Reiber H
Neurochemisches Labor, Universität Göttingen, Germany.
J Neurol Sci. 1994 Apr;122(2):189-203. doi: 10.1016/0022-510x(94)90298-4.
Many neurological diseases are accompanied by increased protein concentrations in the cerebrospinal fluid (CSF), described as a blood-CSF barrier dysfunction. The earlier interpretation as a "leakage" of the blood-CSF barrier for serum proteins could be revised by introduction of a "population variation coefficient" of the CSF/serum quotients for IgG, IgA and IgM (delta Q/Q) which is evaluated as a function of increasing albumin quotients (QAlb). The data presented here are based on specimens from 4380 neurological patients. These population variation coefficients were found to be constant over two orders of magnitude of normal and pathological CSF protein concentrations (QAlb = 1.6.10(-3)-150.10(-3)). This constancy indicates that there was no change in blood-CSF barrier related structures with respect to diffusion controlled protein transfer from blood into CSF and hence no change in molecular size dependent selectivity. The pathological increase of plasma protein concentrations in CSF in neurological diseases could also be explained quantitatively by a decrease of CSF flow rate due to its bifunctional influence on CSF protein concentration: reduced volume exchange, and as newly stated, increased molecular net flux into CSF without change of permeability coefficients. Again, on the basis of a changing CSF flow rate, the hyperbolic functions, which describe empirically the changing quotient ratios between proteins of different size (e.g. QIgG:QAlb) with increasing CSF protein content (QAlb) can likewise be derived from the laws of diffusion as the physiologically relevant description. The hyperbolic discrimination line between brain-derived and blood-derived protein fractions in CSF in the quotient diagrams for CSF diagnosis can be further improved on the basis of the large number of cases investigated. Other physiological and pathological aspects, such as high CSF protein values in the normal newborn, in spinal blockade, in meningeal inflammatory processes, CNS leukemia or polyradiculitis as well as animal species dependent variations can each be interpreted as due to a difference or change in the CSF flow rate.
许多神经系统疾病都伴有脑脊液（CSF）中蛋白质浓度升高，这被描述为血脑屏障功能障碍。通过引入IgG、IgA和IgM的脑脊液/血清商的“群体变异系数”（δQ/Q），可以修正早期将血清蛋白血脑屏障的“渗漏”的解释，该系数是根据白蛋白商（QAlb）的增加来评估的。这里呈现的数据基于4380例神经系统疾病患者的样本。发现这些群体变异系数在正常和病理性脑脊液蛋白质浓度的两个数量级范围内（QAlb = 1.6×10⁻³ - 150×10⁻³）是恒定的。这种恒定性表明，在从血液到脑脊液的扩散控制的蛋白质转运方面，血脑屏障相关结构没有变化，因此在分子大小依赖性选择性方面也没有变化。神经系统疾病中脑脊液中血浆蛋白浓度的病理性升高也可以通过脑脊液流速降低来定量解释，因为脑脊液流速对脑脊液蛋白浓度有双重影响：体积交换减少，并且如新指出的，分子净通量进入脑脊液增加而渗透系数不变。同样，基于不断变化的脑脊液流速，经验性描述不同大小蛋白质（例如QIgG:QAlb）之间商比值随脑脊液蛋白含量（QAlb）增加而变化的双曲线函数同样可以从扩散定律推导出来，作为生理相关描述。在脑脊液诊断的商图中，基于大量研究病例，可以进一步改进脑脊液中脑源性和血源性蛋白质组分之间的双曲线区分线。其他生理和病理方面，如正常新生儿、脊髓阻滞、脑膜炎症过程、中枢神经系统白血病或多发性神经根炎中脑脊液蛋白值升高以及动物物种依赖性变化，都可以解释为脑脊液流速的差异或变化所致。
