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A case of herpes encephalitis diagnosed by brain biopsy and treated with 5-iodo-2-deoxyuridine (IDU) is presented. The infection occurred in a previously well 19-year-old female patient. Plasma and cerebrospinal fluid (CSF) uptake of the substance was determined using 125I labelled IDU. Top CSF levels of IUD and metabolites of less than 4 microgram/ml, about 1/10 of the corresponding plasma level, were obtained after 6 hours of continuous infusion. The result is discussed and compared with a similar study made on 5 healthy beagle dogs where in addition the levels obtained in various parts of the brain were determined. In the animal experiment a mean value of 2.5 microgram/ml of IDU and metabolites was obtained in the CSF after 8 hours, less than 1/20 of the plasma level. The levels in brain tissue were only slightly higher than in the CSF. The causes of therapeutic failures with IDU treatment are discussed.
In order to address an age-dependent alteration in the concentration of beta-amyloid polypeptides (Abetas) within the central nervous system and its probable predisposition to amyloidgenesis in Alzheimer's disease (AD), we measured two species of soluble Abetas, Abeta40 and Abeta42, in cerebrospinal fluids (CSF) from randomly selected Japanese control subjects at various ages (n = 33) and then compared these data with those of probable Japanese AD patients (n = 23). CSF concentrations of Abeta40 and Abeta42 peptides were age-dependent (ANOVA, Bonferroni's multiple comparison; p < 0.01 and p < 0.05, respectively) and were lower in the infant than in adults. From mid-20, the Abeta40 concentrations were decreasing while Abeta42 were rather stable. Abetas in CSF from AD patients (n = 23), whose epsilon4 allele frequency of the apolipoprotein E gene was higher than in controls (n = 83, p < 0.03), were not statistically different from those of age-matched controls (n = 13). A linear relationship was detected between the Abeta40 concentration and the Mini-Mental State Examination score (p < 0.05). The ratio of the Abeta42 to the Abeta40 level measured in the AD CSF samples was approximately 38% decreased compared to age-matched controls (p < 0. 05). These data suggest that the physiological metabolism of soluble Abetas in the brain is regulated in an age-dependent manner, and that the ratio of Abeta42 to Abeta40 level in the CSF would be a useful marker for monitoring progression of AD.
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The arginine vasopressin (AVP) concentrations were determined in plasma and in cerebrospinal fluid (CSF) during a 24-hour period in 7 male patients suffering from hydrocephalus of differing etiologies. Blood and ventricular CSF samples were simultaneously collected every 2 h during the day (08.00-22.00) and every hour during the night (24.00-07.00). In both plasma and CSF, the AVP levels did not show significant time-related circadian variations. No significant correlation was found between the plasma and CSF AVP values during the 24-hour period. The data obtained indicate the absence of the plasma and CSF AVP circadian rhythm in hydrocephalic patients and suggest that in these patients, and possibly in healthy humans, physiological stimuli which are able to induce variations in the plasma AVP concentration during daily life do not alter the CSF AVP content.
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We measured soluble intercellular adhesion molecule-1 (sICAM-1) in the serum and cerebrospinal fluid (CSF) of 35 clinically active relapsing-remitting (RR) multiple sclerosis (MS) patients who underwent both lumbar puncture and gadopentetate dimeglumine (Gd-DTPA)-enhanced MRI within an interval of 1 week, and of 30 neurological controls of whom 17 had noninflammatory neurologic diseases (NIND), 8 bacterial meningitis (BM), and 5 AIDS dementia complex (ADC). Thirteen of the MS patients assumed corticosteroids at the time of the study. While sICAM-1 serum levels were highest in the BM group (p < 0.005), untreated MS patients showed levels higher (p < 0.05) than treated MS and NIND, but similar to ADC. Moreover, the untreated MS group had CSF/serum sICAM-1:CSF/serum albumin (sICAM-1 index) values higher than the treated group (p < 0.01), NIND (p < 0.005), and BM (p < 0.05); high sICAM-1 index was found also in ADC. Untreated MS patients with one or more Gd-DTPA-enhancing MRI lesions (Gd-positive) had higher mean values of CSF/serum albumin ratio (QAlbumin) and CSF mononuclear cells compared to patients without such lesions (Gd-negative). In the untreated Gd-negative patients, sICAM-1 serum levels were higher (p < 0.05) than those in Gd-positive patients. In the latter group, there were positive correlations between the number of CSF mononuclear cells and both IgG (p < 0.01) and sICAM-1 indices (p < 0.05), between QAlbumin and QsICAM-1 (p < 0.005) and between Qalbumin and the Expanded Disability Status Scale score (p = 0.05). There were no significant correlations in the Gd-negative group. These results suggest that sICAM-1 index can be a better marker of intrathecal sICAM-1 synthesis than CSF levels and provide additional insights, in vivo, into the blood-brain barrier mechanisms underlying MRI Gd-enhancement in clinically active RR MS.
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Due to somatic recombination and hypermutation, Ig variable heavy (V(H)) and light (V(L)) regions contain unique immunogenic determinants, idiotopes (Id), which can stimulate T cells. To address the relevance of this in a human disease, monoclonal IgG (mAb)-secreting B cell clones were established from the cerebrospinal fluid (CSF) of two patients with multiple sclerosis (MS). HLA-DR-restricted CD4(+) T cell lines and clones from CSF of both patients specifically recognized autologous CSF mAb. The CSF T cell clones produced IFN-gamma; some also produced TNF-alpha, IL-10 and IL-5. V(H) and V(L) on the monoclonal IgG derived from CSF B cells expressed amino acid replacements due to somatic mutations. A T cell epitope was mapped to a V(H) framework region, where an amino acid replacement was critical for the T cell recognition. The finding of Id-specific T cells and Id-bearing B cells in the CSF indicates that they coexist within the diseased organ, and provide a basis for the study of Id-driven T-B cell collaboration in a human autoimmune disease.
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The diagnosis of congenital syphilis continues to pose a difficult clinical challenge. Because the serodiagnosis of congenital syphilis has significant limitations, the direct detection of Treponema pallidum in suspect neonatal tissues or body fluids represents a desirable alternate diagnostic strategy. We developed and applied the polymerase chain reaction (PCR) for the detection of T. pallidum in clinical material relevant to the diagnosis of congenital syphilis but which typically contain factors inhibitory for the PCR. Four methods of specimen processing were examined to circumvent PCR inhibition; clinical materials included amniotic fluids, neonatal sera, and neonatal cerebrospinal fluids. The PCR was 100% specific for T. T. pallidum compared with the sensitive rabbit infectivity test (RIT) for all clinical materials tested. For amniotic fluids, the PCR was 100% sensitive when correlated with the RIT but had a lesser sensitivity when applied to sera or cerebrospinal fluids, which typically contain few treponemes. The combined sensitivity of the PCR for all clinical samples was 78%. Positive PCR results also were obtained among some clinical specimens for which RIT was not performed; these results correlated well with either stigmata or risk factors for congenital syphilis. The combined results suggest that the PCR can be a useful adjunct to the diagnosis and clinical management of congenital syphilis and that it will provide a valuable tool for investigations of the pathogenesis of the disorder.
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Abnormalities in cerebrospinal fluid associated with meningitis due to Haemophilus influenzae type b were characterized in infant rats. After intranasal inoculation of bacteria, the development of intense bacteremia (greater than 10(4) colony-forming units/ml) correlated with cultures of cerebrospinal fluid positive for H. influenzae, with pleocytosis, and with hisotologic evidence of meningitis. The degree of pleocytosis was related to the age of the animal, the amount of time since inoculation, and the severity of the meningitis.
PURPOSE: Soluble Fas antigen (sFas) and ligand (sFasL), which are associated with apoptosis, have not been evaluated in gastrointestinal or cerebrovascular surgery. The aim of this study was to measure these substances in serum, intra-abdominal fluid, or cerebrospinal fluid, and to speculate a pathophysiologic role for Fas-FasL apoptosis in surgery. MATERIALS AND METHODS: Arterial blood and intraabdominal or cerebrospinal fluid were collected at intervals from 27 gastrointestinal surgical patients, 10 cerebrovascular surgical patients, and 10 spinal anesthesia patients. RESULTS: Serum sFas levels did not change during and after surgery. Intra-abdominal and cerebrospinal sFas levels were identical to and lower than those in serum. Serum sFasL levels did not change during surgery, but decreased after surgery. Intra-abdominal and cerebrospinal sFasL levels were higher than and identical to those in serum. In spinal anesthesia, cerebrospinal sFas and sFasL levels were lower than those in serum. CONCLUSIONS: Serum sFasL decreases after surgery, whereas intra-abdominal or cerebrospinal sFasL increases, although sFas in each site does not change, suggesting redistribution of activated lymphocytes into local surgical wounds and induction of apoptosis in this site.
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