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PubMed1992

Pressure transfer between the perilymph and the cerebrospinal fluid compartments in cats.

This is a review of our studies of the labyrinthine fluid pressure in cats subjected to pressure changes in the middle ear (implosive routes) and the cerebrospinal fluid compartment (explosive routes) as well as to changes in vascular and ambient pressures. The perilymph, cerebrospinal fluid (CSF), middle ear, venous and arterial pressures were measured with the cochlear aqueduct (CA) patent as well as surgically blocked. Experiments on explosive pressure changes revealed that the perilymph pressure was regulated by the CSF in case of CA patency. The CSF influence was dominant enough to obscure any direct effect on the labyrinth from other sources. With the CA obstructed the CSF influence on the labyrinth was apparently mainly via the endolymphatic sac and duct although limited and much delayed. Systemic arterial pressure changes had a pronounced influence on the perilymph pressure, but this effect was revealed only when the CSF influence was reduced by CA obstruction. Experiments on implosive and ambient pressure changes suggested that there was no fundamental difference in the perilymph response to equivalent levels of implosive versus hypobaric pressure. Three factors determined the effect of implosive and hypobaric pressure: the patency of the CA, the rate of the pressure change, and the eustachian tube function.

Air Pressure↗
PubMedDate not supplied

[Tryptophan and tyrosine in blood and cerebrospinal fluid in patients with recent cerebral infarct].

The determinations were carried out in the blood and cerebrospinal fluid of 40 patients with recent cerebral infarction and 30 controls. Tryptophan concentration was determined by the fluorimetric method of Denckla and Dewey, and tyrosine concentration by the method of Waalkes and Udenfried. A statistically significant rise of free tryptophan concentration in the plasma and tryptophan concentration in the cerebrospinal fluid was found which seemed to depend on the stress reaction following brain infarction. No statistically significant changes were observed in the concentration of tyrosine in the cerebrospinal fluid and plasma in patients with brain infarction.

Adult↗
PubMedDate not supplied

[Leukotrienes in cerebrospinal fluid of patients with subacute sclerosing panencephalitis].

In the cerebrospinal fluid of two groups of patients with subacute sclerosing panencephalitis (SSPE), the determinations of LTB4 and LTC4 leukotriene concentrations were performed by radioimmunoassay (RIA). In the first group of 10 patients with chronic SSPE (from 2 to 11 years), the LTB4 and LTC4 levels were 94.8 +/- 17.0 and 97.4 +/- 16.8 pg/ml respectively, and were significantly higher than those in six patients with discopathy, epilepsy and headache (p < 0.01). In the second group of 10 patients with beginning SSPE (disease duration from 1 to 11 months) LTB4 level was lower (was not different from that in the control group), while LTC4 concentration was 97.6 +/- 10.8 pg/ml and again was significantly raised. Higher LTB4 and LTC4 levels in the cerebrospinal fluid of patients with SSPE indicate that these compounds participate in chronic inflammatory reaction around cerebral veins.

Adolescent↗
PubMed2000

Prophylactic percutaneous sealing of lumbar postdural puncture hole with fibrin glue to prevent cerebrospinal fluid leakage in swine.

UNLABELLED: We explored the effect of fibrin glue injection at the site of dural puncture on cerebrospinal fluid (CSF) leakage in a swine model. Pigs were subjected to a lumbar dural CSF puncture in the sitting position with a 17-gauge Tuohy needle. Fibrin glue 1.4 mL was injected through the same needle into the epidural space. Evans blue dye was infused through the cisterna magna 15 min later, and the appearance of dyed CSF through the skin puncture and along the needle trajectory to the dura was inspected and categorized. In seven of eight animals, the CSF leak was sealed with fibrin glue. Control animals were injected with 1.4 mL saline. A sham operation group of animals underwent cisternal dye infusion without a lumbar puncture. CSF pressure at the cisterna magna was recorded throughout the procedure. No significant differences in the leakage indicators were found between the fibrin glue-injected and sham-operated group, whereas both groups showed significant differences with respect to the control group. The fibrin glue seal was effective against CSF pressures of 24.5 [17-31] cm H(2)O. We conclude that percutaneously injected fibrin glue is effective in stopping CSF leaks after dural puncture in this animal model. IMPLICATIONS: In this swine study, we repaired a cerebrospinal fluid leak after a dural puncture by percutaneously injecting tissue adhesive. The technique of percutaneous injection of fibrin glue seems promising for the prophylaxis of headache associated with cerebrospinal fluid leakage, and may be an alternative to an epidural blood patch.

Animals↗
PubMed1983

Age-related changes in the cerebrospinal fluid outflow glycosaminoglycans.

The glycosaminoglycan distribution patterns of the cerebrospinal fluid (CSF) outflow pathway, dura mater and cerebral cortex of young New Zealand red rabbits and 1-, 3- and 12-week-old C-57 mice were identified by analyses of the glycosaminoglycan moieties and by the use of zone electrophoresis. The glycosaminoglycans were identified by specific degradation procedures, i.e., hyaluronate lyase, chondroitin ABC lyase, endo-beta-D-galactosidase and nitrous acid treatment. The CSF outflow pathway and dura mater glycosaminoglycan components were primarily hyaluronic acid and chondroitin sulfate-dermatan sulfate, whereas the cerebral cortex glycosaminoglycan components were hyaluronic acid, chondroitin sulfate-dermatan sulfate, keratan sulfate and heparan sulfate. The glycosaminoglycan components of the dura mater and cerebral cortex decreased and those of the CSF outflow pathway increased as a function of age. These results demonstrate the feasibility of analyses of the CSF outflow pathway glycosaminoglycan components and suggest that topographical changes in the glycosaminoglycan distribution profiles may contribute to the pattern of cerebrospinal fluid outflow.

Age Factors↗
PubMedDate not supplied

[Treatment of cerebrospinal fluid shunt infections using the Perrin and McLaurin technique. Analysis of 11 cases].

Eleven patients with shunt infection (SI) of the cerebrospinal fluid in whom the SI was withdrawn and replaced by a new SI system with reservoir and intraventricular and parenteral antibiotic treatment were reported. The diagnosis was made by culture of the components of the SI and, or, the cerebrospinal fluid. In 9 cases the agent was a staphylococcus. The different therapeutic trials to treat SI infections can be summarized as follows: a) replacement of the SI by an external drainage, antibiotics, and reinsertion of the SI when the cerebrospinal fluid was sterilized; b) withdrawal of the SI and placement of a new SI in the same surgical procedure associated with intraventricular and systemic antibiotic treatment; and c) treatment with intraventricular and, or, systemic antibiotics. It has been demonstrated that the surgical approach (a and b) is more effective. In our series the procedure indicated in B was followed by the control of the infection in all cases. The follow-up of the surgical treatment was 1-3 years. The most currently used SI was the ventriculoperitoneal bypass. Their main complications are pseudocysts which are easily recognized by of abdominal echography and frequently revealed SI infection. Diagnosis and treatment of SI infections should take into account the type of complications and the most appropriate collaboration with other clinical departments.

Adolescent↗
PubMedDate not supplied

Excitatory amino acids in cerebrospinal fluid in neonatal asphyxia.

Of the excitatory amino acids, glutamic and aspartic acid were studied in the cerebrospinal fluid of six infants 4-32 hours after a documented episode of severe neonatal asphyxia. Aspartic acid concentration was definitely increased in the cerebrospinal fluid of these patients, whereas glutamic acid concentration varied considerably. Aspartic acid was always increased, even hours after the period of asphyxia, but values were greater in samples taken less than 12 hours after the asphyxial event. The patients with the highest cerebrospinal fluid aspartic acid concentrations had more severe outcomes.

Aspartic Acid↗
PubMed1983

Severe head trauma and the changes of concentration of neuron-specific enolase in plasma and in cerebrospinal fluid.

In nine patients with severe head trauma, the concentration of neuron-specific enolase in cerebrospinal fluid and in plasma was determined and compared with the activity of creatine kinase and alpha-hydroxybutyrate dehydrogenase, and with the concentration of lactate. In patients who died of the head trauma, a concentration of neuron-specific enolase of 6.8-64 micrograms/l in the plasma (reference range: 3.0-6.0 micrograms/l) and of 2.2-9.0 micrograms/l in the cerebrospinal fluid (reference range: 0.5-2.0 micrograms/l) was detected. Investigations of three patients showed that the changes of the concentration of neuron-specific enolase in plasma and in cerebrospinal fluid were independent of each other. Furthermore, the initial concentration of neuron-specific enolase in the plasma after the accident and the dynamics of its changes during the disease show a close relationship to the outcome.

Adult↗
PubMed1996

Cerebrospinal fluid drainage in the management of CSF leak following acoustic neuroma surgery.

A retrospective analysis was performed on 174 patients operated on from 1992 to 1995 to evaluate the safety and efficacy of continuous lumbar cerebrospinal fluid drainage (CLCFD) in the management of cerebrospinal fluid (CSF) leaks following acoustic neuroma surgery. There was a 17% incidence of CSF leak. CLCFD stopped the leak in 87% of cases. There were no cases of meningitis associated with CLCFD. One deep vein thrombosis was treated without sequelae. It is concluded that CLCFD is safe and efficacious. The authors recommend that CLCFD be implemented immediately when indicated, foregoing a trial of conservative therapy. Indications and precautions are discussed.

Cerebrospinal Fluid↗
PubMed2002

Progression to neuropsychological impairment in human immunodeficiency virus infection predicted by elevated cerebrospinal fluid levels of human immunodeficiency virus RNA.

BACKGROUND: If cerebrospinal fluid (CSF) human immunodeficiency virus (HIV) RNA levels are elevated before the development of neuropsychological (NP) impairment, such an observation would support prospective monitoring of CSF HIV RNA levels as well as therapeutic interventions designed to lower CSF HIV levels. OBJECTIVE: To determine whether increased CSF HIV RNA levels at an earlier time predict subsequent progression to NP impairment in HIV-infected subjects. METHODS: We examined 139 subjects in a prospective cohort study. Comprehensive NP, neuromedical, and laboratory evaluations were performed at initial and follow-up visits at least 6 months apart. Human immunodeficiency virus RNA levels in plasma and CSF were measured with a commercially available, polymerase chain reaction-based assay. To assess the robustness of our findings, we analyzed changes in NP performance over time in 2 ways. First, we used masked clinical ratings of global NP performance to identify individuals who were initially NP normal, and then determined, in a similarly blinded fashion, which of these subjects subsequently became NP impaired. Second, in a separate analysis, we assessed change in subjects' raw scores on each of a series of NP test measures between baseline and follow-up. RESULTS: Among subjects who were not impaired at the initial visit, higher levels of HIV RNA in CSF significantly predicted progression to global NP impairment at the follow-up evaluation. Cerebrospinal fluid HIV RNA levels outperformed other clinical and laboratory measures in predicting progression to NP impairment. Higher CSF HIV RNA levels were associated with worsening performance on tests of attention, learning, and motor function. CONCLUSION: Because elevated CSF HIV RNA levels (>or=200 copies/mL) predict subsequent progression to NP impairment, monitoring of CSF viral load and therapy to reduce CSF HIV RNA levels may be clinically warranted, even if impairment is not identified at the time of lumbar puncture.

Adult↗
PubMed1996

Rapid distribution of intraventricularly administered sucrose into cerebrospinal fluid cisterns via subarachnoid velae in rat.

The intracranial distribution of [14C]sucrose, an extracellular marker infused for 30 s into one lateral ventricle, was determined by autoradiography of frozen-dried brain sections. Within 3.5 min [14C]sucrose appeared in: (i) the third ventricle, including optic, infundibular and mammillary recesses; (ii) the aqueduct of Sylvius; (iii) the velum interpositum, a part of the subarachnoid space that runs along the roof of the third ventricle and contains many blood vessels; (iv) the mesencephalic and fourth ventricles; and (v) the superior medullary velum, a highly vascular extension of the subarachnoid space that terminates at the walls of the mesencephalic and fourth ventricles. Within 5 min, radioactivity was present in the interpeduncular, ambient and quadrigeminal cisterns, which encircle the midbrain. By 10 min, approximately 11% of the radioactivity had passed into the subarachnoid space via a previously undescribed flow pathway that included the velum interpositum and superior medullary velum. At many places along the ventricular system, [14C]sucrose appeared to move from cerebrospinal fluid into the adjacent tissue by simple diffusion, as reported previously (Blasberg R. G. et al. (1974) J. Pharmac. exp. Ther. 195, 73-83; Levin V. A. et al. (1970) Am. J. Physiol. 219, 1528-1533; Patlak C. and Fenstermacher J.D. (1975) Am. J. Physiol. 229, 877-884; Rosenberg G. A. and Kyner W.T. (1980) Brain Res. 193, 56-66; Rosenberg G. A. et al. (1986) Am. J. Physiol 251, F485-F489). Little sucrose was, however, taken up by: (i) circumventricular organs such as the subfornical organ; (ii) medullary and cerebellar tissue next to the lateral recesses; and (iii) the superior and inferior colliculi and cerebral peduncles. For the latter two groups of structures, entry from cerebrospinal fluid was apparently blocked by a thick, multilayered glia limitans. Although [14C]sucrose was virtually absent from the rest of the subarachnoid system after 1 h, it remained in the perivascular spaces and/or walls of pial arteries and arterioles for more than 3 h. Certain transport proteins, protease inhibitors, growth factors and other neurobiologically active materials are present in cerebrospinal fluid, and their distribution to the brain and its blood vessels may be important. The present work shows, in the rat, that the flow of cerebrospinal fluid and the disposition of its constituents is fairly complex and differs among regions. Flow was rapid throughout the ventricular system and into various subarachnoid velae and cisterns, but was surprisingly slow and slight over the cerebral and cerebellar cortices. The cerebrospinal fluid-to-tissue flux of material was relatively free at many interfaces, but was greatly restricted at others, the latter indicating that the old concept of a "cerebrospinal fluid-brain barrier" may hold at such places. Finally, radiolabeled sucrose was retained longer within the walls and perivascular spaces of pial arteries and arterioles than in other subarachnoid tissues; one function of the cerebrospinal fluid system or "third circulation" may thus be delivering factors and agents to these pial blood vessels.

Animals↗