What is "spontaneous" cerebrospinal fluid rhinorrhea? Classification of cerebrospinal fluid leaks.
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We have conducted an in vitro coagulation study consisting of two separate groups of 20 subjects using the thrombelastograph. In the first group, haemodilution was performed with a physiological balanced salt solution similar to plasma, with the exception of calcium, and buffered to a normal pH (Plasmalyte B) at 37 degrees C on blood obtained from consenting volunteers. In the second group, a protein-poor body fluid (cerebrospinal fluid (CSF)) obtained from parturient patients undergoing spinal anaesthesia for Caesarean section was used as the diluent. There were statistically significant differences between the warmed Plasmalyte B treated samples and their untreated controls for all variables measured by the thrombelastograph, except for maximum amplitude, and between the CSF treated samples and their untreated controls for all variables. We conclude that electrolyte and acid-base composition of the diluent fluid had no effect on the observation that crystalloid haemodilution produces hypercoagulability. The marked increase in coagulability produced by addition of CSF cannot be explained on a simple haemodilution basis and confirms previous suggestions of the presence of a procoagulant factor in CSF.
In this study the difference between cerebrospinal fluid (CSF) absorption and formation (A -- F) was measured as a function of CSF pressure in the living and dead dog. We determined this relationship between A -- F and CSF pressure during both increasing and decreasing CSF pressures. A hysteresis effect was identified in 78% of living animals, but was not seen in the dead animals. This suggests that the mechanism of CSF absorption in the living dog is nonpassive and pressure-sensitive.
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beta 2-Transferrin, the desialated form of transferrin normally found only in cerebrospinal fluid (CSF) and aqueous and vitreous humor, is detected by high-resolution immunofixation (IFE). It is not normally found in nasal or aural fluids, saliva, tears, or serum. Detection in nasal fluid has been suggested to document CSF leakage into the nose after skull injury. We measured beta 2-transferrin in 48 samples of CSF. IFE of the CSF was performed on high-resolution agarose gels and stained with Coomassie Blue. beta 2-Transferrin was estimated by quantifying the total transferrin by rate nephelometry and then determining the percentage of transferrin in the beta 2 vs beta 1 region by densitometric scanning of the IFE pattern. We accurately quantified as little beta 2-transferrin as 2.5 mg/L in the CSF samples. The beta 2-transferrin fraction was clearly visible by IFE at concentrations less than 2.5 mg/L, but accurate quantification was difficult. In the samples assayed, the range of beta 2-transferrin was 4.6 +/- 1.9 mg/L. Use of this technique to examine rhinorrhea in a motor-vehicle-accident patient confirmed leakage of CSF into the nasal cavity through a vent in the left olfactory groove.
Although it is often claimed that the presence of a single polymorphonuclear leukocyte (PMN) in the cerebrospinal fluid (CSF) is abnormal, recently some have suggested that a few PMNs are occasionally present in cytocentrifuged differential cell counts of normal CSF. We examined 225 consecutive normal CSF specimens to determine how frequently PMNs occur in normal CSF and to identify factors associated with the presence of PMNs. One or more PMNs were present in 73 cases (32%). The number of CSF PMNs was strongly correlated with the degree of CSF blood contamination and the hematologic PMN count. Of the 163 specimens having 25 red blood cells or less per cubic millimeter, only eight (5%) had three or more PMNs, and these outliers had abnormally high hematologic PMN counts. Of the 36 specimens having 100 red blood cells or more per cubic millimeter, 17 (47%) had six or more PMNs. We conclude that the number of PMNs found on cytocentrifuged differential cell counts is highly dependent on the degree of CSF blood contamination and the patient's hematologic PMN count and that even minimal blood contamination can result in the presence of one to two PMNs in normal CSF.
The objective of this study was to determine whether spinal compression associated with degenerative changes of the lumbar vertebral column induces significant alteration in defined cerebrospinal fluid parameters. Serum and lumbar cerebrospinal fluid were studied in 62 patients and 47 age-matched controls. Patients were grouped according to neurologic status, duration of symptoms, and findings in magnetic resonance imaging. Statistically significant elevations in cerebrospinal fluid/serum albumin ratio, acetylcholinesterase, butyrylcholinesterase activity, and total protein concentration were observed in lumbar cerebrospinal fluid of patients. Patients with neurologic deficits did not exhibit significant differences in cerebrospinal fluid parameters compared with patients lacking neurologic signs. No significant differences were detectable between lateral and medial compression. Acute disk herniation led to practically the same biochemical changes as chronic compression. Biochemical analysis of lumbar cerebrospinal fluid offers additional diagnostic information in patients suffering from back or leg pain associated with degenerative changes of the spine. Pathological damage to meningeal and neural tissues can be demonstrated even if neurologic signs or obvious spinal compression are missing in the radiological examination. An elevated cerebrospinal fluid/serum albumin ratio reflects alteration of the blood/cerebrospinal fluid barrier status. Increased acetylcholinesterase and butyrylcholinesterase activity point to pathophysiological impairment of neural tissues or meninges.
Probenecid blocks the active transport from cerebrospinal fluid to blood of homovanillic acid and 5-hydroxyindoleacetic acid, thus increasing cerebrospinal fluid levels of these products of central monoamine metabolism. The half-life in plasma of probenecid given as a single intravenous infusion (40 mg per kilogram of body weight) to patients with either Huntington's chorea or Parkinson's disease averaged about 6.6 hours. In cerebrospinal fluid, peak values for homovanillic acid and 5-hydroxyindoleactic acid occurred in samples collected 8 hours after the 1-hour probenecid infusion was started. Even after 4 hours, however, levels of both monoamine metabolites were significantly increased. There was a positive correlation between cerebrospinal fluid levels of probenecid and the increase in 5-hydroxyindoleacetic acid but not homovanillic acid. Compared with the oral administration of probenecid, the intravenous infusion technique produced more consistent elevations in plasma and cerebrospinal fluid probenecid levels, greater increases in cerebrospinal fluid homovanillic acid values, and fewer gastrointestinal side effects.
Concentration of alpha-2-macroglobulin, albumin, and chymotrypsin inhibitory capacity representing mainly alpha-1-proteinase inhibitor were estimated in cerebrospinal fluid in disorders of the central nervous system. While chymotrypsin inhibitory capacity was elevated in all cases with derangement of the blood-cerebrospinal fluid barrier, in 30% of the cases alpha-2-macroglobulin levels were in the normal range. The difference can be attributed to the much larger size of the latter. Better correlation between albumin concentration and chymotrypsin inhibitory capacity (r = 0.84) than between albumin and alpha-2-macroglobulin (r = 0.62) supports the view that the rate of entry of proteins from blood into cerebrospinal fluid is inversely related to their size.
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Only limited data on cerebrospinal fluid (CSF) HIV-1 RNA responses and markers of local inflammation in CSF during antiretroviral therapy are available. HIV-RNA, soluble tumor necrosis factor (TNF)-receptor (sTNFr)-II, monocyte chemoattractant protein (MCP)-1, and interferon-gamma-inducible protein (IP)-10 were measured in the peripheral blood and CSF of 26 antiretroviral-naive HIV-1-positive patients, who were treated with ritonavir (RTV)/saquinavir (SQV) (n = 5), RTV/SQV/stavudine (d4T; n = 8) or zidovudine (AZT)/lamivudine (3TC)/abacavir/nevirapine/indinavir (n = 13). After 8 to 12 weeks of treatment, CSF HIV-RNA dropped to <400 copies/ml in 1 of 5 patients in the RTV/SQV group, 8 of 8 patients in the RTV/SQV/d4T group, and 9 of 10 patients in the five-drug group. CSF sTNFr-II and IP-10 levels increased in patients with detectable CSF HIV-RNA. However, increases in CSF chemokine and sTNFr-II concentrations were also observed in some patients with good CSF HIV-RNA responses. Moreover, CSF MCP-1 concentrations increased in the whole population after 2 months of treatment. Ongoing residual HIV replication in the central nervous system, which cannot be detected with CSF HIV-RNA measurements, may account for this phenomenon.
The cell and protein content of the cerebrospinal fluid (CSF) and the CSF/serum ratio of glucose, sodium, potassium, calcium, phosphate and chloride were investigated in 71 children without cerebromeningeal illness and aged 0-4 weeks, 5-8 weeks, 3-6 months, 7-12 months, 1-6 years and 7-14 years. The protein content of the CSF was 730 +/- 146 (530-950) mg/l for the age group 0-4 weeks, and 530 +/- 221 (270-950) mg/l for the age group 5-8 weeks. It was significantly higher than for all subsequent age groups. The CSF glucose accounted for 68-82% of the blood glucose. The serum/CSF ratio for sodium ranged from 101 to 104%, for potassium from 55 to 64%, for calcium from 48 to 70%, for phosphate from 24-29%, and for chloride from 106 to 114%. The decrease in serum and CSF potassium and phosphate concentrations from infancy to school age was significant. The greatest difference was evident in the serum/CSF calcium ratio which was significantly higher in the age groups up to 8 weeks than in the subsequent age groups. The electrolyte concentration of CSF with elevated protein and cell values did not differ significantly from CSF of children without cerebromeningeal disorders.
The gamma globulins in cerebrospinal fluid from almost all patients with multiple sclerosis migrate in agarose electrophoresis as abnormal discrete populations, so-called oligoclonal bands. Such bands have also appeared in cerebrospinal fluid from patients with other types of inflammatory pathology such as neurosyphilis, acute idiopathic polyneuropathy, and subacute sclerosing panencephalitis. The demonstration of cerebrospinal fluid oligoclonal bands may aid in the evaluation of patients with early or atypical multiple sclerosis. This report describes a simple method for demonstrating cerebrospinal fluid oligoclonal bands using readily available commercial reagents and apparatus. Oligoclonal bands were seen in cerebrospinal fluid from all patients with clinically definite multiple sclerosis, even though some had normal cerebrospinal fluid gamma globulin levels, and in most patients with presumptive multiple sclerosis or other inflammatory conditions of the nervous system. They were not seen in cerebrospinal fluid of control patients with a variety of other neurologic diseases.
This study was undertaken to determine if a compound which alters the bulk flow of cerebrospinal fluid (CSF) alters the elimination kinetics of a compound in the CSF. Acetazolamide was chosen as the CSF bulk flow-altering agent. It produces a relatively large effect on the flow process, affecting both choroidal and extrachoroidal CSF production, and has been shown to affect CSF flow following iv administration. The compound monitored was nicotine. Acetazolamide was administered orally for one week before and intravenously during the experiment. Nicotine was administered by a bolus injection directly into the CSF via the cisterna magna. The results indicate that the introduction of acetazolamide into the general circulation increases the rate of removal of nicotine from the CSF. Subjects receiving acetazolamide had elevated CSF pressures. The increase in CSF pressure associated with the administration of acetazolamide suggests pressure as a possible factor in the observed increase in the rate of removal of nicotine.