喹硫平治疗老年期痴呆患者精神行为症状的临床观察

目的探讨喹硫平治疗老年期痴呆患者精神行为症状的临床疗效和不良反应。方法50例老年痴呆患者按入院先后次序分成喹硫平组与阿普唑仑组,并在治疗前及治疗8周后进行评价,采用阿尔茨海默病病理行为评分表（BEHAVE-AD）评价疗效,采用不良反应量表（TESS）及有关实验室检查评价不良反应。结果喹硫平与阿普唑仑对老年期痴呆患者伴发的精神行为症状均有效。喹硫平组有效率为87．5％,阿普唑仑组有效率为66．7％,无统计学差异（χ^2=1．73,P=0．995）。喹硫平治疗8周后BEHAVE—AD总分及各因子分均下降,其中在幻觉、行为紊乱、攻击行为3个因子的得分比阿普唑仑组明显下降。喹硫平的不良反应较阿普唑仑轻,主要的不良反应是嗜睡、头晕和口干。结论喹硫平和阿普唑仑均可用于治疗老年期痴呆的精神行为症状,喹硫平的优势在于治疗老年期痴呆患者的行为和幻觉症状疗效更加明显。     

奥氮平治疗老年期痴呆行为和精神障碍对照研究

目的：探讨奥氮平对老年期痴呆患者的行为和精神症状的疗效及不良反应。方法：80例老年期痴呆患者随机分为奥氮平组38例和奎硫平组42例,疗程8周。采用阿尔茨海默病病理行为评定量表（BEHAV,AD）及治疗中出现的症状量表评定疗效和不良反应。结果：治疗后两组BEHAV—AD评分均显著下降（P〈0．05或P〈0．01）;以奥氮平组BEHAV—AD总分及行为紊乱、抑郁、焦虑评分降低明显（P〈0．05）。结论：奥氮平对老年期痴呆的行为和精神障碍患者安全有效,适合临床应用。     

喹硫平与氟哌啶醇治疗老年期痴呆精神行为症状的对照研究

目的比较喹硫平与氟哌啶醇治疗老年期痴呆患者精神行为症状（BPSD）的疗效、副反应及对认知功能的影响。方法将符合条件的60例老年期痴呆患者随机分为喹硫平组和氟哌啶醇组（各30例）,治疗2个月。采用一般情况调查表（自编）、临床疗效评定量表（CGI）、阿尔茨海默病病理行为评分表（BEHAVE—AD）、简易智力状态检查（MMSE）、药物副反应量表（TESS）进行疗效、副反应和认知功能评估。结果两组有效率分别为85．67％和83．33％,无显著性差异（P〉0．05）。两组BEHAVE—AD评分治疗前后比较均有显著差异（P〈0．05,P〈0．01）,治疗结束后两组间BEHAVE—AD评分无显著差异（P〉0．05）。治疗结束后MMSE评分喹硫平组较氟哌啶醇组高,有显著差异（t=2．24,P〈0．05）。两组锥体外系副反应发生率比较有显著性差异（x2=6．91,P〈0．01）。结论喹硫平与氟哌啶醇对老年期痴呆精神行为症状疗效相似,但副反应小,对认知功能的影响优于氟哌啶醇,故喹硫平更适合于伴有精神行为症状的老年期痴呆患者的治疗。     

美金刚与喹硫平治疗痴呆的行为和精神症状对照研究

目的探讨美金刚与喹硫平治疗痴呆的行为和精神症状(BPSD)的疗效及安全性。方法将78例BPSD患者随机分为美金刚组与喹硫平组,每组39例,观察8周,于治疗前后采用痴呆病理行为评定量表(BEHAVE-AD)评定疗效,简易精神状况检查量表(MMSE)评定认知功能,日常生活能力量表(ADL)评定生活质量,副反应症状量表(TESS)评定不良反应。结果美金刚组BEHAVE-AD评分、MMSE评分、ADL评分、不良反应、锥体外系反应及嗜睡方面均优于喹硫平组,差异有统计学意义(P0.05)。结论美金刚可有效控制BPSD患者的行为和精神症状,改善其认知功能,提高其日常生活能力,且安全性好。     

奎硫平治疗老年期痴呆伴行为和精神障碍对照研究

目的：探讨奎硫平治疗老年期痴呆患者的行为和精神症状疗效及不良反应,并与利培酮对照。方法：对76例老年期痴呆患者随机分为奎硫平组和利培酮组,疗程8周。采用阿尔茨海默病病理行为评定表（BEHAVE-AD）及治疗中出现的症状量表（TESS）评定疗效和不良反应。结果：奎硫平与利培酮对老年期痴呆伴发的精神障碍疗效可靠。有效率奎硫平组94．7％,利培酮组94．9％,不良反应少。结论：奎硫平对老年期痴呆伴发的精神行为障碍患者安全有效,适合临床使用。     

美金刚与奥氮平治疗老年期痴呆的行为和精神症状对照研究

目的 探讨美金刚与奥氮平治疗老年期痴呆的行为和精神症状(BPSD)的疗效及不良反应.方法 将86例老年期BPSD患者分为美金刚组与奥氮平组,治疗8周.在治疗前、治疗2周末、4周末和8周末,采用痴呆病理行为评定量表(BEHAVE-AD)评定疗效,简易精神状况检查量表(MMSE)评定患者认知功能,日常生活能力量表(ADL)评定患者生活质量,治疗中需处理的不良反应症状量表(TESS)评定不良反应.结果 美金刚组在治疗后第2、4、8周末BEHAVE-AD评分较奥氮平组显著下降(t=2.12、t=2.23、t=2.28,P＜0.05).美金刚组在治疗后第8周末MMSE评分较治疗前显著升高(t=2.33,P＜0.05),奥氮平组治疗前后MMSE评分差异无显著性(t=0.42,P＞0.05),两组比较差异有显著性(t=2.04,P＜0.05).两组治疗后第8周末ADL评分显著下降(t1=2.35,t2=2.49,P＜0.05),两组比较差异无显著性(t=0.45,P＞0.05).美金刚组不良反应少于奥氮平组(x2=5.09,P＜0.05),两组在锥体外系反应(EPS)、口干、嗜睡、体质量增加方面差异有显著性(x2=4.62～6.86,P＜0.05).结论 美金刚对老年期痴呆患者的认知功能及行为和精神症状的改善均有效,且安全可靠.     

富马酸喹硫平对精神分裂症患者抑郁症状影响的研究

目的 探讨富马酸喹硫平对精神分裂症的抑郁症状的疗效及副作用.方法 随机抽取广州市民政局精神病院男女各二个病区的住院精神分裂症患者作为研究对象,予以测评中文版卡尔加里精神分裂症抑郁量表（CDSS-C）,评分≥6分判断合并有抑郁症状,将此类患者共96例随机分为两组,治疗组加用富马酸喹硫平,对照组维持原有治疗方法 不变,观察4周,先后于入组前、用药第2周及第4周以CDSS-C及治疗中出现的症状量表（TESS）进行评定及完善体格检查及实验室检查,记录不良事件的发生,以量表分值的变化来判断治疗效果及药物副反应.结果 （1）喹硫平对精神分裂症患者合并抑郁症状的疗效显著,两组比较有统计学差异（有效率分别为81.2%和33.3%,x2=17.425,P=0.000）;（2）研究结束时喹硫平组的CDSS-C评分为（1.64±1.61）,对照组为（2.91±2.46）,两组比较有统计学意义（t=2.735,P=0.008）;研究第2及4周喹硫平组CDSS-C减分值均要明显高于对照组,两组比较有统计学意义（P=0.000及0.001）;（3）药物副反应的严重程度及副反应所引起的痛苦评分以及对实验室检查指标的影响两组间无差异.结论 喹硫平能有效缓解精神分裂症的抑郁症状,无明显药物副作用,可在临床推广使用喹硫平治疗精神分裂症的抑郁症状.     

奎硫平与奥氮平对精神分裂症患者生活质量影响的对照研究

目的比较奎硫平与奥氮平对精神分裂症患者的疗效及生活质量的影响。方法对60例精神分裂症患者,随机分为奎硫平组（30例）与奥氮平组（30例）治疗,疗程12周。分别于治疗前、4周、8周、12周末,采用阳性与阴性症状量表（PANSS）评定疗效,治疗中出现的症状量表（TESS）评定不良反应,于治疗前和12周末采用生活质量综合评定问卷（GQOLI-74）评定生活质量。结果两组均有显著疗效,奎硫平组与奥氮平组均可显著提高生活质量。两组间比较无统计学意义（P〉0．05）。奎硫平组主要不良反应为嗜睡,但两组间比较无显著差异;奥氮平组主要不良反应为体重增加、血糖升高,两组有统计学意义。结论奎硫平与奥氮平对精神分裂症疗效好,不良反应较少,均可提高患者生活质量。     

喹硫平与奥氮平对精神分裂症患者生活质量影响的对照研究

目的 比较喹硫平与奥氮平对精神分裂症患者的疗效及生活质量的影响.方法 对60例精神分裂症患者,随机分为喹硫平组(30例)与奥氮平组(30例)治疗,疗程12周.分别于治疗前、4周、8周、12周末,采用阳性与阴性症状量表( PANSS)评定疗效,治疗中出现的症状量表(TESS)评定不良反应,于治疗前和12周末采用生活质量综...     

阿立哌唑联合奥氮平对精神分裂症患者症状和睡眠的影响

目的 探讨精神分裂症患者服用奥氮平和阿立哌唑治疗的效果及对睡眠质量的影响。方法 选取我院2018年6月～2020年6月收治的105例精神分裂症患者,抽签法随机分为2组,对照组52例给予奥氮平治疗,联合组53例给予奥氮平联合阿立哌唑治疗,均治疗3个月,对比两组睡眠质量、血浆及血清相关指标及精神症状指标变化。结果 治疗3个月后,联合组老年期痴呆患者病理行为量表（Behave-AD）评分、阳性及阴性量表评分、匹兹堡睡眠质量评分表（PSQI）各条目及总分和血清星形胶质源性蛋白100B(S100B)均低于对照组,脑源性神经营养因子（BDNF）高于对照组（P<0.05）,血浆瘦素及神经肽Y水平两组无显著差异（P>0.05）。结论 奥氮平与阿立哌唑联用可有效调节精神分裂症患者血清S100B、BDNF及血浆廋素、神经肽Y水平,改善患者睡眠质量及精神行为症状。     

综合干预对精神分裂症患者睡眠质量的影响

目的探讨综合干预对精神分裂症患者睡眠质量的影响。方法将符合《中国精神障碍分类与诊断标准(第3版)》(CCMD-3)的精神分裂症诊断标准以及伴有睡眠障碍的80例患者,采用"不平衡指数最小分配原则"分为研究组和对照组各40例。对照组只进行睡眠卫生健康教育,研究组接受睡眠卫生健康教育及音乐治疗、刺激控制、渐进性肌肉放松综合干预,疗程一个月。干预前后采用匹茨堡睡眠质量指数(PSQI)测定两组患者睡眠质量。结果干预前,对照组和研究组PSQI总评分分别为(9.70±1.65)分和(9.79±1.88)分,差异无统计学意义(P0.05)。干预后,研究组PSQI主观睡眠质量(1.43±0.68)、入睡时间(2.23±0.56)、睡眠持续性(0.83±0.67)、睡眠障碍(1.49±0.51)、习惯性睡眠效率(0.28±0.50)、日间功能障碍(1.04±0.59)评分及总评分均低于干预前,差异有统计学意义(P0.05)。对照组PSQI各项得分和总得分均高于研究组,差异有统计学意义(P0.05)。结论综合干预可能有助于改善精神分裂症患者的睡眠质量。     

The influence of olanzapine on immune cells in patients with schizophrenia

In vitro and preclinical studies show that biochemical and behavioral effects of olanzapine are quite similar to those of clozapine. In recent years, some cases of reported agranulocytosis due to olanzapine have been published. However, none of these studies compared the hematological and immune parameters before and after treatment. The present study is aimed at investigating the influence of olanzapine on the immune cell parameters by comparing these before and in the third month of olanzapine treatment in patients of schizophrenia. Twenty patients who were diagnosed as schizophrenic depending on the DSM-IV diagnostic criteria were included in the study. The immune parameters of patients were compared by measuring them before the treatment and 3 months after treatment. Immune parameters were analyzed by using flow-cytometry equipment labeled Coulter Epics Elite ESP. The positivity of cell-surface antibody was evaluated as percentage. The rates of CD8 in the third month of the treatment were considerably increased relative to pretreatment. Furthermore, rates of CD4/CD8 were significantly decreased in the third month of the treatment relative to before treatment. These findings suggest that immune impairment may occur during olanzapine treatment in patients with schizophrenia.     

Nocturnal hormone profiles in patients with schizophrenia treated with olanzapine

Nocturnal hormone profiles were measured in patients with schizophrenia with predominantly negative symptoms both under drug-free baseline conditions and after subchronic administration of the atypical antipsychotic olanzapine, with the aim of characterizing its pharmacological properties on the neuroendocrine level. The following hormones were studied in the sleep laboratory under polysomnographic control: adrenocorticotrophic hormone, cortisol, growth hormone (GH), prolactin, testosterone, and melatonin. Blood samples were taken at regular time intervals over the night, and serum concentrations of the hormones were determined. Ten patients completed the study, two of them were excluded from analysis due to incomplete hormone profiles. The dynamics of baseline nocturnal hormone secretion were similar to the patterns known from healthy subjects. After the treatment period of about 4 weeks, hypothalamic-pituitary-adrenal axis activity was reduced with decreased cortisol plasma levels compared to baseline conditions. Olanzapine induced a moderate prolactin elevation. The characteristic GH peak around sleep onset, clearly present under baseline conditions, was markedly reduced after treatment. Testosterone and melatonin secretion were not significantly altered. In conclusion, although interpretation is difficult in some cases due to interference with indirect effects of olanzapine administration and the consequences of the clinical course of the underlying schizophrenic disorder, the neuroendocrine findings are consistent with the receptor-binding profile of olanzapine where, beside the D(2) antagonism, the antiserotonergic properties are most important.     

Effects of olanzapine on slow wave sleep, sleep spindles and sleep-related memory consolidation in schizophrenia

INTRODUCTION: Memory deficits and sleep disturbances are common clinical features of schizophrenia. Sleep is supposed to promote memory consolidation and the antipsychotic olanzapine is suggested to improve both sleep and memory functions. Therefore we performed a study to analyse the acute effects of olanzapine on distinct sleep parameters and sleep-related memory consolidation in parallel. METHODS: We studied 26 patients with schizophrenia on stable antipsychotic medication with amisulpride (age range 19-44 years). Immediately before polysomnography and the morning after we performed neuropsychological tasks. Before the third night in the sleep laboratory, patients received either olanzapine or a placebo. RESULTS: We found a significant positive association for slow wave sleep and declarative memory performance in schizophrenia at baseline. Additionally, Stage 2 sleep spindle density was positively related to overnight memory consolidation. Olanzapine caused a significant increase in the amount of slow wave sleep in accordance with recent studies, but led also to a significant decrease in sleep spindle density, which had not been described before. Memory performance the next morning was not different between the two groups. DISCUSSION: Since not only slow wave sleep but also sleep spindles are supposed to promote sleep-related memory consolidation, we suggest that a putative positive effect on memory performance by slow wave sleep augmentation is neutralised by the decrease in sleep spindles due to olanzapine.     

奥氮平对精神分裂症患者认知功能障碍的改善作用

目的探讨奥氮平对精神分裂症患者认知功能的改善作用。方法使用新韦氏记忆量表(WMSRC)、威斯康星卡片分类测验(WCST)、阳性症状与阴性症状量表(PANSS)、标准化的精神分裂症认知功能成套测验(MCCB)对患者的认知功能进行综合评定。结果治疗8周后,患者的记忆商数较治疗前有显著提高(P0.05);患者总测试次数、随机错误数、持续错误数均显著性下降(P0.05);但分类完成数、正确数无显著性变化(P0.05);患者治疗前后语言记忆及数字序列间存在显著差异(P0.01);治疗前后其迷宫、视觉记忆、空间广度及持续操作测试结果存在显著差异(P0.05),治疗前后患者连线及情绪管理检测结果差异无统计学意义(P0.05);阴性及阳性症状减分值、PANSS总分减分值与患者记忆商数增加值间呈显著正相关关系(P0.05或P0.01);患者PANSS总分减分值和一般病理性症状减分值与随机错误数减分值及阳性/阴性症状减分值与持续错误数减分值间均存在显著正相关关系(P0.05);治疗期间均未出现严重的不良反应。结论奥氮平可以显著改善精神分裂症患者的认知功能障碍,值得临床推广应用。     

Leukocyte telomere length in Hispanic schizophrenia patients under treatment with olanzapine

Different lines of evidence indicate that patients with schizophrenia (SZ) exhibit accelerated aging. Leukocyte telomere length (TL), an aging marker, is associated with age-related and chronic pathologies, including schizophrenia. We analyzed leukocyte TL in 170 SZ patients of Hispanic ancestry grouped based on antipsychotic treatment, compared to 126 matched controls. The group under treatment with atypical antipsychotics was further subdivided according to the risk of medication to cause metabolic syndrome (MetS). Our results show significant erosion in the TL of SZ patients under treatment with the atypical antipsychotics clozapine and olanzapine, which cause high-risk for MetS, compared to healthy controls and patients under treatment with medium and low-risk antipsychotics. However, when the analysis was done separately for clozapine and olanzapine, a significant difference remained only for olanzapine.These findings suggest that atypical antipsychotics that cause high-risk for MetS, particularly olanzapine, may modulate leukocyte TL in SZ patients. Future research is required to elucidate if in fact atypical antipsychotics are involved in TL maintenance in SZ subjects and the mechanism by which this occurs.