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CSF barrier

Tumani, H., et al. (1998). Beta-trace protein in cerebrospinal fluid a blood-CSF barrier-related evaluation in neurological diseases. Ann. Neurol. 44, 882-9. [Pg.385]

The blood-CSF barrier for proteins is defined functionally by nonlinear interaction of the molecular flux and CSF flow rate. [Pg.8]

A blood-CSF barrier dysfunction means decreased CSF flow rate. The structures along the diffusion pathway for proteins between blood and CSF are conservative (no leakage ). [Pg.8]

A blood-CSF barrier dysfunction (i.e., pathologically reduced CSF flow) can have different causes reduced CSF production rate, restricted flow in the subarachnoid space, or restricted passage through the arachnoid villi (F2, R5). [Pg.8]

The blood-CSF barrier is relatively permeable to hydrophilic macromolecules, (i.e., ai-macroglobulin and IgM). In addition, the passage of smaller molecules, which are larger than 500 Da, is facilitated by lipophilicity (i.e., by antibiotics and cytostatic drugs). The composition of the extracellular fluid of the brain parenchyma is unknown. It resembles CSF only in a narrow margin of a few millimeters adjacent to the free CSF space, a zone where a limited diffusion of water-soluble molecules is possible (F2). The composition of CSF is well known because the subarachnoid space can be tapped at its lowest point. Despite the great distance from the site of production, the choroid plexus, it shows all of the characteristics of a filtrate, even in the lumbar sac. [Pg.8]

Thus, for hydrophilic molecules, there is a clear correlation between the CSF/ serum ratio and the hydrodynamic radius of the molecule. This is applicable only in the presence of a steady-state equilibrium (i.e., when the serum concentration is stable and the exchange conditions at the blood-CSF barrier are undisturbed) (Tib). The ratio for water is by definition 1.0. The concentration of the smaller chloride ion is higher in CSF than in serum therefore, in barrier dysfunction, it decreases in comparison to larger molecules. For most amino acids, active... [Pg.8]

Albumin is an excellent marker of the blood-CSF barrier because it originates exclusively in serum. The first attempts to correlate the increase of albumin and IgG assumed a linear rise of both proteins independent of the extent of the barrier alteration. [Pg.9]

This way, it is possible to differentiate the increased concentration of IgG in CSF, which is based on the penetration of this protein from serum under conditions of increased serum concentrations or failure of the blood-CSF barrier. [Pg.9]

Although the examination of total protein in cerebrospinal fluid is quite valuable, it is necessary to mention that this parameter does not provide exact information on the function of the blood-CSF barrier. This is easy to understand. The increased concentration of total protein in cerebrospinal fluid can be based both on the failure of the barrier with a subsequent increase in the concentration of albumin and of other proteins originating from serum and on a more significant intrathecal synthesis of immunoglobulins, especially in levels of IgG. [Pg.11]

The albumin quotient is the most precise, routinely used criterion for assessment of the function of the blood-CSF barrier because albumin in cerebrospinal fluid originates exclusively from serum. Its parallel determination during the monitoring of any CSF protein is necessary because this is the only way to differentiate its increased concentration in cerebrospinal fluid due to passive penetration of the respective serum protein from a more specific increase in the concentration of the monitored protein. It is based on its intrathecal synthesis or on a specific transport mechanism for the given protein across the blood-CSF barrier. Unfortunately, some clinicians disregard this recommendation, and this elementary fact is not sufficiently emphasized in publications on cerebrospinal fluid (A22). [Pg.11]

The blood-CSF barrier of newborns is significantly more permeable than that of adults (F2, R5, SI 1). The albumin ratios continuously decrease during the course of the first month of life, reaching the lowest values between 1 and 3 years of age, and then slowly rise again (Table 4). It is therefore advisable to consider age when assessing the blood-CSF barrier, especially during infancy and old age. [Pg.12]

Concentration of transferrin in CSF does not correlate with serum levels. This suggests consideration of the presence of a speciflc transport system for transferrin in the blood-CSF barrier. This transport system may be similar to that, for instance, for immunoglobulins (transcytosis). Only as an epiphenomenon is there a signiflcant decrease of serum concentrations of transferrin, as in cases of ulcerous meningitis and malignant meningeal inflltration. In this case other methods are required to determine the levels with any degree of precision (A24, Zl). [Pg.14]

In patients with lymphocytic CSF cytological syndromes, elevation of CSF C4 concentrations was observed. Leakage of several proteins across the blood-CSF barrier was also found. Leakage of C4 complement into CSF depends on the functional state of the barrier to a certain extent, being partially selective. Under pathological circumstances, the rate of penetration of protein fractions across the blood-CSF barrier can be modified selectively, which has been proved in CSF acute-phase reactants. They are highly influenced by the production of cytokines. These considerations evoke the question as to whether similar mechanisms of penetration can be expected in cytokines. Elucidation of the pharmacokinetics of interferons in CSF could substantially influence our approach not only to MS patients but to others as well (A18). [Pg.19]

During inflammation, permeability increases in the blood-CSF barrier, elevating levels of sICAM in the CSF. Thus, in settings of acute meningitis, multiple sclerosis, and Guillain-Barre polyradiculoneuritis, CSF concentrations of 44 /rg L 4.5 ixg L and 16.2 /rg L respectively, were measured (R8). A precise, quantitative differentiation between the serum portion and the intrathecal fraction, comparable to the immunoglobulins, is still not possible therefore, the ICAM index represents the best approximation ... [Pg.19]

Fibrinogen. Serum protein, together with the mechanism of hemo-coagulation, is present in normal CSF only in trace concentrations, probably due to its high molecular weight. An increase in CSF concentrations is always connected with severe damage of the blood-CSF barrier or mechanical obstruction in the... [Pg.22]

The CSF/serum ratio of IgG eliminates the individual variation of serum IgG. The quotient of IgG (CSF/serum) to albumin (CSF/serum) eliminates the variation of the IgG quotient by the individual blood-CSF barrier function. Intrathecal IgG is total CSF IgG minus transudative IgG. The first formulas were based on a linear relationship between Q ib and Qigo (Cl, K3, LI, S4). More recent formulas make use of a hyperbolic or exponential function. The application of the latter two formulas reduces the number of false-positive results in the cases of blood-brain barrier disturbances, while sensitivity is maintained. Soeverijn compared Reiber s hyperbolic formula to five other formulas and showed that Reiber s formula produced the best agreement with the lEF gold standard (LI). For the latest modification of the IgG, IgA, and IgM subclasses of immunoglobulins, see Section 3.2.3. [Pg.28]

During the monitoring of any protein in cerebrospinal fluid, it is necessary to bear in mind the functional status of the blood-CSF barrier, serum concentration of the respective protein, and the dimensions of the molecule (or the information based on the molecular weight). These data principally influence the resulting concentration in cerebrospinal fluid. It must also be emphasized again that the parallel determination of albumin in cerebrospinal fluid and serum is necessary. [Pg.34]

Blood—CSF barrier A higher quotient of albumin is frequent owing to a higher permeability of blood-CSF barrier in inflammation... [Pg.36]

Determination of acute-phase proteins (CRP, orosomucoid, haptoglobin, transferrin, prealbumin), immunoglobulins (IgA, IgG, IgM), compressive markers (albumin, fibrinogen), markers of tissue destruction (Apo A-I, A-II, Apo B), components of complement (C3, C4), proteinase inhibitors (antithrombin HI, a -antitrypsin). The measurement was performed simultaneously in CSF and in serum (plasma) by a laser nephelometric method. The functional state of the blood-CSF barrier was evaluated numerically with the help of the quotient Q = Albcsp/s and also by the intrathecal synthesis of immunoglobulins according to Reiber s formula and for each class—IgG, IgM, IgA. [Pg.38]

Out of the examined CSF protein fractions, the elevation of levels occurs especially in acute-phase proteins and in immunoglobulins the destruction of nervous tissue is indicated as well as blood-CSF barrier dysfunction. [Pg.45]

F2. Felgenhauer, K., The filtration concept of the blood-CSF barrier as basis for the differentiation of CSF proteins. In New Concepts of Blood-Brain Barrier (L. Greenwood, D. J. Begley, M. B. Segal, and S. Lightman, eds.), pp. 209-217. Rlenum Rress, London, 1995. [Pg.58]

R2. Reiber, H., The discrimination between different blood-CSF barrier dysfunction and imflamma-tory reactions of the CNS by a recent evaluation graph for the protein profile of CSF. J. Neurol. 224, 89-99 (1980). [Pg.60]


See other pages where CSF barrier is mentioned: [Pg.1035]    [Pg.195]    [Pg.57]    [Pg.57]    [Pg.42]    [Pg.71]    [Pg.1]    [Pg.7]    [Pg.7]    [Pg.7]    [Pg.8]    [Pg.9]    [Pg.10]    [Pg.12]    [Pg.17]    [Pg.18]    [Pg.20]    [Pg.27]    [Pg.27]    [Pg.33]    [Pg.33]    [Pg.45]   
See also in sourсe #XX -- [ Pg.382 , Pg.383 , Pg.383 , Pg.388 ]




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