利培酮治疗难治性精神分裂症临床分析

目的：评价对利培酮对难治性精神分裂症的疗效与副作用。方法：对我住院的难治性精神分裂症３０例换用利培酮治疗２４周。用阳性与阴性症状量表（ＰＡＮＳＳ）评定疗效,用副反应量表（ＴＥＳＳ）及锥体外系副反应量表（ＥＳＲＳ）评定副作用。结果：ＰＡＮＳＳ部分、ＰＡＮＳＳ－Ｇ（一般精神病理）分、ＰＡＮＳＳ－Ｐ（阳性症状）分治疗前后有显著差异。ＰＡＮＳＳ总分及各分量表分均自治疗１２周末起有显著下降,说明自第１２周末开始显效。ＰＡＮＳＳ部分减分率≥２０％者１８例,≥５０％者５例,有效率为６０％。最常见的副作用是ＥＰＳ（６／３０）,但症状多较轻。结论：利培酮对难治精神分裂症有肯定的疗效,副反应轻微。     

维思通与氯氮平治疗慢性精神分裂症的临床对照研究

目的 探讨维思通和氯氮平治疗慢性精神分裂症的临床疗效及副反应。方法 对９６例符合ＣＣＭＤ－２－Ｒ中精神分裂症诊断标准，病程≥５年，ＰＡＮＳＳ总分≥６０分的住院患者并随机分为维思通组（ｎ＝５１例）和氯氮平组（ｎ＝４５例）。研究期限为９周。两组均采用药物固定剂量法，维思通组每日４ｍｇ，氯氮平组每日３７５ｍｇ。分别于研究前、后评定两次ＰＡＮＳＳ量表。以研究前后减分２０分为有效果限值；利用副反应清单比较了     

氯氮平对难治性精神分裂症的疗效与D2受体基因的关系

目的：探讨与氯氮平对难治性精神分裂症疗效有关的Ｄ２受体基因的基因以及其他相关因素。方法：抽取１００例难治性精神分症患者,给予氯氮平≥４００ｍｇ／ｄ的治疗２个月。用阳性症状与阴性症状量表（ＰＡＮＳＳ）评定氯氮平疗效,用多聚酶链式反应扩增及限制性片段长度多态性（ＰＣＲ－ＲＦＬＰｓ）技术测定所研究对象的基因和等位基因。结果：发现氯平对难治性精神分裂症患者的疗铲与患者性别２明显相关,而与Ｄ２受体基因无关,     

利培酮和氯氮平治疗难治性精神分裂症对照观察

目的　了解利培酮和氯氮平对难治性精神分裂症患者疗效。方法　对１３５ 例难治性精神分裂症患者按ＣＣＭＤⅡＲ 标准确诊后,随机分成两组,用利培酮和氯氮平各治疗６ 个月,在治疗前及治疗后２ 、４、６ 个月用ＢＰＲＳ、ＳＡＮＳ、ＳＤＳＳ、ＣＧＩ量表评定疗效。结果　在治疗难治性精神分裂症利培酮有效率３５－３ ％ ,氯氮平有效率３１－３％ ,量表显示二药对难治性精神分裂症疗效相似,利培酮主要以不良反应为轻度静坐不能,震颤,急性肌张力障碍,氯氮平为嗜睡,头晕,恶心,呕吐,流涎。结论　传统的神经阻滞剂治疗难治性精神分裂症无效时,非典型抗精神病药尤其利培酮可作为理想的药物。     

利培酮治疗氯氮平无效的难治性精神分裂症

目的：探讨利培酮对氯氮平治疗无效的难治性精神分裂症是否有效。方法：对３１例氯氮平治疗无效的难治性精神分裂症住院患者改用得培酮治疗。结果：第８周末，阴性与阳性症状量表（ＰＡＮＳＳ）总分较疗前下降≥２０％者１９例（６１．３％）；≥５０％者１２例（３８．７％）。ＰＡＮＳＳ总分、阳必 状和一般精神病理学症状分量表积分的平均秩和于第２周末较疗前显著下降（Ｐ〈０．０５～０．０１）；阴性症状分量表积分于第４周末     

氯氮平的早期副作用治疗窗

寻找氯氮平早期副作用治疗窗。方法 给６６例精神分裂症患者单服氯氮平,并且评价了０周ＰＡＮＳＳ、２周ＴＥＳＳ和血清氯氮平浓度、４周ＰＡＮＳＳ和ＴＥＳＳ。结果 ２周ＴＥＳＳ总分和诸因子分与４周ＰＡＮＳＳ总分减分率均无显著相关性,２周抗α１－肾上腺素因子分在窗内（０～５分）的显效率４７％比窗外的２２％显著为高（Ｐ〈０．０５）,２周氯氮平血清浓度在内（２３０～３３０μｇ／Ｌ）的显效率５１％比窗外的１９％显     

氯氮平对精神分裂症阴性、阳性症状的疗效分析

用氯氮平治疗表现为阴性、阳性症状的精神分裂症病人１３１例，根据阴性症状量表（ＳＡＮＳ）、阳性症状量表（ＳＡＰＳ）评分分为两组，阴性症状组６１例，阳性症状组７０例。分别在治疗前、治疗后２、４、８周使用简明精神病量表、ＳＡＮＳ、ＳＡＰＳ、临床总体印象量表和副反应量表进行盲式评分。结果显示：氯氮平对两组症状均有较好和同等疗效（Ｐ＜０．０１）。对氯氮平的疗效、作用机制、临床应用、副作用及对难治性病例的疗效进行了讨论。     

氯氮平对精神分裂症阴性,阳性症状的疗效分析

用氯氮平治疗表现为阴性、阳性症状的精神分裂症病人１３１例，根据阴性症状量表（ＳＡＮＳ）、阳性症状量表（ＳＡＰＳ）评分分为两组，阴性症状组６１例，阳性症状组７０例。分别在治疗前、治疗后２、４、８周使用简明精神病量表、ＳＡＮＳ、ＳＡＰＳ、临床总体印象量表和副反应量表进行盲式评分。结果显示：氯氮平对两组症状均有较好和同等疗效（Ｐ＜０．０１）。对氯氮平的疗效、作用机制、临床应用、副作用及对难治性病例的疗效     

奥氮平与氯氮平治疗精神分裂症的比较研究

目的：评价奥氮平治疗精神分裂症的临床疗效与安全性,方法 ８０例精神分裂症患者随机分成２组,分别给予奥氮平与氯氮平治疗１２周,采用ＰＡＮＳＳ评价临床疗效,ＴＥＳＳ评价不良反应。结果：全部病人完成疗程,奥氮平组治疗前后ＰＡＮＳＳ减分率４２．４％,有效率为８２．５％,氯氮平组治疗前后ＰＡＮＳＳ减分率３７．５％,有效率为７０％,未见严重的药物不良反应,安全性好。结论：奥氮平是一种有效的治疗精神分裂症的药物     

氯氮平合并利培酮治疗难治性精神分裂症

目的：了解氯氮平全早培酮的治疗难治性精神分裂症的疗效和安全性。方法：２６例符合ＣＣＭＤ－２－Ｒ精神分裂症诊断标准且临床判断属于难治性病人,予氯氮平合并利培酮治疗,疗程８周,分别在治疗前及治疗后进行阳性与阴性症状量表（ＰＡＮＳＳ）和不良瓜症状量表（ＴＥＳＳ）评定。结果：合并治疗８周后部是性,阴性及一般精神病理分治疗前后均有显著差异。ＴＥＳＳＵ叫分治疗前后无显著差异。副反应主要为静坐不能,肌张力增高,     

Involvement of the adenosine A1 and A2A receptors in the antidepressant-like effect of zinc in the forced swimming test

It was previously shown that the acute administration of zinc chloride elicits an antidepressant-like effect in the mouse forced swimming test (FST). We have also shown that the activation of adenosine A₁ and A_2A receptors produces an antidepressant-like effect in FST. Thus, this study investigated the involvement of adenosine receptors in the antidepressant-like effect of zinc in the FST. The antidepressant-like effect of ZnCl₂ (30 mg/kg, i.p.) in the FST was prevented by the pretreatment of animals with caffeine (3 mg/kg, i.p., a non-selective adenosine receptor antagonist), DPCPX (2 mg/kg, i.p., a selective adenosine A₁ receptor antagonist) or ZM241385 (1 mg/kg, i.p., a selective adenosine A_2A receptor antagonist), administered at doses that per se produced no anti-immobility effect. Moreover, the treatment of mice with CHA (0.05 mg/kg, i.p., a selective adenosine A₁ receptor agonist), DPMA (0.1 mg/kg, i.p., a selective adenosine A_2A receptor agonist) or dipyridamole (0.1 µg/site, i.c.v., an adenosine transporter inhibitor) was able to potentiate the action of sub-effective doses of ZnCl₂. Taken together, the results suggest that the antidepressant-like effect of zinc in the mouse FST might involve a direct or indirect activation of adenosine A₁ and A_2A receptors.     

A lipoma of the cerebellum

A lipoma, essentially occupying the superior vermis and related to a branch of the left superior cerebellar artery, was an incidental finding at autopsy of a 75 year old woman who died of renal failure. Localisation of a lipoma to the superior vermis seems to be rare. Besides fatty tissue there were cartilaginous components. Malformation of the convolutional pattern in the immediate vicinity of the tumour suggests its origin from a false mixture of tissue (hamartoma) in the anlage of the cerebellum.     

Subcellular distributions of adenosine A1 and A2A receptors in the rat dorsomedial nucleus of the solitary tract at the level of the area postrema

Adenosine A1 and A2A receptors mediate distinct cardiovascular components of defense reactions that are ascribed, in part, to opposing actions within the nucleus tractus solitarius. To assess the cellular sites of relevance to these actions, we examined the light and electron microscopic immunolabeling of adenosine A1 and A2A receptors in the rat dorsomedial nucleus of the solitary tract at the level of the area postrema (dmNTS-AP), a region crucial for cardiovascular regulation involving vagal baroreceptor afferents. Immunoreactivity for each receptor was independently localized to distinct segments of plasma membranes and endomembranes in somatodendritic, axonal, and glial profiles. The dendritic labeling for each receptor also was detected within and near asymmetric, excitatory-type synapses. Of all peroxidase labeled profiles exclusive of somata, approximately 58% were A1- and 39% were A2A-labeled dendrites. Dendrites and astrocytic glia were the profiles that most often expressed both subtypes of adenosine receptors. The axonal labeling for A2A receptors was seen mainly in unmyelinated axons, whereas the A1 receptors were prominently localized within axon terminals. These terminals often formed single or multisynaptic excitatory-type junctions or single symmetric synapses on dendrites, a few of which expressed A1 and A2A receptors. These results provide the first ultrastructural evidence that A1 and A2A receptors have distributions conductive to their dual involvement in modulating the output of single neurons and glial function in the dmNTS-AP, where the predominate presynaptic effects of adenosine are mediated through A1 receptors.