Cerebrospinal fluid concepts

An alternative system proved to be both simpler and more user friendly (Unger et al., 2004 Machtejevas et al., 2006). Thus far we have used this configuration to analyze human plasma, sputum, urine, cerebrospinal fluid, and rat plasma. For each particular analysis we set up an analytical system based on a simple but specific strategy (Figure 9.5). The analysis concept is based on an online sample preparation and a two-dimensional LC system preseparating the majority of the matrix components from the analytes that are retained on a RAM-SCX column followed by a solvent switch and transfer of the trapped peptides. The SCX elution used five salt steps created by mixing 20 mM phosphate buffer (pH 2.5) (eluent Al) and 20 mM phosphate buffer with 1.5 M sodium chloride (eluent Bl) in the following proportions 85/15 70/30 65/45 45/55 0/100 with at the constant 0.1 mL/min flow rate. Desorption of the... 

Antithrombin HI in cerebrospinal fluid can be easily denoted as an inflammatory marker. Correlations with levels of immunoglobulins, their intrathecal oligo-clonal synthesis, complement components, and acute-phase reactants confirm such concepts. Correlations with apolipoproteins and with the presence of lipophagic macrophages in cytological preparations confirm the elevation of CSF AT III levels when a destructive lesion of the CNS is present. 

Barkai et al. (1978) reported that cerebrospinal fluid levels of inositol were lower in patients with depression than in psychiatrically healthy subjects. We hypothesized that inositol may be deficient in some brain systems in depression. This does not contradict the concept that Li reduces inositol levels and that Li" is an antidepressant, because the PI cycle serves as a second messenger for several balancing and mutually interactive neurotransmitters. Li+ could alleviate depression by reducing inositol and a primary hyperactivity of one hypothetical brain system low inositol levels in another system could cause second messenger dysfunction and thereby depression. 

Cerebral edema occurs in response to a wide variety of insults, including ischemia, hypoxia, infection, and noninfectious inflammation. Shifts in brain water, which is the basis of the cellular swelling, are due to osmotic forces, and result in increases in intra- and extracellular spaces. A reasonable amount of tissue swelling can be tolerated in most parts of the body, however, the restrictions imposed by the rigid tentorium and bony skull cause life-threatening herniation with relatively small increases in the brain compartments. Two early anatomists, Monroe (1733-1817) and Kellie (1758-1829), recognized that increased intracranial pressure due to swelling in the cerebrospinal fluid (CSF), blood, or brain tissue compartments could increase intracranial pressure the concept of limited expansion capacity of the intracranial contents is called the Monroe-Kellie doctrine. 

---