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Radionuclide techniques have commonly been used to assess ventriculovenous shunt function, cerebrospinal fluid dynamics, and for the diagnosis of cerebrospinal fluid leaks. All of these techniques were utilized in this unusual case of retrograde migration of a ventriculoatrial catheter into the neck, with cutaneous fistulization and CSF leak.
The effects of propofol on cerebral blood flow velocity, cerebrospinal fluid pressure, cerebral perfusion pressure and mean arterial pressure were studied during induction in 25 patients scheduled for elective craniotomy. Premedication consisted of only atropine sulphate 0.007 mg/kg (im) 45 min before induction. Measurements were made or derived at time zero and 1, 2, 3, 4 and 5 min after an induction dose of propofol (2.5 mg/kg). Patients were retrospectively stratified into two groups, according to cerebrospinal pressure basal values: (i) lower than 10 mmHg (10 pts) and (ii) higher than 10 mmHg (15 pts). Cerebral blood flow velocity, measured by transcranial Doppler, fell in all the patients, but the reduction was significant at 1, 2, 3 and 4 min only in the group with high CSF pressure, while it never reached the critical value of 10 cm/s. Cerebrospinal fluid pressure and mean arterial pressure decreased in both groups of patients and the fall reached a statistical significance at 1 and 2 min in the group with higher baseline CSF pressure, only at 1 min: a parallel decrease of CPP was recorded, but it was not significant. Thus propofol decreases CSF pressure without hazardous effects on cerebral blood velocity and on cerebral perfusion pressure and seems to be a suitable anaesthetic agent in controlling high cerebrospinal fluid pressure in neuroanaesthesia.
The validity of the hypothesis that some of the neuropsychiatric manifestations of systemic lupus erythematosus (SLE) are mediated by the direct effects of antibody binding to neuronal cell membranes is dependent on the demonstration of antineuronal activity within the central nervous system of patients with active central nervous system disease. Using a radiolabelled staphylococcal protein A assay, we tested cerebrospinal fluid from 27 patients with SLE and central nervous system manifestations, and cerebrospinal fluid from 18 additional patients with SLE but free of central nervous system disease for antibody reactive with the cultured human neuronal cell line SK-N-SH. Cerebrospinal fluid from 20 of 27 patients with active lupus central nervous system disease had increased immunoglobulin G (IgG) antineuronal activity compared with cerebrospinal fluid from two of 18 patients with SLE without central nervous system disease. Ninety percent of the patients with psychosis, organic brain syndrome or generalized seizures had increased IgG antineuronal activity as compared with only 25 percent of the patients who presented with hemiparesis or with chorea/hemiballismus. Antineuronal activity per microgram of IgG was concentrated eightfold in the cerebrospinal fluid of patients with active central nervous system disease as compared with the serum activity. Patients with or without active central nervous system disease did not differ significantly in the amount of serum antineuronal binding activity. The results are consistent with the hypothesis that the more diffuse central nervous system manifestations of SLE are a direct result of the interaction of antibody with neuronal cell membranes.
Rett syndrome is a neurodevelopmental disease affecting girls. The cause is not known. Roles for trophic factors and excitatory neurotransmitters have been postulated. To study the significance of excitatory amino acids in Rett syndrome, we determined glutamate and aspartate concentrations in the cerebrospinal fluid from 11 girls with Rett syndrome (age 8 years 4 months +/- 5.7 years, mean +/- SD) and 11 controls (age 7 +/- 4.2 years). In the patients with Rett syndrome, the mean of cerebrospinal fluid glutamate concentration was 355.2 nmol/L (SD +/- 109.2 nmol/L). In the controls it was 203.9 nmol/L (SD +/- 55.5 nmol/L). In Rett syndrome cases, cerebrospinal fluid glutamate concentrations were significantly higher (P = 0.0006) than in the controls. In the Rett syndrome group, the mean cerebrospinal fluid aspartate concentration was 119.4 nmol/L (SD +/- 43.5 nmol/L). In the control group, it was 90.9 nmol/L (SD +/- 20.9 nmol/L). The difference between the cerebrospinal fluid aspartate values was not significant. Glutamate may therefore play an important role in the primary pathogenesis in Rett syndrome. Further investigations are needed, with recognition of possible actions of neuronal growth factors and excitatory neurotransmitters in the damage mechanisms of Rett syndrome.
An abnormally low level of cystatin C in the cerebrospinal fluid is a diagnostic marker for the hereditary form of brain hemorrhage associated with amyloidosis that was first identified in Iceland. We developed an assay for cystatin C to use in the diagnosis of patients with cerebral amyloid angiopathy and brain hemorrhage. This test consists of a sandwich enzyme-linked immunosorbent assay using monoclonal mouse anticystatin C and polyclonal rabbit anticystatin C antibodies. The cystatin C level was assayed in cerebrospinal fluid samples from 29 patients with brain hemorrhage and 45 control patients with other neurological diseases. Fifteen patients with brain hemorrhage showed low cystatin C levels (less than or equal to 70 ng/ml) in a clinical setting in which the positive and negative findings were compatible with a diagnosis of cerebral amyloid angiopathy. Immunohistological examination of brain tissue obtained by biopsy from two of the 15 patients confirmed the diagnosis of cerebral amyloid angiopathy and identified the deposition of cystatin C and beta-protein. This enzyme-linked immunosorbent assay is simple to perform and may be useful for investigating patients suspected of having cerebral amyloid angiopathy with brain hemorrhage and the deposition of cystatin C.
Indole-3-acetic acid has been identified in human cerebrospinal fluid by the gas chromatographic-mass spectrometric technique called mass fragmentography. A specific and sensitive method for quantitative determination of indole-3-acetic acid down to 2 nanograms per milliliter of cerebrospinal fluid has been developed. Samples of cerebrospinal fluid from 24 patients with depression contained 6.1 +/- 3.1 (range 2.6 to 15.8) nanograms of indole-3-acetic acid per milliliter.
OBJECTIVE AND IMPORTANCE: Four cases of spontaneous cerebrospinal fluid rhinorrhea caused by communication between the subarachnoid space of the middle cranial fossa and a lateral extension of the sphenoid sinus are presented. The cause and management of this unique type of cranial base defect are discussed. CLINICAL PRESENTATION: During the past 10 years, four patients referred to our institution with atraumatic cerebrospinal fluid fistulae were observed to have temporal encephaloceles (encephalomeningoceles) traversing the floor of the middle cranial fossa. Three of the patients had previously undergone unsuccessful transnasal attempts to repair their fistulae by obliteration of the sphenoid sinus. The fourth patient presented before undergoing any treatment. No patient had associated hydrocephalus or tumor. Preoperative computed tomographic cisternograms revealed that all fistulae involved a lateral extension of the sphenoid sinus into the floor of the middle cranial fossa. INTERVENTION: After definitive localization, each patient was operated on transcranially through an anterior middle cranial fossa approach with extradural and/or intradural exploration. The associated temporal encephalocele was amputated or disconnected, and the dehiscent dura and middle cranial fossa floor defect were oversewn and packed with autogenous tissue, respectively. CONCLUSION: The surgical treatment of cerebrospinal fluid rhinorrhea secondary to middle fossa encephalocele associated with lateral extension of the sphenoidal sinus differs from the surgical strategy for more medial sphenoidal fistulae. Fistulae involving a lateral extension of the sphenoid sinus require a transcranial approach for direct visualization and obliteration of the defect, whereas fistulae involving the central portion of the sinus may be successfully obliterated transsphenoidally.
The aim of the present study was to define lipoprotein complexes within cerebrospinal fluid (CSF) in terms of their apolipoprotein composition, using fractionation procedures considered optimal for maintaining lipoprotein structural integrity. Five apolipoproteins were identified, namely apolipoproteins A-I, A-IV, D, E and J. These were differentially distributed amongst lipoprotein particles of which three major subpopulations were identified. CSF-LpAI (20.1 +/- 3.8 nm) was enriched in apolipoprotein A-I and contained the major proportion (> 50%) of apolipoproteins D, E and J. CSF-LpE, of similar size to CSF-LpAI (20.2 +/- 3.1 nm), was composed principally of apolipoprotein E, with minor quantities of apolipoproteins A-I, A-IV, D and J. Elimination of these particles from cerebrospinal fluid by immunoabsorption revealed a third subpopulation of significantly greater diameter (32.0 +/- 6.8 nm). The majority (62%) of apolipoprotein A-IV was also present in this fraction. The study demonstrates the structural and size heterogeneity of lipoproteins in cerebrospinal fluid. This may reflect the lipid transport processes within the central nervous system.
The polyacrylamide disc electrophoresis technique has been applied to the fractionation of ;native' cerebrospinal fluid. Evidence is presented to show that there is an alteration in the protein profile if the fluid is subjected to a concentration stage. A minimum of 22 distinct protein zones have been detected in fluids from patients without structural changes in the nervous system. The method has also been applied to pathological fluids and the differences are discussed.
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1. With the exception of Na, K and Cl clear cerebrospinal fluid (c.s.f.) obtained from chickens varying in age from 6 weeks to 2 years did not reveal significant alterations in composition as could be related to age per se.2. Considerably higher levels of total protein and glucose are found in chicken c.s.f. than are found in mammalian fluid; slightly more chloride is found in chicken than most mammalian c.s.f.'s.3. Intravenous beef insulin depressed chicken cerebrospinal fluid glucose levels; insulin placed intracisternally had no effect on the avian glycogen body glycogen content indicating that c.s.f. glucose constancy, with or without glycogen body assistance, is not responsible for the resistance of the chicken to pharmacological doses of insulin.4. Bovine insulin injected into the cisterna magna of chickens depresses plasma glucose partially by acting over vagal pathways to release endogenous insulin and partially by diffusion across the c.s.f.-blood barrier to exert a peripheral effect.
The lactate, lysozyme, C-reactive protein and serum amyloid-A protein concentrations in cerebrospinal fluid were measured in 11 patients with bacterial meningitis, 27 patients with aseptic meningitis and in 31 control patients. The mean concentration of each parameter was significantly higher (p less than or equal to 0.0001) in patients with bacterial meningitis than in those with aseptic meningitis or those without meningitis. The reliability of these tests in the differential diagnosis of bacterial and aseptic meningitis was compared with leucocyte counts in cerebrospinal fluid. Gram staining for bacteria, and protein and glucose levels. The cerebrospinal fluid lactate level proved to be more sensitive than lysozyme. C-reactive protein or serum amyloid-A protein and had a high degree of specificity.
A conventional method of bacteriological examination of removed cerebrospinal fluid shunts was compared with another method which relies on microscopic and cultural examination of intraluminal fluid. Fifty-five shunts were tested. All eight cases of clinical shunt infection gave positive results with the latter method, whereas a further 23 shunts yielded positive cultures by the conventional method in the absence of clinical infection. The consequences of missed infections due to omission of microscopic examination and overdiagnosis using the conventional culture method are discussed.
Adenosine deaminase (ADA) was estimated in 84 pleural, 140 peritoneal and 136 cerebrospinal fluids to study its diagnostic usefulness as a routine test for tuberculosis. The sensitivity, specificity, positive and negative predictive values for diagnosing tuberculosis in pleural fluids (ADA > 30 U/l) was 67, 92, 78 and 87 per cent respectively, in peritoneal fluids (ADA > 15 U/1) it was 89, 81, 25 and 99 per cent respectively and in cerebrospinal fluids (ADA > 10 U/l) it was 50, 90 21 and 97 per cent respectively. The differences in mean ADA levels between tuberculous (28.0 and 19.5 U/1) and non-tuberculous (9.7 and 4.8 U/1) peritoneal and cerebrospinal fluids although statistically significant (P < 0.001), were of no practical clinical value. A wide scatter in ADA values was seen in both tuberculous and non-tuberculous fluids. ADA estimation in plasma, lymphocytes and cell fractions of fluids was also not diagnostically useful nor did it throw light on the source of elevated ADA in fluids.
Drainage of the cerebrospinal fluid through the olfactory nerves into the nasal lymphatics has been suggested repeatedly. To investigate precisely the morphology of this pathway, India ink was injected into the subarachnoidal space of the rat brain, and samples including the olfactory bulbs, olfactory tracts and the nasal mucosa were observed by light and electron microscopy. Under the dissecting microscope, ink particles were found within the subarachnoid space and along the olfactory nerves. At the nasal mucosa, a lymphatic network stained in black was identified near the olfactory nerves, which finally emptied into the superficial and deep cervical lymph nodes. Light microscopically, ink particles were found in the subarachnoid space, partially distributed around the olfactory nerves and within the lymphatic vessels. By electron microscopy, the subarachnoid space often formed a pocket-like space in the entrance of the fila olfactoria. The olfactory nerves were partially surrounded by ink particles within the space between perineurial cells and epineurial fibroblasts. At the nasal mucosa, the lymphatics were frequently located close to the nerves. These results indicate that the cerebrospinal fluid drains from the subarachnoid space along the olfactory nerves to the nasal lymphatics, which in turn, empties into the cervical lymph nodes. This anatomical communication, thus, allows the central nervous system to connect with the lymphatic system. The presence of this route may play an important role in the movement of antigens from the subarachnoidal space to the extracranial lymphatic vessels, resulting in inducement of an immune response of the central nervous system.
Human arachnoid villi were studied ultrastructurally to clarify the mechanism of cerebrospinal fluid absorption. Arachnoid villi of humans showed quite different features from those of animals. The former were not always invested with endothelial linings as previously reported in the latter. Instead, there was a covering layer of arachnoid cells which consisted of both an electron-lucent outer zone and an electron-dense inner zone. The outer zone had less cytoplasmic filaments and desmosomes than the inner zone. The inner zone was basically indistinguishable from the arachnoid membrane and had numerous cytoplasmic filaments and a series of desmosomes. Often, the covering layer was further encompassed by the thin fibrous capsule which reflected from the dura mater or sinus wall. Both the outer and inner zones were characterized by numerous extracellular cisterns which appeared, electron-optically, to be empty or contain a little 'fuzzy' material. In the villi affected by subarachnoid hemorrhage, extracellular cisterns were distended by intact of disintegrating erythrocytes which appeared to be natural tracers of cerebrospinal fluid. The size of these cisterns measured approximately 10 microns in the maximum diameter. It is suggested that extracellular cisterns may contribute to the bulk outflow of cerebrospinal fluid.
We evaluated the usefulness of the test tape for cerebrospinal fluid (CSF), with which glucose and protein were examined, in aid of rapid diagnosis of various neurological diseases. Twenty-eight patients were examined to estimate the level of CSF glucose and protein using test tape. The data accuracy was confirmed with the data from standard measurements because the data from test tape correlated significantly with the data measured by standard method (glucose, p < 0.05; protein, p < 0.01). The test tape is useful for the rapid examination of CSF. We hope that more accurate test tape method will be developed for CSF glucose and protein determination.
Multiple sclerosis is an uncommon demyelinating condition in Singapore. The commonest mode of presentation here is in the form of Devic's syndrome. Although our patients here have shown classical findings with respect to clinical features, neuroimaging studies and electrophysiologic tests, abnormal cerebrospinal fluid changes have not been reported locally. We report the first case of multiple sclerosis with abnormal cerebrospinal fluid changes. We also reviewed cerebrospinal fluid changes in multiple sclerosis and recent advances in laboratory techniques of cerebrospinal fluid analyses.