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Cerebrospinal fluid pseudocyst of the breast is a rare complication of ventriculoperitoneal shunt placement. Two cases of cerebrospinal pseudocyst of the breast are reported here. The mammography and ultrasound findings in these two cases are described.
The concentration of lead in blood, serum, cerebrospinal fluid, and urine was measured in patients with neurological disease and in control subjects including cases of plumbism. A plot of blood lead versus serum lead resembles the familiar curves of blood lead versus either free erythrocyte porphyrin or urinary delta-aminolaevulinic acid in that serum lead is constant up to a blood lead concentration of 40 micrograms/dl (2 mumol/l) and rises steeply thereafter. The serum lead concentrations yield renal clearances in the range 5-22 ml/min in agreement with values obtained with radiolead on man and predicted from animal studies. The lead content of cerebrospinal fluid is consistently less than that of serum, averaging 50% of the serum concentration for blood leads of less than 20 micrograms/dl (1 mumol/l) but rising to 80-90% in cases of plumbism. Patients with motor neurone disease could not be distinguished from those with other neurological diseases on the basis of the lead content of their serum or cerebrospinal fluid.
STUDY DESIGN: The expression of chondrex (YKL-40, HC gp-39) was measured in the cerebrospinal fluid of from patients with spine diseases. OBJECTIVES: To quantify the levels of chondrex in human cerebrospinal fluid, and to clarify the nature of its expression. SUMMARY OF BACKGROUND DATA: Chondrex is a newly discovered 40-kDa glycoprotein identified originally in the whey secretions of nonlactating cows. It is secreted by a human osteosarcoma cell line, human articular cartilage chondrocytes, and human fibroblasts. However, the function of chondrex in chondrogenesis is unknown, and the expression of chondrex in human cerebrospinal fluid has never been reported. METHODS: The concentration of chondrex in human cerebrospinal fluid was measured by sandwich immunoassay with antihuman chondrex antibodies. Cerebrospinal fluid samples were collected from two groups of patients. Group 1, the control group, consisted of 34 trauma patients. Group 2 consisted of 130 patients with spine diseases: 29 with cervical spondylotic myelopathy, 30 with lumbar disc herniation, 35 with lumbar canal stenosis, and 36 with scoliosis. All values are expressed as the mean +/- standard deviation. RESULTS: The concentration of chondrex in Group 1 (control group) was 113.8 +/- 48.3 ng/mL. The concentrations of chondrex in Group 2 were 245.3 +/- 107.2 ng/mL in cervical myelopathy, 143.2 +/- 53.6 ng/mL in lumbar disc herniation, 241.5 +/- 77.2 ng/mL in lumbar canal stenosis, and 71.4 +/- 33.9 ng/mL in scoliosis. The concentrations of chondrex in cervical myelopathy, lumbar canal stenosis, and lumbar disc herniation were significantly higher than in the control group (P < 0.05). CONCLUSIONS: In this study, the chondrex concentration was high in spine diseases causing spinal stenosis. The authors believe that chondrex is expressed in cerebrospinal fluid as a result of damage or stress to the neural structure, and that it could be a new marker for spine diseases.
BACKGROUND: The attempts to explain the unpredictability of extent of spinal block provided by plain local anesthetic solutions have resulted in many clinical reports; however, causes of this uncertainty are as yet unknown. Recently, normal values of the human cerebrospinal fluid densities have been studied showing important interindividual variations, especially between females and males. The current study was designed to evaluate as primary endpoint the influence of cerebrospinal fluid density values on the extent of spinal block with plain bupivacaine. The ancillary endpoints were search of factors explaining the interindividual differences in cerebrospinal fluid density values reported and determination of the relation between upper extent and regression of spinal anesthesia. METHODS: Sixty-four consecutive patients undergoing peripheral orthopedic surgery with spinal block were enrolled. Spinal anesthesia was performed in the lateral decubitus position with the operated side upward. Two milliliters of cerebrospinal fluid was sampled before injection of 3 ml plain bupivacaine 0.5%. The patient was immediately turned supine and remained in the horizontal position until the end of the study. Maximal sensory block level and time to sensory regression to L4 were determined for each patient enrolled. Cerebrospinal fluid and bupivacaine densities as well as cerebrospinal proteins, glucose, sodium, and chloride concentrations were measured. RESULTS: A highly significant correlation between cerebrospinal fluid density and maximal sensory block level was found (P = 0.0004). However, this correlation was poorly predictive (R(2) = 0.37). Cerebrospinal fluid density, proteins, and glucose concentrations were significantly higher in men than in women: 1.000567 +/- 0.000091 versus 1.000501 +/- 0.000109 g/ml (P = 0.014), 0.46 +/- 0.18 versus 0.32 +/- 0.13 g/l (P = 0.001), and 3.27 +/- 0.7 versus 2.93 +/- 0.5 mM (P = 0.023), respectively. A highly significant (P = 0.0004) and predictive (R(2) = 0.73) inverse correlation was found between maximal upper sensory extent and sensory regression to L4. CONCLUSION: These findings indicate an influence of cerebrospinal fluid density on subarachnoid distribution of 3 ml plain bupivacaine 0.5% and show that with higher cerebrospinal fluid densities, a higher spinal block level can be expected.
Cellular immunocompetence of cerebrospinal fluid lymphocytes was investigated in several neurologic diseases. Microtechniques were developed to enable determination of E-rosetting capacity and phytohemagglutinin responsiveness of scant numbers of cells present in the cerebrospinal fluid specimens studied. Although most individuals had phytohemagglutinin-responsive cells in their CSF, reactivity was somewhat less than that found simultaneously in their blood. Three of eight patients had comparable percentages of E rosettes in their blood and CSF. Int the remainder, the values differed significantly. Although preliminary, these result illustrate a new approach to immunologic characterization of CSF lymphocytes in diseases.
A technique for the measurement of cerebrospinal fluid C4 concentration in unconcentrated specimens has been developed with the methods of electroimmunodiffusion and immunofixation. The method has proved to be reproducible and requires only microliter volumes of undiluted cerebrospinal fluid (CSF). The mean value for CSF C4 concentrations in 16 neurologically normal individuals was 325 +/- 32 mug/100 ml. A positive correlation between CSF C4 concentration and the concentration of CSF albumin and total protein was observed. The positive correlation between the concentrations of CSF C4 and albumin was, however, more clearly defined than the relationship of CSF C4 to total CSF protein.
Plasma and cerebrospinal fluid amino acid values were determined in 29 infants 9 to 30 days of age with a confirmed diagnosis of phenylketonuria. Phenylalanine concentrations in plasma and cerebrospinal fluid were markedly elevated; the degree of elevation in the cerebrospinal fluid had a significant relationship to that of the plasma. The only other significant deviations in the plasma were reductions in the threonine and tyrosine values. Cerebrospinal fluid threonine, alanine, and arginine concentrations were reduced, whereas those of serine, isoleucine, and histidine were elevated. This combined deficiency and excess of amino acids in the central nervous system may have a significant effect on protein synthesis at a time in life when this synthesis and turnover is most active.
Lactate concentrations were determined in the cerebrospinal fluid of patients with purulent, tuberculous and viral meningitis. The control group consisted of 10 patients with meningism (the presence of the meningeal syndrome with a normal cytobiochemical finding of the cerebrospinal fluid). The enzymatic kinetic method of the firm "Behringer" was used. In all the patients with purulent meningitis lactate values were elevated (above 6.2 mmol/l), and the highest values (above 15.0 mmol.l) were found in the patients who also developed respiratory failure. The lactate values in the cerebrospinal fluid of patients with purulent meningitis were higher in statistical significance than in all other examined groups of patients (p less than 0.01). The lactate values were in correlation with the total number of leukocytes (r = 0.78, p less than 0.01) and with the percent of polimorphonuclear leukocytes in the cerebrospinal fluid (r = 0.80, p less than 0.01). Elevated lactate values (above 2.95) were also found in all the patients who had tuberculous meningitis and statistically they differed significantly from the cerebrospinal fluid values of the patients with viral meningitis and meningism (p less than 0.01). There was no difference in the cerebrospinal fluid lactates of patients with viral meningitis and meningism (p greater than 0.05). Elevated lactate values were also found in 2 patients who had paraneoplastic meningitis and in 3 patients with cerebral cysticercosis and hydrocephalus, but without meningitis.(ABSTRACT TRUNCATED AT 250 WORDS)
Plasma and cerebrospinal fluid catecholamines were measured in three patients with multiple sclerosis who had dorsal column stimulators placed at the T5-7 levels. Stimulation for 3 minutes and 20 minutes increased release of plasma norepinephrine, epinephrine, and dopamine, as well as norepinephrine into the cerebrospinal fluid. Neither dopamine nor epinephrine was released into the spinal fluid during or after stimulation. Percutaneous stimulation did not release catecholamines into the plasma or spnal fluid, suggesting that these findings were not simply related to sensory stimulation or stress. Plasma catecholamine levels were inconsistently correlated with pulse rate changes during and after stimulation but not with blood pressure, although the changes in pulse rate and blood pressure were relatively small compared to changes in plasma catecholamines. This study suggests that plasma catecholamines and spinal fluid norepinephrine reflect central activation of sympathetic nervous system pathways and are more reliable indicators of sympathetic activity than changes in cardiovascular function.
Thiobarbituric acid (TBA) reactive substances in serum and cerebrospinal fluid from patients with cerebral apoplexy were determined and their relationship to this disease was studied. TBA reactants in serum were elevated in patients with cerebral apoplexy, but there was no difference between patients with brain tumor or other neurological disease and healthy persons. TBA reactants in cerebrospinal fluid in patients with cerebral aneurysm, cerebral arterial and venous anomalies or intracerebral hematoma, and its levels in patients with cerebral infarction or brain tumor were also higher than in healthy persons. Serum alpha-tocopherol levels were elevated in patients with cerebral infarction, but were relatively low in patients with cerebral aneurysm, cerebral arterial and venous anomalies or intracerebral hematoma. The reverse was the case with cerebrospinal fluid levels of alpha-tocopherol. That is, the sequence of decreasing level of alpha-tocopherol in cerebrospinal fluid was intracerebral hematoma, cerebral aneurysm, cerebral arterial and venous anomalies, and cerebral infarction. The levels of TBA reactive substances in patients with cerebral apoplexy showed a positive correlation between serum and cerebrospinal fluid, and the levels of alpha-tocopherol showed a similar correlation.
OBJECTIVE: Postoperative cerebrospinal fluid leak (CSF) is a serious complication of the cerebellopontine angle surgery. In the current literature, CSF leak rates vary from 8.1 to 20%. The various options in managing this troublesome complication include conservative treatment or invasive surgical repair. The focus of this report is to retrospectively analyze our experience on this specific topic reviewing the incidence of CSF leak and the outcomes of its treatment in a group of patients who underwent surgery for different pathology of the cerebellopontine angle. METHOD: Eighty-five patients who underwent primary surgical procedures performed by a single neurologist were selected for this study. There were 70 surgical removals of acoustic neuromas, and 15 other cerebellopontine lesions. RESULTS: The overall incidence of CSF leak in the total group analyzed was 17.6%. There were five CSF rhinorrheas and 10 wound CSF leaks. Ten acoustic neuromas and five other cerebellopontine angle lesions exhibited this complication. The leak was cured in 53.3% of the cases using a continuous lumbar cerebrospinal fluid drainage (CLCFD). In two patients, the leak was treated with an extradural repair. CONCLUSIONS: Although CLCFD is not routinely used in the treatment of the CSF leak, it proved to be an efficacious and safe option, confirmed by no meningitis observed in our patients treated with this method.
In two cases of cerebrospinal fluid rhinorrhoea in which scinticisternography failed to identify the fistulae, the tracts were demonstrated by positive contrast ventriculography. It is postulated that the fistula communicated with the ventricles but was isolated from the subarachnoid space by adhesions (demonstrated at operation in one case). There was `high pressure rhinorrhoea' in one case. The rhinorrhoea ceased after insertion of ventriculoatrial shunt.
Cerebrospinal fluid (CSF) fistulae can produce leakage through a defect in the bony skull and meninges into the contiguous air-filled cavities at the base of the skull. The major risk is central nervous system infection. When abundant clear rhinorrhea or otorrhea is present, the diagnosis is obvious and imaging is used to localize the fistula. Computed tomography (CT) with millimetric slices and magnetic resonance imaging (MRI) are the most effective diagnostic tools. CT cisternography, an invasive procedure, should only be used when the diagnosis remains uncertain following CT scan and MRI. When CSF leakage is sparse or intermittent, the diagnosis can be made by measuring beta-2 transferrine in the escaping fluid. CT scan followed by MRI are also useful for making the diagnosis and locating the fistula when exterior leakage is absent. CT scan alone is effective for assessing isolated otorrhea. If the diagnosis remains uncertain after all these studies have been used, the patient should be closely followed clinically and isotopic study or surgery should be considered.
We measured 6-mercaptopurine levels in the cerebrospinal fluid and plasma of 15 children undergoing treatment for acute leukemia. Plasma and cerebrospinal fluid samples obtained by lumbar puncture were collected before, during, and after cranial irradiation in order to evaluate a possible change in blood-brain barrier permeability to orally administered 6-mercaptopurine. Considerable interpatient variability has been observed in both plasma and cerebrospinal fluid 6-mercaptopurine levels. No statistical differences in the 6-mercaptopurine cerebrospinal fluid levels under the three different conditions could be detected. Our data suggest that cranial irradiation does not significantly influence the cerebrospinal fluid levels.
Cerebrospinal fluid lipoperoxides, measured as the malondialdehyde-thiobarbituric acid (MDA-TBA) adduct, were quantified by adapting the plasma liquid-chromatographic method of Wong et al. (Clin Chem 1987;33:214-20) to cerebrospinal fluid. Reference values for spinal fluid specimens from 91 adults, ages 17 to 95 y, and 37 children, ages 8 d to 8 y, were determined. Their concentrations were not significantly different (P = 0.222), adults having a mean (and SD) of 0.11 (0.06) mumol and children 0.10 (0.04) mumol of MDA per liter. Their ranges were 0.02-0.26 and 0.04-0.21 mumol of MDA per liter, respectively. We found concentrations in cerebrospinal fluid to be increased in several central nervous system disorders, including seizures, cerebral infarction, alcoholic encephalopathy, and, perhaps, prematurity. The presence of other thiobarbituric acid-reactive substances in cerebrospinal fluid stresses the importance of using highly specific techniques when lipoperoxides are measured in body fluids.
Time and temperature effects on postmortem cerebrospinal fluid samples from 60 adult mongrel dogs were studied. After death the dogs were held at 4, 20, or 37 degrees C for intervals of 3, 6, 12, 24, or 48 h. Antemortem and postmortem cerebrospinal fluid was evaluated for sodium, chloride, potassium, urea nitrogen, glucose, creatinine, calcium, phosphorus, and carbon dioxide. Sodium and urea nitrogen values remained stable. Chloride may be of forensic science value. Low levels of postmortem calcium might indicate antemortem hypocalcemia; high levels of postmortem glucose may indicate antemortem hyperglycemia. Calcium and creatinine levels increased slightly but continually after death; carbon dioxide values dropped.
Cerebrospinal fluid otorhinorrhoea is a well recognized problem. The otolaryngologist has a major role to play in the diagnosis and management of this condition. Five cases are described which illustrate the problems involved; four presented as leaks and one as pneumoencephalus and meningitis. Of the various methods of diagnosis and localization non-invasive techniques, i.e. tomography, CT and flexible endscopy are preferred. The extracranial extradural approach for anterior, middle and posterior fossa leaks allows a direct assault on the fistula. It may be usefully augmented by temporary lumbar drainage.
The effects of sterile meningitis on endothelin-1 (ET-1) and big ET-1 concentrations during hypotension and hypertension were studied in the cerebrospinal fluid and plasma of newborn piglets. Cerebrospinal fluid was obtained via cisterna magna puncture, and blood was obtained from the sagittal sinus vein and left subclavian artery. The study group consisted of 14 newborn piglets injected with 0.5 mL heat-killed group B streptococcus (GBS) (10(9) colony forming unit (cfu) equivalents), into the right cerebral lateral ventricle; the control group consisted of 10 newborn piglets injected with sterile normal saline, in a similar fashion. Hypotension (mean arterial blood pressure (MABP) 20-59 mmHg; 1 mmHg = 133.3 Pa) and hypertension (MABP 110-140 mmHg) were induced 1.5-2 h apart in random sequence in each animal, by inflating balloon-tipped catheters placed at the aortic root and descending aorta, respectively. Cerebral blood flow (CBF) was measured using radiolabeled microspheres, 15 min before and after injection of GBS or saline (normotension), during the hypotension and hypertension episodes, and during recovery normotension, immediately prior to cerebrospinal fluid and blood sampling. ET-1 and big ET-1 concentrations (pg/mL) were measured using radioimmunoassay kits. The combined effect of induced sterile meningitis and induced hypotension resulted in a significant rise in the concentration of cerebrospinal fluid ET-1 (control, 5.1 +/- 0.1; GBS, 9.3 +/- 0.2 pg/mL; p < 0.01), cerebrospinal fluid big ET-1 (control, 0; GBS, 18.1 +/- 2.7 pg/mL; p < 0.01), and sagittal sinus (cerebrovascular) big ET-1 (control, 15.5 +/- 4.2; GBS, 47.5 +/- 9.6 pg/mL; p < 0.01). In contrast, the combined effect of induced sterile meningitis and induced hypertension resulted in a marked elevation in cerebrovascular ET-1 concentrations (control, 9.5 +/- 0.9; GBS, 28.5 +/- 6.1 pg/mL; p < 0.01), with no significant change in cerebrospinal fluid concentrations. In addition, cerebrovascular production of ET-1 increased dramatically during hypertension in the GBS group (control, 0; GBS, 161.7 +/- 13.2 pg.min-1.100 g-1; p < 0.001), and was maintained during the recovery period (133.7 +/- 10.8 pg.min-1.100 g-1). Cerebrovascular ET-1 concentrations correlated significantly with total CBF and MABP in both groups of animals (control, r = 0.49, p < 0.002; GBS, r = 0.64, p < 0.0001), but the response was of a much greater magnitude in the GBS group. There was an inverse relationship between cerebrovascular big ET-1 concentrations and total CBF (r = -0.53, p < 0.0001) and MABP (r = -0.71, p < 0.0001) in the GBS group. In the MABP range of 60-110 mmHg a positive relationship was observed between cerebrovascular ET-1 concentrations and cerebral vascular resistance, in the control group only (r = 0.59, p < 0.002). The combined insult of induced sterile meningitis and induced hypotension or hypertension may be associated with increased cerebrovascular ET-1 and (or) big ET-1 concentrations. Changes in these vasoactive agents may contribute to pressure passivity of CBF in the newborn with meningitis.