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Results for “CEREBROSPINAL FLUID”

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At least 307 records · Page 17Linked to original sources
PubMed1985

[Perinatal relation of the blood-cerebrospinal fluid barrier and its effect on protein composition of the cerebrospinal fluid].

The lumbar spinal fluid of 70 infants aged 238-461 days after conception was examined for total protein with the Cu-Folin-differential test, and for variation of single CSF proteins as a function of developmental age using agar gel electrophoresis. In the early stages of development all CSF fractions as well as total protein are increased compared with adult persons. The absolute amounts decrease after birth more or less rapidly (partly exponentially) and reach a minimum between the 52nd and 57th week of development (prealbumin and beta 1-globulin somewhat earlier, albumin somewhat later). Except for beta 1-globulin this minimum is always lower than the normal adult values. There seems to be a linear correlation between the logarithm of the total protein (also of certain single proteins) and the gestational age over a wide range of development. The behaviour of the haptoglobin and immunoglobulin fractions demonstrates especially well that many independent factors may simultaneously influence the concentration of the CSF proteins (e.g. plasma content of proteins, permeability of the blood/brain or blood/CSF barrier) and that these factors themselves depend on both the developmental state (gestational age) and chronological age (birth). This study, in agreement with the results of other authors suggests that in human neonates the reference range of those CSF parameters which depend on barrier conditions should be related to the gestational age rather than to the chronological age.

Alpha-Globulins↗
PubMed2002

[Design and development of cerebrospinal fluid container].

The cerebrospinal fluid container is a device for storage of medicaments. By means of surgical operation, a ventricle catheter can be embedded in the ventricle of the brain. This safe and reliable device provides for neurosurgeons a new method of intracranical therapy and reestablishment of the circulating passage of the cerebrospinal fluid.

Brain Diseases↗
PubMed1990

The use of magnetic resonance imaging to assess slow fluid flow in a model cerebrospinal fluid shunt system.

Cerebrospinal fluid (CSF) shunt malfunction in patients with hydrocephalus is common and can result in prolonged hospitalisation, operative exploration or progressive neurologic damage. The evaluation of shunt function usually requires invasive techniques that can be inaccurate or cause complications. Magnetic Resonance Imaging (MRI), which has been used to study both intraluminal blood flow and intraventricular CSF flow, may offer an alternative noninvasive test of shunt function. The MR characteristics of flow related enhancement were studied in a model shunt system. A special section of tubing for MRI was inserted into the system proximal to the valve. Flow through the system could be varied from 0 to 20 ml/h. Multiple spin echo images were made (TR2000, TE20) transverse to the specialised tubing. The intensity of the intraluminal MR signal at specific locations along this tubing and from a 'no flow' standard were measured. The signal intensity varied as a linear function of flow rate from 2.5 ml/h to 20 ml/h. These results suggest that MRI has potential for evaluating the slow flow in CSF shunts.

Cerebrospinal Fluid Shunts↗
PubMed1994

Pharmacokinetics of fluconazole in cerebrospinal fluid and serum of rabbits: validation of an animal model used to measure drug concentrations in cerebrospinal fluid.

Complete concentration-time data describing the pharmacokinetics of fluconazole in the cerebrospinal fluid (CSF) following a single dose are not available for humans or animals. We studied the pharmacokinetics of fluconazole with an indwelling intracisternal needle as described by R.G. Dacey and M.A. Sande (Antimicrob. Agents Chemother. 6:437-441, 1974). To determine whether the presence of an intracisternal needle alters pharmacokinetics in the CSF, we validated this model with uninfected rabbits by measuring pharmacokinetic constants following direct intracisternal and intravenous administration of fluconazole. Following direct injection, there was no alteration of elimination rates in the CSF with increasing sample number or time. Following intravenous administration, the penetration and kinetic constants were the same in individual animals from which multiple CSF samples were obtained as in a composite subject constructed by pooling virgin samples from different animals. The presence of the intracisternal needle did not alter CSF chemistry or leukocyte counts, and erythrocyte contamination was < 0.001%. While drug concentrations were measured by a microbiological assay, we also compared the sensitivity and reproducibility of a high-performance liquid chromatography (HPLC) assay with those of the microbiological assay. Following a single intravenous dose, the maximum concentration of the drug in serum, the time to maximum concentration of the drug in serum, the terminal elimination half-life in the CSF, and the percent penetration by fluconazole were 6.12 micrograms/ml, 1 h, 9.0 h, and 84.3%, respectively. We conclude that the sampling of CSF via an indwelling needle does not alter fluconazole pharmacokinetics, cause inflammation, or alter chemical parameters; that the microbiological assay is at least equivalent in sensitivity and reproducibility to the HPLC assay; and that robust parameters describing the pharmacokinetics of fluconazole are possible with this model.

Animals↗
PubMed2005

Herniation secondary to critical postcraniotomy cerebrospinal fluid hypovolemia.

OBJECTIVE: Cerebrospinal fluid hypovolemia resulting in postural headaches is a well-known clinical entity, but severe forms of cerebrospinal fluid hypovolemia with altered mental status and signs of transtentorial herniation ("brain sag") have rarely been reported. This article describes the clinical features of brain sag after craniotomy in an attempt to increase recognition of this syndrome. METHODS: Between April 2001 and January 2003, 220 consecutive patients with subarachnoid hemorrhage were prospectively enrolled in the Columbia Subarachnoid Hemorrhage Outcomes Project; 137 underwent craniotomy for aneurysm clipping. Among these patients, the diagnosis of brain sag was made when all three of the following criteria were present: clinical signs of transtentorial herniation, head computed tomographic scans revealing effacement of the basal cisterns with an oblong brainstem, and improvement of symptoms after placement of the patient in the Trendelenburg position (-15 to -30 degrees). For each patient, the symptoms, clinical course, and subsequent response to treatment were characterized. In addition, brainstem dimensions were measured on computed tomographic scans taken before, during, and after resolution of brain sag. A "sag ratio" was generated for these time points by dividing the maximum anteroposterior distance by the maximum bipeduncular distance. RESULTS: Eleven (8.0%) of 137 aneurysmal subarachnoid hemorrhage patients treated by craniotomy and an intraoperative spinal drain met the criteria for brain sag. Signs of transtentorial herniation developed most commonly between 2 and 4 days postoperatively. Pupillary asymmetry was noted in 10 (91.0%) of 11 patients, whereas the other patient demonstrated extensor posturing. The Trendelenburg position reversed the symptoms in all patients. The mean sag ratios before, during, and after resolution of brain sag were 0.91 +/- 0.03 (mean +/- standard error), 1.18 +/- 0.03, and 0.91 +/- 0.03, respectively. This represented a 30.9% elongation of the brainstem during sag (P < 0.001) and a 23.6% change back to baseline after resolution of the syndrome (P < 0.002). There was no significant difference between the presag and postsag ratios. CONCLUSION: Severe cerebrospinal fluid hypovolemia after craniotomy may produce a dramatic herniation syndrome that is completely reversed by the Trendelenburg position. Brain sag should be included in the differential diagnosis for acute postoperative clinical deterioration in this patient population.

Adult↗
PubMed1999

Elevated levels of tau in cerebrospinal fluid: implications for the antemortem diagnosis of Alzheimer's disease elevated levels of tau in cerebrospinal fluid: implications for the antemortem diagnosis of Alzheimer's disease.

Alzheimer's disease (AD) is a heterogeneous group of dementias characterized by progressive cognitive impairments as well as by the accumulation of abundant extracellular deposits of Ass and intra-neuronal neurofibrillary lesions in selective-ly vulnerable regions of the AD brain. The latter abnormalities (e.g. neurofibrillary tangles, dystrophic neurites, neuropil threads) are aggregates of paired helical filaments (PHFs) formed from altered tau proteins (PHFtau). Although PHF tau and normal central nervous system (CNS) tau are phosphorylated at nearly the same sites, PHFtau is phosphorylated to a greater extent, and alterations in the activity of CNS kinases and phosphatases most likely contribute to the pathogenesis of PHFtau. Since the abundance of neurofibrillary lesions correlates with the dementia in AD, the generation of PHFtau and the formation of neurofibrillary lesions may be part of a cell death pathway leading to massive neuron loss and dementia in AD. Building upon these and other insights into altered tau metabolism in AD, a series of studies suggest that the diagnosis of AD may be supported in living patients by determining the concentration of tau in cerebrospinal fluid (CSF). We review these promising studies here, and discuss them in the context of current understanding of the pathobiology of AD.

Journal Article↗
PubMed1988

Reduction of cerebrospinal fluid pressure by hypocapnia: changes in cerebral blood volume, cerebrospinal fluid volume and brain tissue water and electrolytes. II. Effects of anesthetics.

Part I of these studies (Artru, 1987) examined how cerebral blood volume (CBV), CSF volume, and brain tissue water and electrolytes determined CSF pressure during 4 h of hypocapnia in sedated dogs. The three groups reported were: hypocapnia (PaCO2 20 mm Hg) with no intracranial mass (group 1), intracranial mass (epidural balloon, CSF pressure 35 cm H2O) but no hypocapnia (group 2), and intracranial mass with hypocapnia used to lower CSF pressure (group 3). It was found that in dogs with an intracranial mass (group 3) the CSF pressure-lowering effect of hypocapnia was sustained for 4 h due to improved reabsorption of CSF, decrease of CSF volume to offset reexpansion of CBV and no increase in the sum of CSF volume and CBV. The present Part II studies (groups 4-8) examine the effects of anesthetics on CSF pressure during conditions like those used for group 3, namely, intracranial mass present and hypocapnia used to lower CSF pressure. When halothane or enflurane were used for anesthesia, the CSF pressure-lowering effect of hypocapnia was not sustained. CSF pressure increased from 17.3 +/- 4.7 and 19.0 +/- 4.1 cm H2O, respectively (mean +/- SD), at 10 min to 50.3 +/- 12.8 and 43.2 +/- 12.8 cm H2O, respectively at 4 h. Increase of CSF pressure was associated with increased resistance to reabsorption of CSF (Ra) and increase in the sum of CSF volume and CBV. With halothane the intracranial volume increase was comprised chiefly of cerebral blood and with enflurane the intracranial volume increase was comprised chiefly of CSF. When isoflurane, fentanyl, or thiopental were used for anesthesia, the CSF pressure-lowering effect of hypocapnia was sustained. Ra did not increase and the sum of CBV and CSF volume remained reduced.

Anesthetics↗