Yellow spinal fluid. Diagnostic significance of cerebrospinal fluid in jaundiced patients.
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
1. Concentrations of angiotensin II (ANG II) were measured by radioimmunoassay in cerebrospinal fluid and plasma from neurosurgical patients and patients having spinal anaesthesia. Cerebrospinal fluid concentrations of renin, renin substrate and ANG I were also measured. 2. Cerebrospinal fluid concentrations of ANG II measured with antiserum 30/VI were low in neurosurgical patients (mean 6 pmol/l, range < 2 - 12 pmol/l, n = 7) and lower in spinal anaesthesia patients (mean 1 pmol/l, range < 2 - 4 pmol/l, n = 14) and unrelated to concurrent plasma concentrations of ANG II. 3. A second more sensitive immunoassay with ANG II antiserum 9/P gave higher cerebrospinal fluid concentrations of ANG II in spinal anaesthesia patients (mean 15 +/- 1 pmol/l, n = 7, P < 0.01). 4. Paper chromatography showed that the ANG II immunoreactive material measured with antiserum 9/P was not ANG I, ANG II, ANG II-(2-8), ANG II-(3-8) or ANG II-(4-8). 5. The concentration of ANG I in cerebrospinal fluid was low (4 +/- 0.04 pmol/l, n = 7). No renin was detected (n = 32) and the concentration of renin substrate was 45 +/- 2.6 nmol/l (n = 24). 6. Much of the immunoreactive ANG II in human cerebrospinal fluid is an immunoassay artifact.
A technique for ventriculolumbar perfusion of the cerebrospinal fluid space has been used to study the neuromuscular effects of low concentrations of magnesium and calcium in the cerebrospinal fluid of conscious sheep. Perfusion with synthetic cerebrospinal fluid solutions containing less than 0-6 mg magnesium/100 ml produced episodes of tetany which were abolished by perfusion with a solution of normal magnesium concentration. This suggests that the low cerebrospinal fluid magnesium concentrations reported in cases of hypomagneseamic tetany may result in changes within the central nervous system that could produce the nervous signs. Perfusates with a calcium concentration below 2-0 mg/100 ml caused hyperpnoea and continuous muscle tremors. Magnesium (0-6 mg/100 ml) and calcium (2-0 mg/100 ml) perfused simultaneously acted synergistically to produce signs characteristic of low levels of each of the ions.
Cerebrospinal fluid cholinesterase activity was determined in 5 species of domestic animals. Suitable samples of cerebrospinal fluid could be obtained repeatedly from sheep, calves, and dogs without killing, but not from pigs and rabbits. The cholinesterase activity among erythrocytes, plasma, and cerebrospinal fluid of these species was also compared statistically.
Cochlear dysplasia associated with defect in stapes footplate can be a cause of cerebrospinal fluid leak. Repair of cerebrospinal fluid leak in these cases is usually done by packing the vestibule with muscle or fascia. This traditional method of repair has 30-60% failure rate. Cerebrospinal fluid leak in four such patients was successfully repaired using multiple layer packing of vestibule, reinforced by pedicle temporalis muscle graft. Intraoperatively continuous lumbar drain was done. Magnetic resonance imaging of inner ear using 3D FSE T2WI and 3D FIESTA sequences was found helpful noninvasive investigation to localize site and route of cerebrospinal fluid leak.
Twenty-one amino acids were determined in serum and cerebrospinal fluid of 12 patients with endemic, and in the cerebrospinal fluid of 22 patients with epidemic optic neuropathy. For the endemic patients, there was a decrease in aspartate and taurine in the serum with respect to controls. The ratios aspartate/taurine and taurine/valine were decreased, and glutamate/taurine was increased in the serum. Some of the altered amino acid ratios indicate preponderance of excitatory to inhibitory molecules. The ratio with valine corresponded to the decrease in taurine and the maintenance of valine concentration, an amino acid related to anthropometric parameters. A typical malnutrition pattern was not observed, as the levels of essential amino acids were not significantly modified. In the cerebrospinal fluid there were increases in aspartate, glutamate and threonine, the first two probably indicating a neurodegenerative disorder or some type of metabolic alteration, primary or secondary to the disease. The increase in threonine could be related to lipid metabolism, but it is not clear at present. A wide variety of amino acid ratios were increased in the cerebrospinal fluid of patients with endemic optic neuropathy, mainly pointing to an excitatory condition and some metabolic alterations. In the cerebrospinal fluid of patients with epidemic optic neuropathy there was an increase in aspartate and glutamate, and increase in glutamate/taurine, glutamate/glycine, and gamma-aminobutyric acid/glycine ratios. Interesting differences were also observed between patients from different periods of time, but with the same clinical features, and the modifications of amino acid concentrations in the cerebrospinal fluid, such as glutamine, threonine and tryptophan. The present results indicate a disorder in the metabolism of amino acids, support a specific deficit, especially for taurine, an imbalance between excitatory and inhibitory amino acids, and a possible relation to viral infections.
OBJECTIVE: To describe the clinical presentation, diagnosis, surgical management, and outcome of patients with spontaneous cerebrospinal fluid otorrhea. STUDY DESIGN: Retrospective case series. SETTING: Tertiary referral center. METHODS: The authors conducted a chart review of all previously unreported cases of surgically confirmed cerebrospinal fluid otorrhea at their institution between September 1996 and February 2005. Acquired cases were excluded from this study. Eleven cases of spontaneous cerebrospinal fluid otorrhea were identified among 10 patients. RESULTS: Nine of the 10 patients presenting with spontaneous cerebrospinal fluid otorrhea were women. Ages ranged from 34 to 79 years. Eight patients presented with serous otitis media, and two women presented with meningitis. High-resolution computed tomography demonstrated a tegmen defect with a sensitivity of 80%. Nine tegmen defects were repaired using a transmastoid approach without recurrence. One patient with a contracted mastoid and a meningoencephalocele herniating from the tegmen tympani into the attic required the temporal craniotomy approach for definitive repair. Another patient with a tegmen tympani defect developed a recurrence of cerebrospinal fluid otorrhea 8 years after a transmastoid repair using only fascia and fibrin glue. A recurrent tegmen defect in this patient was repaired using a transmastoid approach and a multilayered closure technique. CONCLUSION: The diagnosis of spontaneous cerebrospinal fluid otorrhea requires clinical suspicion in the setting of persistent serous otitis media. High-resolution computed tomography can confirm the diagnosis. The authors' findings indicate that repair through a transmastoid approach is effective if the tegmen defect can be widely visualized. The authors advocate a multilayered closure technique.
OBJECTIVE: To evaluate the clinical manifestation and surgical technique of Mondini dysplasia with cerebrospinal fluid (CSF) leakage. METHOD: Three Mondini dysplasia with spontaneous cerebrospinal fluid leakage were treated by the authors. A transcanal tympanotomy were used to pack the vestibular cavity with muscle. RESULT: Three children were first manifested with recurrent meningitis and spontaneous cerebrospinal fluid rhinorrhea. Further examinations found that the leakages were otogenic. One side or both sides Mondini dysplasia were confirmed by CT scanning of temporal bones. The leakages were all stopped by the primary surgical closure. CONCLUSION: Mondini dysplasia should be considered in children with spantaneous cerebrospinal fluid otorhinorrhea. A temporal bone CT scan can confirmed the diagnosis. A transtympanic closure is very effective in the management.