 2002–2004
    • Tzu Chi University
      • • Department of Psychiatry
      • • Institute of Neuroscience
      Hua-lien, Taiwan, Taiwan
  • 1993–2004
    • Taipei City Hospital
      T’ai-pei, Taipei, Taiwan