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PubMed1977

[Normal range of free amino acids in cerebrospinal fluid of children (author's transl)].

UNLABELLED: Free amino acids were determined quantitatively in cerebrospinal fluid of 80 boys and 69 girls (ages 1 month-14years). On the basis of the cliniclal criterions these children were considered to be ""healthy''. The total number of examined children was 2000. Cerebrospinal fluid was mixed with an equal volume of 5% sulphosalicylic acid and the amino acids were separated by ion exchange column chromatography. RESULTS: 1. The sexspecific investigation of the 1 month -2 years old children showed that the boys had a statistical significant hgher concentration of lysine and that no statistical significant differences existed between the groups of 2-14 years old children. 2. The age specific comparison revealed that the amino acid concentrations ofaspartic acid, citrulline, histidine, lysine, serine, threonine and tyrosine were in the cerebrospinal fluid of the younger boys statistical significant higher as compared to the older boys and that the concentration of serine in the cerebrospinal fluid of the younger girls was statistical significant higher than in the group of older girls.

Adolescent↗
PubMed2001

Increased HTLV-I proviral load and preferential expansion of HTLV-I Tax-specific CD8+ T cells in cerebrospinal fluid from patients with HAM/TSP.

To date, high human T-cell lymphotropic virus type I proviral load in patients with human T-cell lymphotropic virus type I-associated myelopathy/tropical spastic paraparesis has been reported and is thought to be related to the pathogenesis of human T-cell lymphotropic virus type I-associated myelopathy/tropical spastic paraparesis. However, the proviral load in cerebrospinal fluid has not been well investigated. We measured human T-cell lymphotropic virus type I proviral load in cerebrospinal fluid cells from human T-cell lymphotropic virus type I-associated myelopathy/tropical spastic paraparesis patients using real-time quantitative polymerase chain reaction (TaqMan). Human T-cell lymphotropic virus type I proviral load in cerebrospinal fluid cells were significantly higher than that of the matched peripheral blood mononuclear cells, and a high ratio of human T-cell lymphotropic virus type I proviral load in cerebrospinal fluid cells to peripheral blood mononuclear cells were observed in patients with short duration of illness. Human T-cell lymphotropic virus type I Tax-specific CD8+ T cells, as detected by peptide-loaded HLA tetramers, accumulated in cerebrospinal fluid compared with that in peripheral blood mononuclear cells, while the frequency of cytomegalovirus-specific CD8+ T cells in cerebrospinal fluid was reduced. These observations suggest that accumulation of both human T-cell lymphotropic virus type I-infected cells and preferential expansion of human T-cell lymphotropic virus type I-specific CD8+ cells in cerebrospinal fluid may play a role in the pathogenesis of human T-cell lymphotropic virus type I-associated myelopathy/tropical spastic paraparesis.

Adolescent↗
PubMed1991

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.

Child↗
PubMed1998

Detection of a gliotoxic activity in the cerebrospinal fluid from multiple sclerosis patients.

We recently showed that peripheral blood cell supernatants from multiple sclerosis (MS) patients, containing reverse transcriptase activity and retroviral RNA from the newly human identified multiple sclerosis retrovirus (MSRV), also secrete a cytotoxin which induces death of primary mouse cortical glial cells. We have hypothesized that macrophages could release this cytotoxin in the cerebrospinal fluid. The cerebrospinal fluid cytotoxicity from 166 patients with various neurological diseases (including MS patients) was tested on glial cells in vitro. Our bioassay shows that a glial cytotoxic activity is significantly present in cerebrospinal fluid from patients with relapsing-remitting MS at relapse. Since this cytotoxic activity seems to correlate with active cases of MS, it may represent a critical pathogenic factor in the neuropathology of MS.

Adult↗
PubMed1983

Detection of fungi in cerebrospinal fluid.

With the exception of Cryptococcus neoformans, fungi are rarely detected in cerebrospinal fluid obtained from patients having or suspected of having fungal meningitis. A review of the literature reveals that several fungi have been either isolated, observed, or both in cerebrospinal fluid specimens. These fungi include Acremonium species, Aspergillus amstelodami, A. flavus, A. fumigatus, A. oryzae, A. terreus, Blastomyces dermatitidis, Candida albicans, C. tropicalis, C. viswanathii, Coccidioides immitis, Cryptococcus albidus, C. neoformans, Histoplasma capsulatum, Paecilomyces variotii, Paracoccidioides brasiliensis, Pseudallescheria boydii, Schizophyllum species, and Sporothrix schenckii. Laboratory findings for cerebrospinal fluid specimens obtained from such patients and clinical presentations are summarized.

Aspergillus↗
PubMed1993

Oligoclonal IgG in cerebrospinal fluid detected by isoelectric focusing using PhastSystem.

Identification of oligoclonal immunoglobulin G (IgG) in cerebrospinal fluid (CSF) is one of the major laboratory signs in multiple sclerosis (MS). Oligoclonal IgG can also be seen in other immunostimulating central nervous system diseases, e.g. meningitis caused by Borrelia spirochetes. A convenient isoelectric focusing (IEF) method combined with polyethyleneglycol-enhanced (PEG) immunofixation and silverstaining using PhastSystem for detection of oligoclonal IgG bands in serum and unconcentrated spinal fluid was developed. Serum and cerebrospinal fluid samples earlier investigated using agarose IEF combined with immunoblotting and avidin-biotin amplified double-antibody peroxidase staining (= A-IEF) were blindly re-analysed using PhastGel IEF 3-9 modified with addition of Pharmalyte 8-10.5 followed by immunofixation and silver staining (= PhastIEF). PhastSystem IEF using PhastGel had the same capability to separate and visualize oligoclonal IgG bands as the conventional agarose IEF. However, PhastIEF was more convenient and less time-consuming than A-IEF. PhastIEF combined with immunofixation and silver staining using application of standardized amounts of IgG for both the serum and CSF samples (40-60 ng IgG/lane is fast, well-standardized and reproducible. The method is sensitive and uses only a minute volume of unconcentrated cerebrospinal fluid for the investigation of CSF IgG pattern.

Cost-Benefit Analysis↗
PubMed1984

Cerebrospinal fluid enolase in stroke.

This study relates the level of alpha and gamma enolase in cerebrospinal fluid sampled within 4 days of a stroke to the volume of the cerebral infarct measured on the CT image and to the clinical outcome of the patient. Twenty-eight patients were studied, two with transient ischaemic attacks and 26 with completed stroke due to infarction. The cerebrospinal fluid enolase was raised in the two patients with transient ischaemic attacks and 23 with completed stroke. There was a positive correlation between the volume of the infarct and the level of cerebrospinal fluid alpha and gamma enolase. A high cerebrospinal fluid enolase was always associated with a poor prognosis.

Adult↗
PubMed2000

[Beta-trace protein in diagnosis of cerebrospinal fluid fistula].

Beta-trace protein is a lipocalin that was recently identified as prostaglandin D synthase and represents a major constituent of human cerebrospinal fluid. Beta-trace protein, similar to beta 2-transferrin, has been used as an immunological marker for the detection of cerebrospinal fluid. Between 1982 and 1999, 130 specimens from 101 patients with suspected cerebrospinal fluid leaks of the anterior or lateral skull base have been investigated for beta-trace protein. The specimens were analyzed by one-dimensional immunoelectrophoresis using Laurrell's electroimmunoassay. In all, beta-trace protein could be detected in 57 specimens and was absent in 73. All case notes were studied retrospectively. In correlation with the clinical course and the findings of CT of the paranasal sinuses, high resolution CT of the petrous bones, CT cisternography, NMR, 111In-DTPA radionuclide cisternography, intraoperative findings, visualization of sodium-fluorescein stained cerebrospinal fluid using endoscopic blue light or testing for glucose, there was no false-positive result. A false-negative result occurred in two cases. These findings show that the beta-trace test has a sensitivity of 97.3% and a specificity of nearly 100%. Our findings show that analysis of beta-trace protein can be a valuable test for detecting CSF leakage and has certain advantages in comparison with the beta 2-transferrin assay.

Adolescent↗
PubMed1979

An improved method for the concentration of cerebrospinal fluid cells by suction tip and sedimentation chamber.

To concentrate cells from cerebrospinal fluid, a new method was developed. The technique is a modification of the cell sedimentation method of Sayk. The fluid is absorbed after passing through a Nuclepore filter, pore size 0.4 micron. With the aid of simple utensils it is possible to obtain a cell preparation of high quality using only 0.3 ml of cerebrospinal fluid. The cytomorphology is as good as that achieved by Sayk's sedimentation technique. The cell yield was determined using an accurate and precise method to estimate the number of cells present in the cerebrospinal fluid. The average cell yield is 90%, and all staining methods are applicable. The system is easily modified, and can be suited to many other fluids and purposes.

Cerebrospinal Fluid↗
PubMed1993

Cerebrospinal fluid proteins as indicators of nerve root compression in patients with sciatica caused by disc herniation.

Patients with sciatica caused by lumbar disc herniation were studied to identify biochemical changes in the cerebrospinal fluid related to myelographic findings and clinical observations. One hundred forty-three patients were evaluated by myelography with regard to involvement of the dural sac and the nerve root. A medial group (20 patients) with evidence of dural sac impingement was compared to a lateral group (63 patients) and an extreme lateral group (9 patients) whose condition primarily affected the nerve root. The remaining 51 patients comprised a mixed group with involvement of both the dural sac and the nerve root. The mean cerebrospinal fluid/serum albumin ratio, cerebrospinal fluid/serum immunoglobulin G ratio, and cerebrospinal fluid total proteins showed a significantly increasing trend from the medial through the lateral to the extreme lateral groups. Patients with lateral lumbar disc herniations more often showed neurologic deficits. These results indicate that the elevated cerebrospinal fluid total protein found in the patients with sciatica is due to leaking of plasma proteins primarily from the nerve root into the cerebrospinal fluid. The cerebrospinal fluid proteins may be used as diagnostic parameters of nerve root compression, especially when surgery is a consideration or in patients in whom sciatica is unlikely.

Adolescent↗
PubMed1985

Extractive acylation and mass spectrometric assay of 3-methoxytyramine, normetanephrine, and metanephrine in cerebrospinal fluid.

The chemical analysis of 3-methoxytyramine, normetanephrine, and metanephrine in tissues, blood, and cerebrospinal fluid is complicated by the low levels in which they occur and the amphoteric nature of the functional groups, which hampers their isolation from aqueous media. In the present report, we describe a practical and simple method for the routine isolation and derivatization of 3-methoxytyramine, normetanephrine, and metanephrine in high yield from aqueous samples like cerebrospinal fluid. The metabolites are simultaneously derivatized with pentafluoropropionic anhydride and extracted into an organic solvent. After further treatment with pentafluoropropionic anhydride under anhydrous conditions, the samples are ready for GC/MS analysis. The method is able to exploit the theoretical maximal sensitivity available in the electron capture negative-ion chemical ionization mode without any apparent losses during extraction and derivatization, giving limits of detection in the low picogram range. Mean levels of free 3-methoxytyramine, normetanephrine, and metanephrine in human cerebrospinal fluid were 3.77, 5.20, and 0.40 pmol/ml. Assay of pools of squirrel monkey, human, and canine cerebrospinal fluid with and without previous enzymatic hydrolysis demonstrated that the three metabolites occur predominantly in a conjugated form.

Acylation↗
PubMed1986

Abnormal proteins in the cerebrospinal fluid of patients with Creutzfeldt-Jakob disease.

We studied more than 300 cerebrospinal fluid proteins from 21 patients with Creutzfeldt-Jakob disease. We also examined cerebrospinal fluid from 100 normal controls and more than 400 patients with various neurologic disorders other than Creutzfeldt-Jakob disease. Four abnormal proteins that were identified in the patients with Creutzfeldt-Jakob disease were absent in the normal persons. Two of these proteins (Mr [relative molecular mass], 40,000; pl [isoelectric point], 5.7 and Mr 40,000; pl 5.9) were also present in some patients with multiple sclerosis, herpes simplex encephalitis, schizophrenia, Parkinson's disease, or Guillain-Barré or Behçet's syndrome. Two proteins (Mr 26,000; pl 5.2 and Mr 29,000; pl 5.1) were present in all patients with Creutzfeldt-Jakob disease and in 5 of 10 patients with herpes simplex encephalitis, but in none of the other control groups. A subsequent blinded study of these cerebrospinal fluid proteins from patients with Creutzfeldt-Jakob disease, Alzheimer's disease, Huntington's disease, multi-infarct dementia, parkinsonism dementia of Guam, or the specific dementia of the acquired immunodeficiency syndrome resulted in the ability to distinguish all cases of Creutzfeldt-Jakob disease from the other types of dementia. Although the identity and origin of the abnormal spinal fluid proteins are not yet known, these preliminary results suggest that their presence may help in the diagnosis of Creutzfeldt-Jakob disease.

Cerebrospinal Fluid Proteins↗
PubMed1989

Cerebrospinal fluid pressure in pyogenic meningitis.

The pressure of cerebrospinal fluid taken at lumbar puncture was recorded objectively by strain gauge pressure measurement in 35 infants and children with pyogenic meningitis. Raised pressures were found in 33 children. The median pressure was 15 mm Hg (range 4-70 mm Hg) in all age groups. The pressure level varied throughout the infection, but a higher median pressure (19 mm Hg) was found when this was measured on the day of admission. The clinical features of the meningitis in these patients suggest that many of the presenting symptoms and signs are those of pressure. These results show that high pressure is frequently present in childhood meningitis, not just in those who die from cones or who have radiological evidence of hydrocephalus. We conclude that raised cerebrospinal fluid pressure is a frequent accompaniment of childhood meningitis and may need treatment in its own right and is therefore one further important factor influencing the course and outcome of childhood meningitis.

Adolescent↗
PubMed1979

Clearance of bacteria from cerebrospinal fluid to blood in experimental meningitis.

The occurrence and importance of secondary bacteremia in the pathogenesis of and response to therapy in meningitis is uncertain. Streptococcus pneumoniae type III was injected into the cerebrospinal fluid of the cisterna magna in anesthetized, curarized dogs, and sequential simultaneous samples were obtained from the superior sagittal sinus, cisterna magna, and peripheral blood. The results show that: (i) bacteria are rapidly transported from the cerebrospinal fluid to blood but only after active multiplication within the cerebrospinal fluid, and (ii) entrance into the blood from the cerebrospinal fluid occurs before the height of the febrile response or cerebrospinal fluid pleocytosis.

Animals↗
PubMed1979

Decreased cerebrospinal fluid cyclic adenosine 3',5'-monophosphate in bacterial meningitis.

The concentration of cyclic adenosine 3',5'-monophosphate (cAMP) in 16 cerebrospinal fluid samples from eight patients with bacterial meningitis due to several different organisms was determined. An age- and sex-matched control group of 12 patients with a variety of acute, noninfectious systemic and neurological diseases was also examined. To quantitate the amount of cAMP, a new, improved radioimmunoassay was used with the ability to measure 2.5 X 10(-15) mol of cAMP. The mean concentration of cAMP in the cerebrospinal fluid from patients with meningitis was 0.05 nM, and from patients in the control group it was 1.18 nM. The difference between these two values is statistically significant. The decreased cAMP concentration in the cerebrospinal fluid from patients with bacterial meningitis did not seem to be secondary to metabolism by bacteria or leukocytes, increased enzymatic degradation within the cerebrospinal fluid, or an artifact introduced by the collection and storage procedure. Since the concentration of cAMP in the cerebrospinal fluid is normally found to be within narrow limits and probably reflects intracellular cAMP levels, the results described in this study suggest that interference with cAMP metabolism in central nervous system tissue occurs in bacterial meningitis. This finding seems to be independent of the causative organism and might explain the pathogenesis of selected, neurological manifestations of this disease.

Adolescent↗
PubMed1981

Daily rhythms in cortisol and melatonin in primate cerebrospinal fluid. Effects of constant light and dark.

Cerebrospinal fluid was continuously collected from the cisternal-cervical subarachnoid space of chair-restrained rhesus monkeys. The concentrations of melatonin and cortisol were measured in the cerebrospinal fluid. Under diurnal lighting (light:dark, 12:12 h) melatonin concentrations were elevated during darkness and low during illumination. The melatonin rhythm persisted in constant darkness but was suppressed in constant illumination. Under diurnal lighting, cortisol concentrations were elevated in the early portion of the light period. This daily rhythmicicty of cortisol secretion was not altered by constant illumination or constant darkness. The differential response of the two hormones to constant light suggest that the daily fluctuation of melatonin secretion was not responsible for the daily rhythmicity of cortisol secretion in the rhesus monkey.

Animals↗
PubMed1976

[Detection of HBSAG in cerebrospinal fluid by means of a radioimmunoassay technique (author's transl)].

HBSAg was demonstrated radioimmunologically in cerebrospinal fluid in 7 out of 11 seropositive children with acute viral hepatitis B (1/2), fulminant viral hepatitis (0/1), chronic active hepatitis (2/4), chronic persistent hepatitis (1/1), cirrhosis (1/1), and asymptomatic carrier status (2/2). Counterelectrophoresis and complement fixation test lacked the necessary sensitivity to detect the antigen even in patients with high serum concentrations. The pass over of the cerebrospinal barrier appears to be dependent of the serum titer. Some neurologic symptoms in the early stage of acute viral hepatitis are probably connected with the appearance of HBSAg in cerebrospinal fluid. It is however unlikely that central-nervous-system dysfunctions observed in association with fulminant viral hepatitis and coma result from a direct effect of HBSAg or hepatitis B-virus. In chronic carriers the cerebrospinal fluid probably contains the antigen more frequent. The cerebrospinal fluid of HBSAg-positive patients has to be regarded as an infectious agent.

Acute Disease↗
PubMed1999

Markers of nerve tissue injury in the cerebrospinal fluid in patients with lumbar disc herniation and sciatica.

STUDY DESIGN: The light subunit of neurofilament protein, S-100 protein, neuron-specific enolase, and glial fibrillary acidic protein were determined in the cerebrospinal fluid in patients with lumbar disc herniation and in control patients. OBJECTIVES: To determine whether nerve root injury caused by disc herniation increases the levels of nerve and glial cell injury markers in the cerebrospinal fluid. SUMMARY OF BACKGROUND DATA: Markers of nerve tissue injury can be analyzed in the cerebrospinal fluid, allowing characterization of the cell types involved and the degree of disease in patients with neurologic disorders. METHODS: Cerebrospinal fluid samples were obtained by preoperative lumbar puncture in patients who underwent surgery for lumbar disc herniation and in patients who underwent lower extremity surgery (control group), neurofilament protein (light subunit) and glial fibrillary acidic protein were analyzed by enzyme-linked immunosorbent assay and S-100 protein and neuron-specific enolase by radioimmunoassay and luminescence immunoassay, respectively. In the disc herniation group the concentrations of the four markers were evaluated regarding possible correlation to patient history, computed tomographic findings, and clinical findings. RESULTS: Cerebrospinal fluid concentration of neurofilament protein (light subunit) and S-100 were increased in the disc herniation group compared with that in control subjects (1158 +/- 383 ng/L vs. 152 +/- 14 ng/L, P < 0.01; 1963 +/- 231 ng/L vs. 1003 +/- 152 ng/L, P < 0.05, respectively). No statistical differences in neuron-specific enolase and glial fibrillary acidic protein concentrations were observed between the groups. Disc herniation patients with fewer than 3 months' duration of subjective symptoms had higher neurofilament protein levels than did patients with longer duration. None of the markers was related to preoperative clinical or computed tomographic findings. Patients with persistent neurologic findings at follow-up 2-3 months after surgery had higher levels of neurofilament protein before surgery compared with-those without sequelae. CONCLUSIONS: Patients with disc herniation and sciatica have increased concentrations of neurofilament protein and S-100 in the cerebrospinal fluid, which indicates damage of axons and Schwann cells in the affected nerve root.

Adult↗