Binswanger病脑血流及红细胞变形性的研究

本文测定了Ｂｉｎｓｗａｎｇｅｒ病患者和相应对照组的局部大脑血流量及红细胞滤过指数的变化。结果发现，疾病组双侧大脑皮质及白质血流值间均无明显差异，大脑白质血流明显低于健康对照组和各病例对照组，疾病组红细胞滤过指数明显高于各对照组、提示Ｂｉｎｓｗａｎｇｅｒ病患者存在红细胞变形能力低下，检测脑血流对于鉴别不同类型的大脑白质疏松症具有一定的参考价值。     

Binswanger病血液流变学及血液成份的观察

本文测定了３５例老年Ｂｉｎｓｗａｎｇｅｒ病患者的部分血液流变学及血液成份的变化。结果发现，与健康对照组和脑动脉硬化组比较，疾病组高切变率全血粘度显著升高，红细胞变形能力明显降低，血液成份ＨＧ、ＭＣＶ、ＭＣＨ、ＭＣＨＣ、ＲＤＷ显著增加。提示红细胞的老化性改变参与了Ｂｉｎｓｗａｎｇｅｒ病的发生，设法提高患者红细胞变形能力和降低血粘度将有益于阻止该病的进展。     

Binswanger病患者载脂蛋白多态性的初步研究

探讨Ｂｉｎｓｗａｎｇｅｒ病患者核心家庭成员的载脂蛋白（ａ）和载脂蛋白Ｅ多态性分布和等位基因频率。方法：疾病组患者３５例,配偶组３３例,子女组３１例,对照组６３例。采用免疫印迹技术检测ａｐｏ（ａ）和ａｐｏＥ多态性分布,并推算等位基因频率。     

Binswanger脑病动态血压及动态心电图观察

采用动态检测技术观察３１例Ｂｉｎｓｗａｎｇｅｒ脑病和对照组３１例健康人血压和心率的变异性。结果显示，患者均存在动态血压异常，其中平均收缩压、平均舒张压超过正常值者２７例（８７％），夜间基底血压异常升高２２例（７１％），血压异常波动２０例（６４％），昼夜节律逆转４例（１３％）。患者２４小时内５ｍｉｎ节段正常心动周期的标准差明显低于对照组，患者的收缩压与心率间无显著相关性。提示血压波动及持续的夜间升压现象在Ｂｉｎｓｗａｎｇｅｒ脑病中起着一定作用，而这种异常可能与患者存在植物神经系统功能失调有关。     

Binswanger病的临床与MRI

近年来，随着ＣＴ和ＭＲＩ检查手段的问世，尤其是ＭＲＩ在临床上的广泛应用，Ｂｉｎｓｗａｎｇｅｒ病的诊断率明显提高。我院１９９５年～１９９７年４月收治６８例Ｂｉｎｓｗａｎｇｅｒ病患者，现报告如下。１临床资料１．１一般资料本组男６２例，女６例，年龄６０～９...     

临床神经病学杂志2002年第15卷文题索引

(按汉语拼音字母顺序排列 )ＡＡｌｚｈｅｉｍｅｒ病　Ａｌｚｈｅｉｍｅｒ病患者脑脊液Ｔａｕ蛋白水平的检测及其临床意义　 (王　琳等 ) 3 5 2　Ａｌｚｈｅｉｍｅｒ病患者血清和脑脊液中ＩＬ 6及ｓＩＬ 6Ｒ水平的研究　 (吴崇巍等 ) 163阿司匹林　阿司匹林对大鼠局灶性脑缺血再灌注损伤中血ＮＯ、ＥＴ、ＴＮＦ含量的影响　 (周庆博等 ) 3 2 6Ｂβ淀粉样蛋白　β淀粉样蛋白对大鼠额叶和海马细胞外液单胺类递质的影响　 (刘春风等 ) 2 60Ｂｉｎｓｗａｎｇｅｒ病　Ｂｉｎｓｗａｎｇｅｒ病的诊断　 (郭洪志等 ) 3 77巴曲酶　巴曲酶对ＮＪＳ小鼠…     

Binswanger氏病临床与CT,MR分析

Ｂｉｎｓｗａｎｇｅｒ氏病临床与ＣＴ、ＭＲ分析吴跃，杨秀卿Ｂｉｎｓｗａｎｇｅｒ氏病（ＢＤ）又称皮质下动脉硬化性脑病。现将我院１９８９～１９９２年６月共收治的１２例病人临床表现和ＣＴ、ＭＲ资料报告如下：临床资料一、一般资料本组１２例中，男８例，女４例。４...     

Binswanger＇s病若干临床问题探讨

回顾１９８９～１９９３年住院的２６例Ｂｉｎｓｗａｎｇｅｒ＇ｓ病，复习文献，对其临床表现。诊断及鉴别诊断进行探讨．对ＣＴ和ＭＲＩ在Ｂｉｎｓｗａｎｇｅｒ＇ｓ病的诊断价值进行讨论。     

中风与神经疾病杂志1996年第13卷文题索引

中风与神经疾病杂志１９９６年第１３卷文题索引（按汉语拼音字母顺序排列）ＡＡｌｚｈｅｉｍｅｒ病实验性Ａｌｚｈｅｉｍｅｒ模型鼠脑组织５－羟色胺含量改变的研究（３）：１５０ＢＢｉｎｓｗａｎｇｅｒ病Ｂｉｎｓｗｉｎｇｅｒ病临床研究（４）：２３０Ｃ迟发性神经元坏...     

Binswangere脑病动态血压及动态心电图观察

采用动态检测技术观察３１例Ｂｉｎｓｗａｎｇｅｒ脑病和对照组３１例健康人血压和心率的变异性。     

Increased plasma homocysteine levels without signs of vitamin B12 deficiency in patients with multiple sclerosis assessed by blood and cerebrospinal fluid homocysteine and methylmalonic acid

OBJECTIVE: The aim of this study was to evaluate if multiple sclerosis (MS) is associated with vitamin B12 (cobalamin) deficiency. METHODS: We measured serum vitamin B12, plasma folate, serum methylmalonic acid (MMA), plasma homocysteine (tHcy) and also cerebrospinal fluid (CSF) MMA and tHcy in 72 patients with MS and 23 controls. RESULTS: The mean plasma tHcy level was significantly increased in MS patients (11.6 micromol/L) compared with controls (7.4 micromol/L) (P = 0.002). Seven patients showed low serum vitamin B12 levels but only one of them had concomitant high plasma tHcy. None of them showed high serum MMA. Plasma or blood folate levels did not differ between MS patients and controls. We found no significant differences in mean values or frequency of pathological tests of serum B12, serum MMA, mean corpuscular volume (MCV), haemoglobin concentration, CSF tHcy or CSF MMA between patients and healthy subjects. There were no correlations between CSF and serum/plasma levels of MMA or tHcy. Serum vitamin B12, serum MMA, plasma tHcy, CSF Hcy or CSF MMA were not correlated to disability status, activity of disease, duration of disease or age. CONCLUSIONS: The relevance of the increased mean value of plasma tHcy thus seems uncertain and does not indicate functional vitamin B12 deficiency. We can not, however, exclude the possibility of a genetically induced dysfunction of the homocysteine metabolism relevant for the development of neuroinflammation/degeneration. Our findings indicate that, regardless of a significant increase in plasma tHcy in MS patients, the MS disease is not generally associated with vitamin B12 deficiency since we did not find any other factors indicating vitamin B12 deficiency. Analysis of CSF MMA and CSF tHcy, which probably reflects the brain vitamin B12 status better than serum, are not warranted in MS. We conclude that B12 deficiency, in general, is not associated with MS.     

Cerebrospinal fluid C3 and C4 indexes in immunological disorders of the central nervous system

OBJECTIVES: Validation of cerebrospinal fluid (CSF) indexes as a measure for intrathecal C3 and C4 production. Examination of their role in differential diagnosis of immunological disorders of the central nervous system (CNS). MATERIAL AND METHODS: Correlative study in controls (low back pain without disk herniation) between the CSF/serum ratio (Q) for albumin, and Q C3 and Q C4. Comparative study of C3 and C4 indexes in patients with CNS dysfunction due to relapsing-remitting (RR) multiple sclerosis (MS), secondary progressive (SP) MS, systemic lupus erythematosus (SLE), and human immunodeficiency virus (HIV) infection. RESULTS: Strong and statistically highly significant correlations between Q albumin and Q C3 (r=0.89, P=0.0001), and Q C4 (r=0.68, P= 0.0001). In MS patients decreased mean values for serum (RR, SP) and CSF (RR) C3, and increased C3 index mean value (RR, SP). In CNS SLE increase of mean C3 and C4 index values. In CNS HIV increase of mean C3 and C4 index values, and CSF C3 and C4 concentrations. Most individual index values were within the reference range. CONCLUSION: CSF index is a valid tool to detect intrathecal C3 or C4 production. C3 or C4 index contributes little to the differential diagnosis of immunological CNS disorders. C3 might play a pathogenic role in various immunological CNS disorders.     

Serum and CSF PDGF‐AA and FGF‐2 in relapsing‐remitting multiple sclerosis: a case–control study

Background and purpose: Fibroblast growth factor‐2 (FGF‐2) and platelet‐derived growth factor‐A (PDGF‐AA) are potent modulators of oligodendrocytes, the main responsible cells for myelin regeneration. We measured FGF‐2 and PDGF‐AA in the sera and cerebrospinal fluid (CSF) of patients with relapsing‐remitting multiple sclerosis (RR‐MS) and compared these values with control subjects. Methods: Twenty‐three patients with RR‐MS and 23 subjects without inflammatory and demyelinating diseases were included. Serum samples of the patients were collected in both relapse and remission phases and were analyzed with ELISA method. CSF was drawn during the relapse period. Blood and CSF were drawn from control subjects for comparison. Wilcoxon and Mann–Whitney U‐test and Spearman’s rank correlation were used for analysis. P values of <0.05 were considered significant. Results: Age and sex distribution were similar in both groups. Serum values of FGF‐2 were higher in relapse phase compared with remission phase, with a trend toward significance (P = 0.052). CSF PDGF‐AA showed significant negative correlation with disease duration (correlation coefficient = ?0.58, P = 0.004). Serum levels of PDGF did not differ between two phases significantly. There was no difference in serum and CSF values of these factors between patients and controls. When we compared patients with prolonged disease with controls, a significant difference between the CSF levels of PDGF‐AA was observed (mean ± SEM 2.78 ± 0.8 in controls vs. 0.55 ± 0.29 in patients with MS ≥ 2 years, P < 0.05). Conclusion: Our study was the first to show that CSF PDGF‐AA is related to disease duration. Supporting previous findings we showed that serum and CSF levels of these factors are weak indicators of disease severity.     

Cerebrospinal fluid Flt3 ligand level in patients with amyotrophic lateral sclerosis

OBJECTIVES: The Flt3 ligand (FL) is a cytokine with a neurotrophic and antiapoptotic activity in the central nervous system that induces the survival of neurons. The aim of the study was to measure levels of FL in amyotrophic lateral sclerosis (ALS) patients. MATERIALS AND METHODS: The study involved 23 ALS patients and 23 people in the control group. The measurement of FL in the cerebrospinal fluid (CSF) and serum was performed by the enzyme-linked immunosorbent method. RESULTS: Results showed that CSF FL levels were significantly increased in ALS patients compared with the controls (P < 0.05) but the serum levels of this cytokine did not differ from the controls (P > 0.05). There was no significant correlation between CSF and serum FL levels and clinical parameters of ALS (P > 0.05). The difference in CSF/serum ratio of FL between ALS patients and controls was not statistically significant (P > 0.05). CONCLUSION: An increase in CSF FL levels in ALS patients, observed in this study, could be a compensative response for neurodegeneration but may also reflect increased diffusion of this cytokine into the central nervous system caused by blood-CSF barrier dysfunction.     

Postmortem Brain,Cerebrospinal Fluid,and Blood Neurotrophic Factor Levels in Alzheimer’s Disease: A Systematic Review and Meta-Analysis

Accumulating evidence suggest that aberrations of neurotrophic factors are involved in the etiology and pathogenesis of Alzheimer’s disease (AD), but clinical data were inconsistent. Therefore, a meta-analysis on neurotrophic factor levels in AD is necessary. We performed a systematic review of blood, CSF, and post-mortem brain neurotrophic factor levels in patients with AD compared with controls and quantitatively summarized the clinical data in blood and CSF with a meta-analytical technique. A systematic search of PubMed and Web of Science identified 98 articles in this study (with samples more than 9000). Random effects meta-analysis demonstrated that peripheral blood BDNF levels were significantly decreased in AD patients compared with controls. However, blood NGF, IGF, and VEGF did not show significant differences between cases and controls. In CSF, random effects meta-analysis showed significantly deceased BDNF and increased NGF levels in patients with AD, whereas IGF and VEGF did not show significant differences between the AD group and control group. In addition, 23 post-mortem studies were included in the systematic review. Although data from post-mortem brains were not always consistent across studies, most studies suggested decreased BDNF and increased (pro)NGF levels in hippocampus and neocortex of patients with AD. These results provide strong clinical evidence that AD is accompanied by an aberrant neurotrophin profile, and future investigations into neurotrophins as biomarkers (especially CSF BDNF and NGF) and therapeutic targets for AD may be warranted.     

Monocyte and microglial activation in patients with mood-stabilized bipolar disorder

Background

Bipolar disorder is associated with medical comorbidities that have been linked to systemic inflammatory mechanisms. There is, however, limited evidence supporting a role of neuroinflammation in bipolar disorder. Here we tested whether microglial activation and associated tissue remodelling processes are related to bipolar disorder by analyzing markers in cerebrospinal fluid (CSF) and serum from patients and healthy controls.

Methods

Serum was sampled from euthymic patients with bipolar disorder and healthy controls, and CSF was sampled from a large subset of these individuals. The levels of monocyte chemoattractant protein-1 (MCP-1), YKL-40, soluble cluster of differentiation 14 (sCD14), tissue inhibitor of metalloproteinases-1 (TIMP-1) and tissue inhibitor of metalloproteinases-2 (TIMP-2), were measured, and we adjusted comparisons between patients and controls for confounding factors.

Results

We obtained serum samples from 221 patients and 112 controls and CSF samples from 125 patients and 87 controls. We found increased CSF levels of MCP-1 and YKL-40 and increased serum levels of sCD14 and YKL-40 in patients compared with controls; these differences remained after controlling for confounding factors, such as age, sex, smoking, blood–CSF barrier function, acute-phase proteins and body mass index. The CSF levels of MCP-1 and YKL-40 correlated with the serum levels, whereas the differences between patients and controls in CSF levels of MCP-1 and YKL-40 were independent of serum levels.

Limitations

The cross-sectional study design precludes conclusions about causality.

Conclusion

Our results suggest that both neuroinflammatory and systemic inflammatory processes are involved in the pathophysiology of bipolar disorder. Importantly, markers of immunological processes in the brain were independent of peripheral immunological activity.     

CSF and plasma GABA levels in Parkinson's disease

CSF gamma-aminobutyric acid (GABA) levels were reduced in patients with idiopathic Parkinson's disease when compared with age matched controls, but the difference was not significant. However, when the Parkinsonian patients were subdivided, CSF GABA levels were lower in the levodopa treated group than in the untreated group and the controls. There was no difference in plasma GABA levels between Parkinsonian patients and controls.     

High cerebrospinal fluid concentration of glial fibrillary acidic protein (GFAP) in patients with normal pressure hydrocephalus

The concentration of glial fibrillary acidic protein (GFAP) in lumbar cerebrospinal fluid (CSF) was measured in 12 patients with normal pressure hydrocephalus (NPH) 11 patients with primary degenerative dementia (PDD), 8 patients with various other neurological diseases, and 18 patients without signs of organic nervous disease (controls).

Mean CSF GFAP concentration was significantly higher in NPH patients: 96 ± 23 ng/ml (SEM) when compared with PDD patients: 8.2 ± 1.9 ng/ml (P < 0.01), or with controls: 4.3 ± 0.7 ng/ml (P < 0.01). Only 2 NPH patients had a GFAP concentration within the range of the control group (2–14 ng GFAP/ml CSF). No significant differences were found between the PDD patients and the control group, or between the group of patients with other neurological diseases and the control group.

In addition, a rostro-caudal gradient of GFAP in CSF could be demonstrated. In 6 NPH and 2 PDD patients both ventricular and lumbar CSF samples were investigated. In all cases the ventricular GFAP concentration was higher than the lumbar concentration. The difference was statistically significant (P < 0.01).

Our results suggest that determination of CSF GFAP concentration might be of diagnostic value in discrimination between NPH patients and patients with enlarged ventricles associated with degenerative brain disease.     

Elevated levels of interleukin-12 and interferon-gamma in patients with human T lymphotropic virus type I-associated myelopathy

The levels of interleukin-12 (IL-12) (p70 heterodimer), total IL-12 (p70 heterodimer plus p40 chains), interferon-gamma (IFN-gamma) as Th1 cytokine, and those of interleukin-4 (IL-4) and interleukin-10 (IL-10) as Th2 cytokines in sera and cerebrospinal fluid (CSF) from 22 patients with human T lymphotropic virus type I (HTLV-I)-associated myelopathy (HAM) were compared with those of 22 patients with other neurological diseases (OND), including nine anti-HTLV-I-seropositive carriers. Both serum IL-12 (total and p70 heterodimer) and CSF IFN-gamma, measured by the enzyme-linked immunosorbent assay (ELISA), were significantly elevated in patients with HAM as compared to the patients with OND, including the anti-HTLV-I-seropositive carriers. Serum IFN-gamma also was significantly elevated in the HAM patients as compared to the controls. There was no significant difference in the CSF levels of IL-12 (total and p70 heterodimer) between the HAM patients and controls, whereas, for the Th2 cytokines IL-4 was detected in the CSF of four anti-HTLV-I-seropositive carriers of the 13 control patients but not in any of the patients with HAM. No significant difference was found in the serum levels of IL-4 and IL-10, nor in the CSF levels of IL-10 in the patients with HAM and in the controls. These findings indicate that in patients with HAM, the immunological balance of helper T lymphocytes between Th1 and Th2 is toward Th1 in the periphery and that Th1-mediated immunological status in the central nervous system is involved in the pathogenesis of HAM.