利培酮和氯丙嗪治疗时血糖代谢变化

目的:研究使用抗精神病药影响血糖代谢的特点。方法:198例未曾治疗或停药3个月以上的精神分裂症住院患者给予氯丙嗪或利培酮治疗。于入院时及治疗1、2、3和6个月时检测血糖浓度。结果:氯丙嗪组治疗2个月餐后2 h糖耐量试验(2hPG)、6个月后糖化血红蛋白(HbA1C)浓度均明显高于治疗前。治疗6个月血葡萄糖调节受损(IGR),氯丙嗪组有15.54%,利培酮组有7.37%;≥40岁者2hPG和HbA1C明显高于<40岁者。结论:2hPG和HbA1C浓度增高是糖代谢异常的早期表现,早期干预有利于防止IGR。     

首次使用氯丙嗪和利培酮对精神分裂症患者血糖代谢的影响

目的 探讨首次使用氯丙嗪和利培酮对精神分裂症患者血糖代谢的影响。方法 114例住院精神分裂症患者随机分为氯丙嗪组和利培酮组。治疗前及治疗后第1、2．3、6个月及12个月后分别测定多项血糖指标浓度，并进行对照分析。结果 治疗3个月时的空腹血糖（FPC）、2小时糖耐量（2HPG）及餐后2小时血糖（2HPBG），以及治疗6个月时的糖化血红蛋白（HbAlc）浓度明显高于治疗前；治疗12个月后有15．79％的患者发生血糖调节功能受损（ICR），其中氯丙嗪组为11．65％，明显高于利培酮组6．32％；随着精神病发病年龄的增长，上述血糖浓度也逐步提高；发病年龄、疗前糖耐量及脂蛋白p浓度接近正常上限可能是ICR的诱因。结论 首次使用氯丙嗪和利培酮即可影响糖代谢，应早期监测血糖，早期干预。     

氯丙嗪和利培酮对精神分裂症患者血糖调节功能影响的动态观察

目的观察抗精神病药在治疗的不同时间精神分裂症患者血糖代谢的变化特点,探讨预防血糖调节功能损害(IGR)的有效方法。方法将213例住院精神分裂症患者分为氯丙嗪组(108例,200~650mg/d)和利培酮组(105例,3~6mg/d),均单一用药,分别于入院时、治疗第1,2,3,6个月末及1年末测定多项血糖浓度并进行对照研究。结果(1)治疗后随时间延长,两组血糖浓度均不断上升。治疗第3个月末餐后2h血糖(2hPBG)和2h糖耐量(2hPG)浓度开始升高,治疗第6个月末空腹血糖(FPG)和空腹糖化血红蛋白(HbA1c)开始升高,治疗1年末所有血糖指标均升高(均P<0.05~0.01)。(2)组内治疗前后比较,氯丙嗪组治疗第3个月末2hPG[(5.77±1.28)mmol/L]和2hPBG[(5.93±1.10)mmol/L]、治疗第6个月末HbA1c[(5.49±0.76)mmol/L]、治疗1年FPG浓度[(5.29±0.71)mmol/L]均高于治疗前[分别为(mmol/L)5.31±0.58,5.48±0.60,5.22±0.50和4.96±0.49],均P<0.05~0.01;利培酮组治疗1年末2hPBG浓度[(5.70±0.89)mmol/L]高于治疗前[(5.35±0.77)mmol/L;P<0.05]。(3)两组比较,氯丙嗪组治疗第3个月末2hPBG和HbA1c[(5.41±0.63)mmol/L]、治疗1年末2hPG[(5.92±1.34)mmol/L]和FPG[(5.29±0.71)mmol/L]浓度均高于利培酮组[分别为(mmol/L)5.55±0.83,5.23±0.50,5.54±0.91,5.08±0.59],均P<0.05~0.01。1年末,两种药物日剂量与各血糖浓度之间无显著相关性(P>0.05)。(4)两组治疗后各时间点IGR的发生率均上升;治疗1年末,氯丙嗪组IGR发生率达36.1%,高于利培酮组(22.9%;P<0.05)。(5)在完成1年观察的198例患者中,51例(25.8%)至少有1次符合IGR血糖浓度标准,但两组间的差异无统计学意义(P>0.05)。结论血糖浓度随药物治疗时间的延长而上升,其中氯丙嗪比利培酮更易引起IGR。     

抗精神病药对体重和血糖的影响

目的：了解氯丙嗪、氯氮平和利培酮对体重和血糖的影响。方法：对84例首发精神分裂症患者随机分为3组，单用氯丙嗪、氯氮平和利培酮治疗，疗程8周，分别在治疗前及治疗后2、4、6、8周末观察体重及血糖的变化。结果：3组患者治疗后体重均有非常明显的增加，其中氯丙嗪、氯氮平组治疗4组末，利培酮组治疗6周末体重已比治疗前有明显增加。氯氮平组治疗4周末血糖有明显升高，体重与血糖升高有非常明显的正相关。结论：氯氮平、氯丙嗪和利培酮均能引起体重增加，氯氮平引起的血糖升高可能与此有关。结论：氯氮平、氯丙嗪和利培酮均能引起体重增加，氯氮平引起的血糖升高可能与此有关，应予以关注。     

住院精神分裂症并发糖尿病患者与抗精神病药物应用的关系分析

目的探索抗精神病药物与精神分裂症伴发糖尿病的临床关系。方法观察445例住院精神分裂症患，将氯丙嗪、氯氮平、利培酮及氯氮平合并氯丙嗪分组比较，研究药物种类、住院治疗时间对血糖的影响程度。结果血糖增高和糖尿病的发生率分别为19．78％和12．13％，都以氯氮平合并氯丙嗪组最高，氯氮平次之；氯丙嗪组、氯氮平组及氯氮平合并氯丙嗪组末次血糖浓度明显高于首次血糖浓度。除利培酮组外，住院治疗1～10年的血糖浓度明显增高，但10年后氯氮平组仍有增高趋势。结论氯氮平合并氯丙嗪对血糖代谢影响最大，氯氮平具有更长远的不利影响，使用抗精神病药物时应定期监测血糖。     

氯氮平与氯丙嗪对儿童少年精神分裂症患儿血糖浓度的影响

目的研究氯氮平与氯丙嗪对儿童少年精神分裂症患者血糖浓度的影响。方法对80例儿童少年精神分裂症患儿平均分为氯氮平组和氯丙嗪组,治疗六周。用血生化法分别测定治疗前后的空腹血糖浓度及其体重。结果氯氮平组治疗后血糖增高,体重明显增加,治疗前后有显著性差异;氯丙嗪组治疗后血糖无明显升高,体重增加不明显,治疗前后无显著性差异。结论氯氮平治疗可明显增加儿童少年精神分裂症患儿的血糖浓度及体重,在使用氯氮平治疗儿童少年精神分裂症时监测血糖浓度有临床意义。     

氯丙嗪或利培酮治疗首发精神分裂症患者发生代谢综合征风险的1年观察

目的比较首发精神分裂症患者接受氯丙嗪或利培酮治疗1年后发生代谢综合征的风险，探索干预新模式以降低抗精神病药物导致的代谢综合征。方法首发精神分裂症住院患者分别给予氯丙嗪或利培酮治疗。于人组时、治疗第1、3、6及12个月末，检测空腹血糖、餐后2小时血糖、糖化血红蛋白、高密度脂蛋白、低密度脂蛋白、总胆固醇、三酰甘油水平和血压、体重等。结果共入组198例患者。入院时及治疗第12个月末代谢综合征阳性分别为22例（11．1％）和28例（14．1％），差异有统计学意义（x2=26．21，P〈0．01）。氯丙嗪组，入组时和治疗1年后发生代谢综合征阳性人数分别为12例（11．7％）和17例（16．5％），差异有统计学意义（校正x2=20．85，P〈0．01）。利培酮组分别为10例（10．5％）和11例（11．6％），差别无统计学意义（校正x2=1．97，P=0．16）。治疗第12个月末，利培酮组血浆三酰甘油水平、空腹血糖、餐后2小时血糖、糖化血红蛋白含量低于氯丙嗪组，差异有统计学意义。代谢综合征的发生与患者入组时的代谢异常（r=0．36，P〈0．01）和男性（r=0．17，P：0．02）有关，与治疗药物无关（r=0．07，P=0．32）。结论氯丙嗪和利培酮可引起或加重首发精神分裂症患者代谢综合征。抗精神病药物对患者的影响尚需要进一步的研究。     

利培酮对首发精神分裂症患者糖代谢的影响

目的:探讨利培酮对首发精神分裂症患者糖代谢的影响.方法:46例首发精神分裂症患者予利培酮治疗,于治疗前和治疗4周末测定空腹血糖(FPG)及餐后2 h血糖(2hPG)、三酰甘油、胆固醇、胰岛素、瘦素、胰岛素抗体,并测量身高、腰围、体质量,计算体质量指数(BMI),量表采用阳性与阴性症状量表(PANSS).结果:治疗第4周末与治疗前相比,2hPG、瘦素、BMI、腰围、血脂、糖耐量异常率明显增高,PANSS总分明显减低.治疗前2hPG与胆固醇、腰围均呈正相关,空腹血糖与BMI呈正相关;治疗4周末2hPG、FPG与腰围均呈正相关.患者年龄、用药剂量是糖耐量异常的有关危险因素.结论:精神分裂症患者在药物治疗的初期就应进行2hPG检测,尤其是年长者和药量较大者.     

糖化血红蛋白对抗精神病药治疗时血糖的监测

目的:探讨糖化血红蛋白(HbA1C)在抗精神病药治疗中对血糖变化的监测作用.方法:对198例单用氯丙嗪或利培酮治疗的精神分裂症住院患者于治疗前、治疗1、2、3、6、12个月测定HbA1C及血糖浓度并与常规血糖检测指标进行比较.结果:HbA1C浓度随治疗时间延长而增高,与血糖浓度变化呈显著正相关,与血葡萄糖调节受损(IGR)的发生呈平行发展,治疗1年后异常率为11.6%.结论:HbA1C检测稳定性好,结合空腹血糖等常规指标,是抗精神病药治疗中观察血糖变化的有效指标.     

阿立哌唑、利培酮及氯丙嗪对精神分裂症疗效及认知功能的影响

目的探讨非经典抗精神病药阿立哌唑、利培酮及传统抗精神病药氯丙嗪治疗精神分裂症的疗效及对认知功能的影响。方法将148例符合CCMD-3诊断标准的精神分裂症病人随机分为阿立哌唑组（48例）、利培酮组（52例）和氯丙嗪组（48例），观察12周，分别于治疗前及治疗后4、8、12周采用阳性症状与阴性症状量表（PANSS）、不良反应量表（TESS）评定疗效和不良反应；治疗前及治疗后12周采用韦氏成人记忆测检（WMS）及威斯康星卡片分类测验（WCST）测定。结果与治疗前比较，三组治疗后12周PANSS总分及各因子分显著下降（P〈0．01），但三组之间无显著差异；利培酮、氯丙嗪组的不良反应发生率高于阿立哌唑组（P〈0．05），主要表现为肌强直、震颤等锥体外系等不良反应；阿立哌唑、利培酮组WMS和WCST评分均有显著改善，而氯丙嗪组治疗前后则无差异。结论阿立哌唑、利培酮及氯丙嗪治疗精神分裂症均有效，且疗效相当，阿立哌唑所致锥体外系不良反应较少，阿立哌唑、利培酮对认知功能有改善作用，而氯丙嗪则对认知功能无影响。     

Development of the projection from the nucleus of the brachium of the inferior colliculus to the superior colliculus in the ferret

Neurons in the deeper layers of the superior colliculus (SC) have spatially tuned receptive fields that are arranged to form a map of auditory space. The spatial tuning of these neurons emerges gradually in an experience-dependent manner after the onset of hearing, but the relative contributions of peripheral and central factors in this process of maturation are unknown. We have studied the postnatal development of the projection to the ferret SC from the nucleus of the brachium of the inferior colliculus (nBIC), its main source of auditory input, to determine whether the emergence of auditory map topography can be attributed to anatomical rewiring of this projection. The pattern of retrograde labeling produced by injections of fluorescent microspheres in the SC on postnatal day (P) 0 and just after the age of hearing onset (P29), showed that the nBIC-SC projection is topographically organized in the rostrocaudal axis, along which sound azimuth is represented, from birth. Injections of biotinylated dextran amine-fluorescein into the nBIC at different ages (P30, 60, and 90) labeled axons with numerous terminals and en passant boutons throughout the deeper layers of the SC. This labeling covered the entire mediolateral extent of the SC, but, in keeping with the pattern of retrograde labeling following microsphere injections in the SC, was more restricted rostrocaudally. No systematic changes were observed with age. The stability of the nBIC-SC projection over this period suggests that developmental changes in auditory spatial tuning involve other processes, rather than a gross refinement of the projection from the nBIC.     

Mechanisms of the suppression of the nociceptive reflex of the opening of the mouth during stimulation of the structures of the limbic brain

The comparative effectiveness of the inhibitory influence of tetanic stimulation of hypothalamus, amygdala and limbic cortex on EMG-response of m. digastricus evoked by electrical stimulation of tooth pulp nociceptive afferents was studied in cats anesthetized with a mixture of chloralose and nembutal. It was found that inhibition of the EMG-component of the jaw-opening reflex is most pronounced in case of stimulation of medial and lateral region of the hypothalamus, the inhibitory effect of central and medial nuclei of the amygdala is less pronounced and the effect of the limbic cortex is the weakest. It was shown that the mechanism of the antinociceptive effect of tetanic stimulation of the hypothalamus is not related to the concomitant increase of the blood pressure. After stabilization of the blood pressure the suppressive effect of the hypothalamus remains without changes, that points out to a direct, primary, not baro-afferent mechanism of the inhibition of the activity of nociceptive neurons of the trigeminal sensory nuclei. Noradrenaline, injected intravenously, induced a large increase of the blood pressure accompanied by a pronounced inhibition of the pain reflex. Angiotensin causes the same degree of blood pressure elevation without changes in the amplitude of the EMG-response of the pain reflex. Hypothalamic and noradrenergic mechanisms for control of pain sensitivity are discussed.     

The organization of the connections between the cortex and the claustrum in the monkey

The distribution of labelled cells and of extracellular granules in the claustrum has been studied after injections of horseradish peroxidase in several areas of the neocortex. The frontal and parietal lobes are related to the anterior and posterior halves respectively of the claustrum, and the occipital and temporal cortex to the posterior and inferior margins. Parts of the claustrum related to areas of the cortex in the frontal lobe overlap considerably in the antero-posterior dimension with parts related to widely separated but interconnected areas of the parieto-temporal cortex. Areas of cortex within one lobe which are interconnected are related to parts of the claustrum which overlap in the dorsoventral dimension.     

Experimental study of the projections of the nucleus of the tractus solitarius and the area postrema in the cat

Projections from the area postrema and adjacent parts of the medial solitary nucleus are demonstrated with the Nauta method following lesions limited exclusively to these structures. Experiments are controlled with lesions involving adjacent bulbar regions, cerebellum, and spinal cord. Ascending pathways in the dorsal and lateral columns of the spinal cord project ipsilaterally to the area postrema and bilaterally to a para-alar nucleus in the ventral periphery of the nucleus gracilis. Neurons in the area postrema project mainly inspilaterally to the dorsal and medial regions of the medial solitary nucleus. Neurons in the posterior half of the medical solitary nucleus project ipsilaterally to the lateral solitary nucleus, dorsal vagal nucleus, ambigus, retrofacial nucleus, and dorsal and lateral bulbar reticular formation. Projections to nuclei intercalatus and prepositus hypoglossi, bilaterally, and to the ipsilateral dorsal tegmental nucleus by way of the dorsal longitudinal fasciculus are also shown. No direct projections to the diencephalon are demonstrated. Control lesions in the dorsal column nuclei reveal projections to the contralateral inferior olive and thalamic reticular and ventrobasal nuclei, but not to the projection sites of the solitary nucleus. Evidence is given to support the hypothesis that ascening visceral pathways are interruped in the bulbar reticular formation and dorsal tegmental nucleus before reaching the diencephalon. Correlations are suggested with functional aspects of the central autonomic and reticular activating systems.