脑脊液免疫球蛋白作为神经梅毒诊断和愈后判断指标的研究

目的探讨脑脊液免疫球蛋白对神经梅毒的诊断和愈合判断的价值。方法回顾36例多次住院神经梅毒临床和实验室检查等资料,采用SPSS 17.0进行统计分析。结果36例神经梅毒患者中无症状神经梅毒13例,麻痹性痴呆11例,脑膜血管梅毒5例,脊髓痨5例,脑膜神经梅毒2例。初次检查脑脊液免疫球蛋白(Ig)IgG、白细胞、IgM、IgA和蛋白升高分别为35例(97.2%)、30例(83.3%)、29例(80.6%)、26例(72.2%)、25例(69.4%)。血清甲苯胺红不加热试验(TRUST),脑脊液TRUST、IgA、IgG、IgM、白细胞、蛋白皆较治疗前降低,差异有统计学意义(P<0.05)。结论脑脊液中的免疫球蛋白可以作为神经梅毒的诊断和愈后判断的新指标。     

Presence of aldosterone-like immunoreactivity in cerebrospinal fluid in normotensive subjects.

Accumulating evidence, including a wide distribution of specific receptors for aldosterone in the brain, has revealed a potential role of aldosterone in the central nervous system. However, whether or not aldosterone is present in cerebrospinal fluid remains unclear. We attempted to detect aldosterone in cerebrospinal fluid in 14 normotensive subjects. Cerebrospinal fluid was obtained by lumbar puncture. Aldosterone-like immunoreactivity was detected in cerebrospinal fluid (163 +/- 5 pmol/l, range 139-211 pmol/l) and was found to significantly correlate to both plasma aldosterone (r = 0.70, p less than 0.01) and plasma renin activity (r = 0.68, p less than 0.01). However, no significant relationship was found between aldosterone-like immunoreactivity in cerebrospinal fluid and the level of sodium or potassium in cerebrospinal fluid or mean blood pressure. Although we confirmed the presence of aldosterone-like immunoreactivity in cerebrospinal fluid of normotensive subjects, the physiological role of aldosterone in cerebrospinal fluid has yet to be elucidated. Further study will thus be needed to determine the role of cerebrospinal fluid aldosterone.     

The effect of chronic and acute changes in plasma composition on vasopressin secretion and cerebrospinal fluid in the rat.

The effects of chronic and acute changes in plasma composition on the osmolality and sodium concentration of cerebrospinal fluid and plasma vasopressin (AVP) concentration have been examined. Chronic elevation of plasma osmolality in three strains of genetically AVP-deficient rats (Brattleboro and New Zealand hypertensive and normotensive Brattleboro) was associated with increased cerebrospinal fluid osmolality by comparison with AVP-replete controls (Long Evans and New Zealand genetically hypertensive and normotensive rats). The linear correlation between plasma and cerebrospinal fluid osmolality did not reflect a similar relationship between plasma and cerebrospinal fluid sodium concentration. Hypertensive animals exhibited a threefold higher plasma AVP concentration in association with significantly elevated cerebrospinal fluid osmolality by comparison with normotensive controls. Although ip hypertonic saline injection elicited parallel increases in plasma and cerebrospinal fluid osmolality and sodium concentration in both hypertensive and normotensive rats, only in the normotensives did this result in an increase in plasma AVP concentration. These results indicate that cerebrospinal fluid is subject to modest chronic and acute changes in osmolality and sodium concentration which may contribute to the osmotic control of AVP secretion. The disturbed control of vasopressin secretion in hypertensive rats may in part be related to the abnormal cerebrospinal fluid composition in these animals.     

Apolipoproteins in human cerebrospinal fluid.

The presence of apolipoproteins A-I, E, C-II, and C-III and the absence of apolipoprotein B was demonstrated in human cerebrospinal fluid. The concentration of apolipoproteins was measured by electroimmunoassay. Apolipoproteins E, C-II, and C-III were present in cerebrospinal fluid at 3--5% of their concentration in plasma; the cerebrospinal fluid level of apolipoprotein A-I was 0.4%. Most of the cerebrospinal fluid apolipoproteins were present in the rho less than 1.21 g/ml lipoprotein fraction. The major apolipoporteins of cerebrospinal fluid are E and A-I. The possible mechanism of transfer and the physiological and pathophysiological role of apolipoproteins in cerebrospinal fluid are postulated.     

腰椎穿刺脑脊液置换对动脉瘤性蛛网膜下腔出血患者血管内栓塞术后脑脊液核因子κB和转归的影响

目的 探讨动脉瘤性蛛网膜下腔出血(aneurysmal subarachnoid hemorrhage,aSAH)患者动脉瘤栓塞术后早期脑脊液置换对脑脊液核因子-κB(nuclear factor-κB,NF-κB)水平和临床转归的影响.方法 纳入接受动脉瘤栓塞术的aSAH患者,按治疗方案分为脑脊液置换组与非脑脊液置换组.所有患者均在入院3d内行脑动脉瘤弹簧圈栓塞,脑脊液置换组在弹簧圈栓塞后24 h内进行腰椎穿刺脑脊液置换,隔日1次,每次置换脑脊液20 ～30 ml,鞘内注射地塞米松3 mg.在弹簧圈栓塞治疗后1、7和14d检测脑脊液NF-κB水平.主要转归指标为发病后3个月时改良Rankin量表(modified Rankin Scale,mRS)和格拉斯哥转归量表(Glasgow Outcome Scale,GOS)判定的临床转归,转归良好定义为mRS评分0～2分或GOS评分＞3分.次要转归指标包括严重并发症(脑积水、脑动脉痉挛、脑梗死、再出血)和死亡.结果 共纳入81例接受动脉瘤栓塞术的aSAH患者,其中脑脊液置换组42例,非脑脊液置换组39例.脑脊液置换组基线资料与非脑脊液置换组无显著性差异(P均＞0.05).脑脊液置换组颈强直持续时间显著短于非脑脊液置换组[(11.3±3.2)d对(16.5±3.5)d;t =6.985,P＜0.001].脑脊液置换组和非脑脊液置换组在弹簧圈栓塞治疗后1d、7d和14 d时脑脊液NF-κB水平均呈进行性降低(P均＜0.05),但在各时间点脑脊液置换组脑脊液NF-κB水平均显著低于非脑脊液置换组(P均＜0.01).脑脊液置换组在治疗后3个月时根据mRS评分(92.9％对56.4％;x2=14.446,P＜0.001)和GOS评分(97.6％对76.9％∥=8.004,P=0.005)评价的转归良好率均显著高于非脑脊液置换组,脑血管痉挛发生率显著低于非脑脊液置换组(14.3％对33.3％;x2 =4.086,P=0.043).结论 脑脊液置换治疗可降低接受动脉瘤栓塞术的aSAH患者的脑血管痉挛发生率并改善临床转归,其机制可能与降低脑脊液NF-κB水平有关.     

Zoster encephalitis. Isolation of virus and measurement of varicella-zoster-specific antibodies in cerebrospinal fluid

Varicella-zoster virus (VZV) was isolated on two occasions from the cerebrospinal fluid of an elderly woman with encephalomyelitis complicating thoracic zoster. Antibodies to ZV-induced membrane antigen (FAMA) were present in cerebrospinal fluid in a titer of 1:64; serum antibodies were 64-fold higher. Further evidence for local antibody production was derived from simultaneous measurements of immunoglobulin G and albumin in cerebrospinal fluid and serum and calculation of a cerebrospinal fluid-IgG index.     

结核性脑膜炎脑脊液中糖浓度与临床表现关系的研究

目的探讨脑脊液(CSF)中糖浓度<1.0mmol/L结核性脑膜炎患者的临床特点,治疗和预后。方法回顾分析2001年11月至2006年5月在华中科技大学附属同济医院临床确诊为结核性脑膜炎114例患者的临床资料,按CSF中糖浓度是否低于1.0mmol/L分成两组,并对两组患者的临床症状、体征、CSF各项指标,影像学结果以及预后情况进行分析比较。结果CSF中糖浓度低于1.0mmol/L的结核性脑膜炎患者可能主诉症状持续时间(P=0.007),病情程度,共济失调(P<0.01),意识模糊(P<0.01),人格改变(P=0.014),失禁(P=0.030),小脑性共济失调(P<0.01),Glasgow昏迷等级(P=0.023),新发脑梗死(P<0.01)和1年后的预后不良(P<0.01)较对照组严重。结论结核性脑膜炎CSF中糖浓度低于1.0mmol/L的患者入院病情较重,可能遗留更多的持续性神经功能缺损。     

Pressor response to small elevations of cerebroventricular pressure in conscious rats

Acute relationships between cerebrospinal fluid hydrostatic pressure and arterial pressure were quantified in conscious rats. The rats were catheterized with a left femoral artery catheter, and a double set of catheters was implanted into the third cerebral ventricle. In three groups of rats, artificial cerebrospinal fluid with various sodium concentrations (142, 152, and 162 mM) was infused into the third ventricle for 3 hours at 1.0 microliter/min. Mean arterial pressure (MAP) and third ventricular pressure were monitored simultaneously, and both increased progressively over the 3-hour infusion period; the rate of rise was significantly greater with infusion of the hypertonic solution. There were no significant differences between the rat groups infused with low, normal, or high artificial cerebrospinal fluid sodium in either the slope or the intercept of the regression equation relating cerebrospinal fluid pressure and MAP: a 1 cm H2O rise of cerebrospinal fluid pressure was always associated with nearly a 1 mm Hg rise in MAP. In other rats, changes in both cerebrospinal fluid pressure and MAP were shown to be highly dependent on the rate of ventricular infusion. We conclude that elevations of systemic arterial pressure are associated with only small elevations of cerebrospinal fluid pressure and that physiological changes of cerebrospinal sodium (+/- 10 mM) influence arterial pressure by altering intravascular hydrostatic pressure rather than sodium or osmosensitive receptors in the cerebral ventricles.     

The enzyme-linked immunosorbent assay method for IgG antibody to purified protein derivative in cerebrospinal fluid of patients with tuberculous meningitis

Three patients with culture-proven Mycobacterium tuberculosis meningitis were studied. Analysis of cerebrospinal fluid with an enzyme-linked immunosorbent assay (ELISA) method measuring IgG antibody to purified protein derivative rapidly yielded positive results, whereas results of acid-fast smears were negative and cultures took several weeks before growth appeared. We did serial studies of cerebrospinal fluid and sera from one patient. Initially, greater amounts of IgG antibody to purified protein derivative were present in the cerebrospinal fluid than in the serum. The antibody level in the cerebrospinal fluid paralleled the patient's clinical course, cerebrospinal fluid cell count, protein level, and glucose level. Cerebrospinal fluid samples from 33 hospitalized control patients were negative for antibody to purified protein derivative. The ELISA method measuring IgG antibody to purified protein derivative should be evaluated as a means of early diagnosis and management of patients with suspected tuberculous meningitis.     

Cerebrospinal fluid and human immunodeficiency virus. Findings in healthy, asymptomatic, seropositive men

Involvement of the central nervous system by human immunodeficiency virus is an important cause of morbidity and mortality. We have undertaken a longitudinal study of asymptomatic individuals found to be human immunodeficiency virus seropositive to identify and characterize cerebrospinal fluid abnormalities early in the disease process. Our findings in 25 individuals have been notable for a frequent incidence of cerebrospinal fluid abnormalities. Pleocytosis or elevated cerebrospinal fluid protein was found in 12 (48%) of 15 patients studied. Oligoclonal banding was present in 6 (26%) of 23 patients. Human immunodeficiency virus was isolated by culture in 4 asymptomatic patients. The cerebrospinal fluid abnormalities we observed indicate an active process occurring in the central nervous system, even in early human immunodeficiency virus infection in asymptomatic patients. Serial observation of these patients for development of neuropsychiatric findings may provide answers to the significance of cerebrospinal fluid abnormalities identified in these patients.     

Nephritis associated with a diphtheroid-infected cerebrospinal fluid shunt

Hypocomplementemic proliferative glomerulonephritis occurred during diphtheroid infection of a ventricular decompression shunt for cerebrospinal fluid diversion (cerebrospinal fluid shunt) in a young man. Granular deposits of immunoglobulin M (IgM) and the third component of complement (C₃) were found along the glomerular basement membrane. This report provides supportive evidence for immune complex-mediated glomerular injury due to diphtheroid infection in a cerebrospinal fluid shunt.     

Cerebrospinal fluid flow abnormalities in patients with neoplastic meningitis. An evaluation using 111indium-DTPA ventriculography

Cerebrospinal fluid flow dynamics were evaluated by 111Indium-diethylenetriamine pentaacetic acid (111In-DTPA) ventriculography in 27 patients with neoplastic meningitis. Nineteen patients (70 percent) had evidence of cerebrospinal fluid flow disturbances. These occurred as ventricular outlet obstructions, abnormalities of flow in the spinal canal, or flow distrubances over the cortical convexities. Tumor histology, physical examination, cerebrospinal fluid analysis, myelograms, and computerized axial tomographic scans were not sufficient to predict cerebrospinal fluid flow patterns. These data indicate that cerebrospinal fluid flow abnormalities are common in patients with neoplastic meningitis and that 111In-DTPA cerebrospinal fluid flow imaging is useful in characterizing these abnormalities. This technique provides insight into the distribution of intraventricularly administered chemotherapy and may provide explanations for treatment failure and drug-induced neurotoxicity in patients with neoplastic meningitis.     

Monitoring of neurotransmitter amino acids by means of an indwelling cisterna magna catheter: a comparison of two rodent models of fulminant liver failure.

Alterations of brain and cerebrospinal fluid amino acids have consistently been described in human and experimental fulminant liver failure. To evaluate the significance of such changes in the pathogenesis of hepatic encephalopathy in fulminant liver failure, brain and cerebrospinal fluid amino acids (glutamate, aspartate, GABA, glycine, taurine) were measured at various stages during the development of neurological dysfunction in rats after hepatic devascularization or thioacetamide treatment to induce acute liver failure. To facilitate repetitive removal of cerebrospinal fluid, a technique employing long-term implantation of cisterna magna catheters in conscious, freely moving rats was developed. Brain but not cerebrospinal fluid concentrations of the excitatory amino acids glutamate and aspartate were reduced in both animal models of fulminant liver failure in parallel with deterioration of neurological status. Brain and cerebrospinal fluid GABA levels were not significantly altered. Cerebrospinal fluid glycine levels were increased two to three times in parallel with increasing brain glycine content in the devascularized rat but were unchanged in thioacetamide-induced liver failure, suggesting distinct pathophysiological mechanisms in these two experimental situations. On the other hand, onset of coma in both animal models of fulminant liver failure was accompanied by significantly increased cerebrospinal fluid taurine levels. We suggest that such changes result from taurine release from astrocytes in brain into the extracellular fluid; this is consistent with taurine's role in the regulation of intracellular osmolarity in brain. Sequential measurements of amino acids in the cerebrospinal fluid of small rodents with indwelling cisterna magna catheters adds a useful new approach for exploring the neurobiology of hepatic encephalopathy in fulminant liver failure.     

Cerebrospinal fluid to serum glucose ratios in diabetes mellitus and bacterial meningitis

Although calculation of the cerebrospinal fluid to serum glucose ratio is widely recommended as a way to identify pathologic hypoglycorrhachia, few data are available to document its accuracy. In order to provide a better basis for interpretation of this quotient, simultaneous cerebrospinal fluid and serum glucose concentrations from patients with diabetes mellitus and noninflammatory cerebrospinal fluid and patients with acute bacterial meningitis were compared. Cerebrospinal fluid to serum glucose ratios were significantly lower in the patients with meningitis (Mann-Whitney U Test, p < O.001). A ratio of 0.31 provided the best differentiation between the two groups. Ratios were below this level in 45 of 64 patients with meningitis, including 10 in whom the absolute cerebrospinal fluid glucose concentration was not below 40 mg/dl. In 35 of 36 uninfected diabetic subjects, ratios were 0.31 or greater. In the sole exception, concentrated glucose solution had been given intravenously shortly before lumbar puncture. Use of the cerebrospinal fluid to serum ratio, in addition to the absolute cerebrospinal fluid glucose concentration, increases sensitivity in detecting pathologic hypoglycorrhachia with little loss in specificity.     

Detection of granulocyte-macrophage colony-stimulating factor in cerebrospinal fluid of patients with aseptic meningitis

The level of granulocyte-macrophage colony-stimulating factor (GM-CSF) in the cerebrospinal fluid from 14 infants and children with meningitis and 6 patients who suffered other diseases besides meningitis was measured by our sensitive enzyme linked immunosorbent assay for GM-CSF. The minimal detection level of GM-CSF was 40 pg/ml. Six of 9 patients (67%) with aseptic meningitis had detectable GM-CSF in cerebrospinal fluid and the concentrations of GM-CSF ranged from 49 to 114 pg/ml (mean 72 pg/ml), whereas none of 5 patients with bacterial meningitis or 6 patients with other diseases besides meningitis had detectable GM-CSF levels. There was no clear correlation between the GM-CSF levels in cerebrospinal fluid and the leukocyte count in either peripheral blood or cerebrospinal fluid, or the concentration of protein or glucose in cerebrospinal fluid.     

Efficacy and frequency of cerebrospinal fluid drainage in operative management of thoracoabdominal aortic aneurysms

BACKGROUND: Paraplegia remains the most dreaded complication following thoracoabdominal aortic repair. We investigated the efficacy of cerebrospinal fluid drainage as a spinal cord-protecting modality. We also evaluated the correlation between the frequency of cerebrospinal fluid drainage and the Crawford classification. METHODS: Spinal cord function was monitored during 20 open surgical procedures (group I) and 27 stent-graft implantations (group II). Evoked potentials and intracranial pressure were monitored in each operation. If intracranial pressure exceeded 15 mmHg, cerebrospinal fluid was drained. RESULTS: Cerebrospinal fluid drainage was necessary in 75 % of patients in group I (Crawford type I: 33 %, type II: 40 %, type III: 20 %, type IV: 7 %) and in 22 % of patients in group II (Crawford type I: 33 %, type II: 66 %). Evoked potential alterations correlated with an increase in intracranial pressure. Timely cerebrospinal fluid drainage reversed these changes in 72 %. Three patients remained paraplegic. CONCLUSION: Cerebrospinal fluid drainage is a valuable neuroprotective interventional tool to lower the risk of spinal cord ischemia. The combination of neurophysiological monitoring and cerebrospinal fluid drainage optimizes the prevention of paraplegia during aortic repair.     

Immunoreactive ACTH in the cerebrospinal fluid of the rat: decrease after mediobasal hypothalamic lesion and hypophysectomy, increase after adrenalectomy.

The effect of various anaesthetics and of the manipulations of the hypothalamo-pituitary-adrenocortical system (hypophysectomy, adrenalectomy and lesion of the mediobasal hypothalamus) was studied on immunoreactive-ACTH levels in the plasma and in the cerebrospinal fluid in the rat. The anaesthetics used (Hypnorm, pentobarbital, urethan and Ketanest) were without effect on immunoreactive-ACTH concentration in the cerebrospinal fluid. Immunoreactive-ACTH was significantly decreased after hypophysectomy and elevated after adrenalectomy in both cerebrospinal fluid and plasma. Destruction of the mediobasal hypothalamus resulted in reduced immunoreactive-ACTH content in the cerebrospinal fluid (about 20% of control) in both experiments, whereas immunoreactive-ACTH levels in the plasma of the lesioned rats were lower only in one of the two experiments performed. These data suggest that the main source of the immunoreactive-ACTH in the cerebrospinal fluid of the rat is the hypothalamus; the contribution of the pituitary gland being less than 50% of the radioimmunoassayable ACTH.     

Anticardiolipin antibodies and interleukin-6 in cerebrospinal fluid and blood of Chinese patients with neuro-Beh?et's syndrome.

Anticardiolipin antibodies of the IgG, IgM and IgA isotypes and soluble IL-6 were measured in paired serum and cerebrospinal fluid samples from five patients with neuro-Beh?et's syndrome. Another five patients with non-inflammatory neurological diseases were also studied as a control group. Anticardiolipin antibodies, especially the IgM isotype, and IL-6 were highly elevated in the cerebrospinal fluid of patients with neuro-Beh?et's. Levels of both IgM isotype anticardiolipin antibodies and IL-6 in the cerebrospinal fluid dropped after disease activity subsided. These results suggest that the increase in IgM isotype anticardiolipin antibodies and IL-6 in cerebrospinal fluid may be involved in the immune response of neuro-Beh?et's within the central nervous system. Serial measurements of IgM isotype anticardiolipin antibodies and IL-6 in the cerebrospinal fluid may be useful in evaluating disease activity in neuro-Beh?et's.     

手足口病合并病毒性脑炎患儿脑脊液和血清NSE测定及意义

目的探讨手足口病（HFMD）合并病毒性脑炎（VE）患儿脑脊液和血清神经元特异性烯醇化酶（NSE）含量变化的临床意义。方法采用酶联免疫吸附试验双抗体夹心法对32例HFMD合并VE、30例单纯HFMD和26例非神经系统疾病患儿的脑脊液和血清NSE进行测定,比较各组NSE水平及惊厥/抽搐组与无惊厥/抽搐组、嗜睡/昏睡组与无意识障碍组脑脊液和血清NSE水平的差异。结果与对照组相比,HFMD合并VE组脑脊液和血清NSE水平均有统计学差异（P〈0.05）,单纯HFMD组脑脊液和血清NSE水平无统计学差异（P〉0.05）;HFMD合并VE患儿惊厥/抽搐组脑脊液和血清NSE水平高于无惊厥/抽搐组,意识障碍组脑脊液和血清NSE水平高于无意识障碍组（P均〈0.01）;患儿脑脊液和血清NSE含量呈正相关（r=0.87,P〈0.01）。结论 HFMD合并VE患儿脑脊液和血清NSE水平与疾病的严重程度相关,检测HFMD患儿脑脊液及血清NSE水平的变化有助于判定脑组织受损的严重程度及评估预后。     

Management of neurosyphilis: time for a new approach?

Given the long term sequelae of untreated neurosyphilis and insensitive tests to detect treponemes in the cerebrospinal fluid, questions regarding the utility of a lumbar puncture and cerebrospinal fluid analysis either to confirm or exclude neurosyphilis are raised.