中枢神经组织内微量注射：注入体积,浓度与扩散范…

采用微量注射法在猫脊髓内注射不同体积和浓度的伊文思蓝溶液，发现染料在中枢神经组织中的扩散范围与注射体积有关，而与伊文思蓝的浓度无关。２￣３μｌ扩散范围为２．５２￣３．４３ｍｍ，最适于对靶点进行生理验证。本研究为功能性疾病靶点验证时注入利多卡因的体积和浓度提供了参考依据。     

单唾液酸神经节苷脂鞘内注射治疗恢复期脊髓损伤的临床研究

目的观察单唾液酸神经节苷脂(GM1)鞘内注射治疗恢复期脊髓损伤的临床疗效。方法 46例脊髓损伤恢复期患者随机分为2组,对照组(n=23)给予综合性康复训练;治疗组(n=23)在对照组基础上给予GM1 40mg鞘内注射,每周1次,共3次。分别在治疗前和治疗第2个月末,采用ASIA评分标准对所有患者进行功能评定。结果治疗后2组患者ASIA评分均较治疗前显著增高(P0.05),治疗组与对照组相比明显增高(P0.05);3例鞘内注射后次日双下肢肌力明显增加;所有穿刺脑脊液压力均在正常范围内,脑脊液常规、生化和细胞学检测均未见异常;治疗中未出现严重不良反应。结论鞘内注射GM1治疗恢复期脊髓损伤效果良好,费用低廉,安全可行。     

尿中微量白蛋白与脑梗死患者病情严重程度、预后及复发的关系

目的：探讨尿中微量白蛋白与脑梗死患者病情严重程度、预后及复发的关系。方法采用前瞻性队列研究方法,86例脑梗死患者根据尿白蛋白排泄率（UAER）分为2组：尿微量白蛋白组（MAU 组）36例（尿白蛋白排泄率30~300 mg/24 h）;尿白蛋白正常组（NAU 组）50例（尿白蛋白排泄率〈30 mg/24 h）,入院时采用美国国立卫生院卒中评分（National Institutes of Health Stroke Scale,NIHSS）及格拉斯哥昏迷量表（Glasgow Coma Stroke,GCS）评分评定患者的病情严重程度;用 Barthel 生活指数（Barthel index,BI）评定患者的日常生活能力,用改良的 Rankin 量表（modified Rankin Scale,mRS）评定患者的病残程度,并于脑梗死后3、12、24月时再次进行 BI 及 mRS 评分,并随访2年以观察脑梗死复发情况。结果MAU 组入院时 NIHSS 评分（7.09±2.24）分,高于 NAU 组（4.96±2.11）分（P 〈0.05）,GCS 评分（13.4±2.62）分,低于 NAU 组（14.5±2.87）分（P 〈0.05）;MAU 组 BI 评分在入院时、脑梗死后3、12、24月均低于 NAU 组（P 〈0.05）;MAU 组在入院时、脑梗死后3、12、24月 BI 评分、mRS 评分均高于 NAU 组（P 〈0.05）。随访2年,MAU 组再发1次6例（16.67%）,再发2次3例（8.33%）,再发3次及以上者1例（2.78%）;NAU 组再发1次5例（10%）,再发2次2例（4%）,再发3次及以上者0例（0%）;MAU 组均高于 NAU 组（P 〈0.05）。结论脑梗死伴 MAU 患者与脑梗死 NAU 患者比较,前者病情较重、预后较差,复发率更高。     

血尿酸、尿微量白蛋白与2型糖尿病颈动脉内膜病变的关系

目的探讨血尿酸（UA）、尿微量白蛋白（UMP）与2型糖尿病颈动脉内膜病变的相关性。方法选取我院自2007-03-2010-05收治的106例2型糖尿病患者作为研究对象,分为A组（UAER〈200μg/min,血尿酸水平正常）51例和B组（UAER≥200μg/min,高尿酸血症）55例,同时选取同期我院体检的非糖尿病健康者50例作为C组（对照组）,检测3组患者的血尿酸、尿微量白蛋白及空腹血糖、甘油三酯、胆固醇、颈动脉内膜-中膜厚度水平,分析研究结果。结果 3组患者TG、TC比较差异无统计学意义（P〉0.05）;A、B 2组UA、UMP、FBG、IMT与C组比较均有明显差异（P〈0.05,P〈0.01）;A组与B组UA、UMP、IMT比较差异有统计学意义（P〈0.01）。UA、UMP与IMT呈显著正相关（r=0.685、0.362、0.574）。结论 UA、UMP与2型糖尿病颈动脉内膜病变具有显著相关性,对早期防治糖尿病周围血管病变有重要价值。     

急性脑梗死患者微量白蛋白尿与卒中相关 危险因素的关系探讨

目的 探讨微量白蛋白尿（microalbuminuria,MAU）与急性脑梗死危险因素及其病情严重程度的关系。
方法 采用前瞻性研究方法,连续收集2011年7月～2013年7月在上海市第一人民医院分院神经内科
住院且发病时间72 h内的急性脑梗死患者166例为研究对象,其中男89例,女77例,应用免疫比浊法
测定患者的尿微量白蛋白水平,根据检测结果将所有患者分成MAU阳性组（81例）和MAU阴性组（85
例）。比较两组间一般临床资料及生化指标是否存在差异,并采用Logistic回归分析评估MAU与脑梗死
危险因素的相关性。
结果 166例患者中,有81例（48.8%）存在MAU。MAU阳性组与阴性组比较,糖尿病（χ2=8.116,
P =0.004）、收缩压（t =2.735,P =0.007）、美国国立卫生研究院卒中量表（National Institutes of Health
Stroke Scale,NIHSS）（t =2.612,P =0.01）、血糖（t =2.68,P =0.008）、低密度脂蛋白胆固醇（t =2.217,
P =0.028）和C反应蛋白（t =5.548,P =0.000）差异有显著性。Logistic回归分析显示,糖尿病［优势比
（odds ratio,OR）为1.51,95%可信区间（confidence interval,CI）1.26～2.47,P =0.01］、收缩压（OR 1.47,
95%CI 1.01～1.17,P =0.004）、低密度脂蛋白胆固醇（OR 2.43,95%CI 1.01～5.37,P =0.03）和C反应蛋
白（OR 1.79,95%CI 1.09～1.21,P =0.005）均为MAU的独立危险因素。
结论 MAU与高血压、糖尿病、C反应蛋白、血脂等脑梗死危险因素密切相关。     

间断鞘内注射罗哌卡因和布比卡因对大鼠后肢感觉、运动功能的影响

目的 探讨间断鞘内注射不同浓度罗哌卡因、布比卡因后大鼠后肢感觉、运动功能及脊髓背根神经细胞的变化.方法 SD大鼠30只,采用随机数字表法分为5组(n=6).按改良法于L3-4蛛网膜下腔置管.分别经导管注入0.75%罗哌卡因(R1组)、1%罗哌卡因(R2组)、2%罗哌卡因(R3组)和2%布比卡因(B组)40μL,对照组(N组)注入人工脑脊液40μL,每1.5小时一次,共3次.于注药后1 d开始对5组大鼠进行热板仪、压痛仪及后肢撑力实验.以评价5组大鼠的感觉、运动功能.结果 N、R1、R2组感觉、运动功能及脊髓背根神经节病理学结果基本正常;R3组出现暂时性感觉异常,且神经元有轻度改变;B组出现暂时性肌力下降和不可逆性感觉异常,神经元表现为空泡形成、变性.结论 大鼠蛛网膜下腔间断注射浓度低于2%的罗哌卡因对脊神经无永久性损伤.而注射2%罗哌卡因和2%布比卡因均可造成大鼠后肢神经毒性损伤.且后者损伤程度大于前者.     

脑干与脊髓内肿物的组织病理和超微结构研究

目的：研究脑干与脊髓内肿物的类别、分布和组织病理与超微结构特点。方法：取７２例脑干与脊髓内肿物的活检材料，做半薄和超薄切片，光镜与电镜观察。结果：脑干肿瘤２３例，脊髓内肿瘤１５例，脑干血管畸形１９例，脊髓内血管畸形４例，其中３例伴有肿瘤。脑干肿瘤中星形细胞瘤最多，室管膜瘤很少。脊髓内肿瘤中室管膜瘤最多，星形细胞瘤次之，９例脊髓内肿瘤，包括６例室管膜瘤，两极有空洞形成，洞壁淤血水肿。血管畸形中海绵状血管畸形最多，静脉性和毛细血管扩张型较少，可见毛细血管扩张型向海绵状血管畸形的过渡和复合型。结论：星形细胞瘤在光镜下适于按ＷＨＯ的新分级法分为四级。在电镜下需根据核异型的程度和数量及胞质内细胞器的增减来考虑恶性度。室管膜瘤、神经鞘瘤、黑色素瘤和血管外被细胞瘤在电镜下常有特异的微细结构作为确切的诊断依据。脊髓内肿瘤两极的空洞形成，考虑与肿瘤压迫，循环障碍，水肿液蓄积有关。３例脊髓内海绵状血管畸形有肿瘤与空洞并存，其发生可能与肿瘤长期压迫、循环障碍、毛细血管持续扩张有关。     

脑脊液置换联合万古霉素与地塞米松鞘内注射治疗术后颅内感染的临床研究

目的探讨脑脊液置换联合万古霉素与地塞米松鞘内注射治疗术后颅内感染的疗效。方法2002~2012年收治67例术后颅内感染患者,均给与脑脊液置换治疗;在此基础上,25例给予静脉滴注头孢曲松治疗（对照组）,42例给予鞘内注射万古霉素和地塞米松治疗（治疗组）。结果治疗组14 d治愈率（64.3%,27/42）、20 d治愈率（83.3%,33/42）和总治愈率（100%）均明显高于对照组[（分别为20.0%,5/25;56.5%（13/25）;84.0%（21/25）;P〈0.05）。治疗组平均治愈时间[（13.21±4.52）d]较对照组[（22.51±5.74）d]显著缩短（P〈0.05）。两组脑萎缩、脑积水、神经根刺激症状等并发症发生率无统计学差异（P〉0.05）。结论脑脊液置换联合万古霉素和地塞米松联合鞘内注射治疗术后颅内感染疗效显著,实用安全。     

鞘内注射胶质细胞抑制剂对背根神经节压迫大鼠脊髓星形胶质细胞的影响

BACKGROUND： Astrocytes are considered to provide nutritional support in the central nervous system. However, recent studies have confirmed that astrocytes also play an important role in chronic pain.
OBJECTIVE： To investigate the effects of intrathecal injection of fluorocitrate, minocycline or both on astrocyte activation and proliferation in the spinal dorsal horn of compressed dorsal root ganglion in rats.
DESIGN, TIME AND SETTING： The neurology randomized controlled animal study was performed at the Jiangsu Institute of Anesthesia Medicine, from September 2006 to April 2007. MATERIALS： A total of 96 male Sprague Dawley rats, aged 6-8 weeks, were selected for this study. Following intrathecal catheterization, 80 rats underwent steel bar insertion into the L4-5 intervertebral foramina to make a stable compression on the L4-5 posterior root ganglion. Thus rat models of ganglion compression were established. Minocycline and fluorocitrate were purchased from Sigma, USA.
METHODS： A total of 96 rats were randomly and equally divided into six groups. Rat L4, L5 transverse process and intervertebral foramina were exposed in the sham operation group, but without steel bar insertion. The model group did not receive any manipulations. Rats in the phosphate buffered saline （PBS） group were intrathecally injected with 0.01 mmol/L PBS （20 μL）. Rats in the fluorocitrate group were subjected to 1 μmol/L fluorocitrate （20 μL）. Rats in the minocycline group were intrathecally injected with 5 g/L minocycline （20 μL）. Rats in the minocycline and fluorocitrate group received a mixture （20 μL） of 5 g/L minocycline and 1 μmol/L fluorocitrate. Following model establishment, drugs were administered once a day.
MAIN OUTCOME MEASURES： At 7 and 14 days following model induction, glial fibrillary acidic protein expression in the spinal dorsal horn was measured by immunofluorescence microscopy. Six sections with significant glial fibrillary acidic protein -positive expression were obtained to count astrocytes under an inverted microscope.
RESULTS： No significant differences in astrocyte count were detected between the fluorocitrate and model groups. Cell bodies were small with a few processes in the fluorocitrate group, compared with the model group. The astrocyte count decreased significantly in the minocycline group and the minocycline and fluorocitrate group compared with the sham operation, model, PBS and fluorocitrate groups （P 〈 0.01）. The decrease in astrocyte count was mainly found in layers Ⅲ–Ⅳ of the spinal dorsal horn. Cell body volume was smaller and process numbers were fewer in the minocycline group and the minocycline and fluorocitrate group, compared with the model and PBS groups.
CONCLUSION： Fluorocitrate can inhibit astrocyte activation, but does not affect astrocyte proliferation. However, minocycline can inhibit the activation and proliferation of astrocytes.     

癫痫患儿服用苯巴比妥时血清浓度、血清游离浓度和唾液浓度的关系与临床意义

目的 :探讨苯巴比妥 (PB)治疗癫痫时的血清浓度 (Cp)、血清游离浓度 (FCp)、唾液中浓度 (Cs)的关系。方法 :用Waters高效液相色谱法检测 5 6例单服PB的癫痫患儿的 3种PB浓度。结果 :不同年龄组癫痫患儿之间PB的平均Cp、FCp、Cs差别无显著意义 ;Cp与FCp ,FCp与Cs有较好的相关性 ,而Cp与Cs之间相关性不明显。结论 :测定Cs可反映FCp的水平 ,因此可通过测定PB的Cs水平检测PB实际抗癫痫药物浓度     

N-Acetylserotonin in the central nervous system

1. N-acetylserotonin has been identified by immunohistochemistry in specific brain areas separate from melatonin and serotonin. N-acetylserotonin is widely distributed within the brain stem, cerebellum and hippocampus and in the brain stem it is contained within reticular formation nuclei and motor nuclei. Like serotonin, N-acetylserotonin appears to be derived from tryptophan as tryptophan hydroxylase inhibition leads to a lowering in innunoreactive N-acetylserotonin in brain and blood. Beta adrenergic drugs influence N-acetylserotonin neurons with beta adrenergic agonists causing a rise in immunoreactive N-acetylserotonin. The presence of N-acetylserotonin in brain has been confirmed by gas chromatography, mass spectrometry and radioimmunoassay.

2. At this point little is known of the possible role of N-acetylserotonin in the brain. In the hippocampus N-acetylserotonin is present in granule cells and its appearance parallels the appearance of those cells. High affinity binding of tritiated N-acetylserotonin is found in brain and in various brain areas and this radioligand appears to label serotonergic receptors. Preliminary iontophoretic studies performed on hippocampal slices indicate an inhibitory action of N-acetylserotonin on glutamate induced firing of pyramidal cells.

3. Taken together these findings suggest that N-acetylserotonin may have a role in the central nervous system distinct from that of being a precursor for melatonin. If this hypothesis is correct it would suggest that indoleamines have certain similarities to catecholamines. Thus for the catecholamines, dopamine, norepinephrine and epinephrine form a synthetic sequence and yet have independent roles as neurotransmitters and/or hormones. The three indoleamines serotonin, N-acetylserotonin and melatonin also form a synthetic sequence and these three substances may also have independent roles as neurotransmitters and/or hormones.     

Immunolocalization of cathepsin D in the human central nervous system and central nervous system neoplasms

The cellular distribution of the lysosomal proteinase cathepsin D was studied in a series of 76 neoplasms and 18 non-neoplastic tissues from the human central nervous system, using a well-characterized polyclonal antibody in a peroxidase-antiperoxidase technique. In the normal and developing brain, cathepsin D is confined to neurons and choroid plexus epithelium. Strong granular cytoplasmic staining was present in neuronal and choroid plexus neoplasms, and in reactive macrophages. A large variety of other neoplasms also exhibited positive cytoplasmic staining, albeit usually of a weaker diffuse type. Cathepsin D cannot be considered a specific marker for neuronal or choroid plexus neoplasms, but the antiserum used in this study may be of value in antibody panels for the investigation of these tumours. Its localization may also be of value in embryological studies, particularly in the cerebellum, and in investigations of steroid hormone receptor-associated proteins in meningiomas and Schwannomas.     

Introduction: ecology and the central nervous system

Behavioral ecology, the study of the survival value or function of behavior, has developed for a time by confining cognition to convenient black boxes that were assumed to be rigged by natural selection to direct an animal to the right decision for a given set of circumstances. However, the interpretation of test results concerning functional hypotheses about behavior depends crucially on assumptions made about their ability to collect and process information: cognition. Clearly, progress in behavioral ecology requires that the cognitive black boxes be opened and studied. This need coincides with an explosive growth of interest in animal cognition that has promoted and enhanced the level of interaction between behavioral ecologists and animal cognition scientists. The result promises to be profitable to the extent that it will raise interest and research in a number of new areas such as the costs in terms of survival value of evolving increased cognitive capacity or even the possibility of exploring brain morphology using a functional approach.     

FosB expression in the central nervous system following isotonic volume expansion in unanesthetized rats

We examined c-Fos and FosB staining in the central nervous system 8 and 24 h following acute volume expansion in unanesthetized rats. Male rats were instrumented with a femoral artery catheter for measurement of blood pressure and heart rate (HR), a jugular venous catheter for measurement of central venous pressure (CVP), and a femoral vein catheter for i.v. infusion. After 48 h, rats were volume expanded with isotonic saline (10% of body weight for 10 min i.v.) or given a control infusion (0.01 ml/min for 10 min i.v.). After a period of 8 or 24 h, the rats were deeply anesthetized and perfused transcardially with 4% paraformaldehyde. Separate sets of serial sections of the hypothalamus were processed for either FosB (Santa Cruz) or c-Fos (Oncogene AB-5) immunocytochemistry. The volume expansion protocol significantly increased central venous pressure but did not affect blood pressure or heart rate. Volume expansion produced a significant increase in FosB-positive cells in the paraventricular nucleus (PVN) of the hypothalamus, the supraoptic nucleus (SON), the perinuclear zone (PNZ) of the supraoptic nucleus, the nucleus of the solitary tract (NST), and the caudal ventrolateral medulla (CVL) in both the 8- and 24-h groups. In the area postrema (AP), the number of FosB-positive cells was significantly increased only at 8 h post-infusion. However, c-Fos was not significantly increased above control levels at either time point. The results demonstrate that FosB activation is maintained for at least 24 h following an acute increase in central venous pressure.     

Lactoferrin in the central nervous system

Lactoferrin (LF) is a protein secreted by the tissues of ectodermal origin. Its structure is similar to transferrin. LF appeared to be multifunctional, but its main functions are connected with the natural defense system of mammals. The biological role and origin of LF within brain in normal and disease processes are as yet uncharted. LF expression is greatly upregulated during neurodegenerative disorders and in elderly brains. LF may exert an antiinflammatory function via its inhibitory effect on hydroxyl radical formation. By antioxydative properties, LF prevents DNA damage and consequently tumor formation in the CNS. Moreover, LF specifically transactivates the p53 tumor suppressor gene. LF suppresses distress perception via opioid mediated mechanism and prevents a decrease of the immune system activity caused by psychosocial stress. Furthermore, LF possibly modulates behavior in man and in animals.     

HIV and the central nervous system

Central nervous system complications are common in HIV-1 infected patients and occur either as a result of concomitant immunosuppression (opportunistic infections, lymphoma and tumors), as a primary manifestation of HIV infection, or as an adverse effect of therapy (immune restoration and toxicity). These complications contribute largely to patient morbidity and mortality. In the era of highly active antiretroviral therapy (HAART) these disease states have changed in presentation, outcome and incidence. We review in detail the epidemiology, pathogenesis, clinical features, diagnosis, and management of these disorders.