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Contemporary aspects of cerebrospinal fluid analysis are discussed, including the relationship to neuro-infective, autoimmune and other neurological diseases. The actual state of cerebrospinal fluid microbiological and cytological investigation and analysis of cerebrospinal fluid protein fractions are described in detail.
Cerebrospinal fluid from 100 patients with clinically diagnosed meningitis was examined for alpha-interferon. In the laboratory four patient groups were identified: bacterial meningitis (n = 12), viral meningitis (n = 15), normal cerebrospinal fluid (n = 57) and abnormal cerebrospinal fluid (n = 16). A further 14 patients with cerebrospinal fluid shunts but no abnormality in the cerebrospinal fluid provided a control group for alpha-interferon determinations. The group with viral meningitis and the group with abnormal cerebrospinal fluid had significantly higher alpha-interferon concentrations (p less than 0.001) when compared with those of the three other groups. This assay had great predictive value in determining those patients with abnormal cerebrospinal fluid who did not have a bacterial cause of meningitis. As the groups with abnormal cerebrospinal fluid and viral meningitis had a similar spread in alpha-interferon values it is likely that both reflect viral infection of the central nervous system.
The diffusion of oxyphenbutazone into synovial and cerebrospinal fluids and synovium and joint cartilage was investigated in 25 patients receiving short-term treatment. In the synovial fluid, the mean oxyphenbutazone concentration, was 57.1 +/- 13.4% of the plasma level, due to its excellent diffusion into the joint cavity. In synovial tissue, the oxyphenbutazone level was higher in patients with severe inflammation than in those with no or little inflammation. Penetration into joint cartilage is less than into synovial tissue. In cerebrospinal fluid the concentration was close to the level of free plasma oxyphenbutazone. The findings show increased diffusion of oxyphenbutazone towards its site of action in inflammation.
The cerebrospinal fluid from five patients with Alzheimer disease and five age-matched controls was fractionated into 7 to 9 fractions utilizing chromatographic techniques. The cerebrospinal fluid from each of the five Alzheimer disease patients contained two fractions (fractions B and C) which were lacking in the cerebrospinal fluid of the five age-matched controls. In addition, when the elution profiles of the Alzheimer disease and control cerebrospinal fluid were compared, fraction A, which was found in every cerebrospinal fluid sample studied, was eluted slightly faster in the Alzheimer disease samples than in the cerebrospinal fluid samples from the age-matched controls. Furthermore, it is believed that fraction A isolated from the control cerebrospinal fluid consists of aggregated immunoglobulin molecules and that fraction A isolated from the Alzheimer disease patients' cerebrospinal fluid might consist of immune complexes. Each of the purified cerebrospinal fluid fractions from both control and Alzheimer disease patients was studied for its ability to inhibit macrophage mediated tumor cytotoxicity as well as activate macrophages to kill tumor cells. Each activate macrophages to kill tumor cells. None of the purified cerebrospinal fluid fractions obtained from the controls could inhibit macrophage mediated tumor cytotoxicity whereas 4 of the 9 purified fractions isolated from the Alzheimer disease patients inhibited macrophage mediated cytotoxicity by more than 50%. When fractions B and C were examined for their ability to either activate macrophages or inhibit macrophage mediated cytotoxicity, it was found that fraction B inhibited macrophage mediated cytotoxicity but was not able to activate macrophages to kill tumor cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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A total of 592 computed tomography examinations of the brain in children were studied from the aspect of age and development. The series was divided into 3 groups with respect to neurologic development: 1) normal without neurologic symptoms, 2) normal or subnormal with neurologic symptoms, and 3) moderately to severely retarded. For evaluation, a method of visual grading was applied for each cerebrospinal fluid space. Concerning the ventricular system, the most significant changes in size with increasing age were noted in the lateral ventricles. There were no significant changes in the third and fourth ventricles. Among the three groups, the enlargement was most prominent in group 3 and less prominent in groups 1 and 2. Concerning the extraventricular spaces, the enlarged bifrontal fluid collection area, the sylvian fissure, the interhemispheric fissure, and the cerebral sulci vanished with increasing age. Similarly to the ventricular system, the enlargement was most prominent in group 3, and less prominent in groups 1 and 2, above the age of 1 year. The relation of these results to age and developmental factors are discussed.
T-lymphocytes in the cerebrospinal fluid of patients with multiple sclerosis are predominantly CD4+ (inducer) as opposed to CD8+ (suppressor/cytotoxic) T cells. The CD4+ lymphocytes can be subdivided into populations that express high densities of the CDw29 (4B4) determinant and have helper inducer function or express high densities of CD45R (2H4) determinant and have suppressor inducer function. In the present study, we characterized the nature of these CD4+ T cells in the cerebrospinal fluid of patients with multiple sclerosis by performing flow cytometric analysis on paired samples of blood and cerebrospinal fluid. There were significantly lower percentages of CD4+2H4+ T cells in the cerebrospinal fluid than in the peripheral blood (p = 0.001, paired t test). In contrast, there were increased percentages of helper inducer (CD4+4B4+) T cells in the cerebrospinal fluid (p = 0.001, paired t test), compared with the peripheral blood. Analysis of subjects with other inflammatory disorders of the central nervous system did not show significant decreases in CD4+2H4+ T cells in cerebrospinal fluid, though in some, decreases were also observed. These results indicate that the CD4+ T cells in the cerebrospinal fluid of patients with multiple sclerosis are predominantly helper inducer, as opposed to suppressor inducer T cells, and that the relative decrease of suppressor inducer cells in the peripheral blood of multiple sclerosis patients is not due to their migration to the cerebrospinal fluid. Furthermore, the increased numbers of helper inducer cells in the cerebrospinal fluid may contribute to local autoimmune processes in the central nervous system compartment of multiple sclerosis patients.
beta-Trace, a 23.5 kDa glycoprotein of unknown biological functions, is present in all body fluids tested. It is found in higher concentration in human seminal fluid and cerebrospinal fluid (CSF) than in serum. A one-step procedure for the isolation of beta-trace from pooled CSF is described, by affinity chromatography using a specific antibody made against beta-trace. Amino terminal sequence analysis yields the sequence A P E A Q V S V Q P N F Q Q D K F L G with no homology to known proteins, indicating that beta-trace is a novel CSF protein.
OBJECTIVE: Persistent cerebrospinal fluid leaks in the human population are rarely found in otherwise healthy individuals, but occur in patients with comorbid illnesses. These leaks are frequently resistant to dural suturing or closure of the defect site with connective tissue, cartilage, or plastic materials. In this study, fibrin sealant (ViGuard Fibrin Sealant was used to adhere muscle grafts to surgically created dural defects to close cerebrospinal fluid leaks in chinchillas. Histologic evaluation of the defect sites were conducted to assess healing and tissue response in the test and control groups. METHOD: In 20 chinchillas, after a skin incision, a 6 mm X 6 mm window was created in the right superior bulla exposing the underlying bony tegmen. Using a microcutting burr, a 3 mm X 3 mm area of tegmen was drilled out and the exposed dura was resected to create a large cerebrospinal fluid (CSF) leak. In the control group (n = 10), a small muscle graft from the surrounding tissue was placed into the defect site. In the test group (n = 10), the muscle graft was glued into the defect with ViGuard Fibrin Sealant. Bulla and skin were then closed. All animals were killed at 3 weeks into the experiment, and tissue was harvested for histologic examination. SETTING: The Department of Otolaryngology, Head and Neck Surgery Research Laboratory. University of Illinois, Chicago. RESULTS: Three weeks after surgery in the test group the tegmen defects were found to be closed by bone or connective tissue or both. Meninges had regrown, and the underlying brain appeared histologically normal. There was no evidence of CSF leak, toxicity, infection or other deleterious tissue reactions. In the control group, again the meningeal and bony tegmen defects were seen to be closed by connective tissue or bone or both. Brain tissues appeared histologically normal. There was no evidence of CSF leak, toxicity, or other deleterious tissue reactions. One animal of the test group died of unknown causes. On autopsy, no signs of meningitis or encephalitis could be detected and the cause of death was unapparent. CONCLUSION: Fibrin Sealant, made from pooled donor blood and treated with viral elimination procedures, was found in combination with muscle grafts to securely close induced CSF leaks in the chinchilla model. Inflammation, infection, or toxic reactions were not observed. We believe that ViGuard Fibrin Sealant has stronger bonding power compared with available autologous fibrin tissue adhesives.
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The localization of a cerebrospinal fluid fistula producing cerebrospinal fluid otorrhea can be very difficult. However, the exact anatomic localization of the bony defect is important when selecting the surgical approach to repair. Case reports of two patients in whom spontaneous cerebrospinal fluid otorrhea occurred following pressure equalization tube placement for middle-ear effusion are presented. Nuclear magnetic imaging supplemented CT scan findings, providing noninvasive localization of the defect. Preoperative impressions were confirmed at surgery. In addition to discussing the use of magnetic resonance imaging in evaluating cerebrospinal fluid otorrhea, the literature will also be reviewed.
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Cerebrospinal rhinorrhoea is potentially serious due to the risk from infection. In patients presenting with a nasal discharge of clear fluid it is important to identify the nature of the fluid. Cerebrospinal fluid is readily identified by the presence of asialo-transferrin (tau protein). A method is presented for the identification of tau protein based upon agarose electrophoresis, followed by transfer onto cellulose nitrate membrane and immunochemical detection of transferrin. The method is reliable, sensitive and simple, and requires only basic electrophoresis apparatus.