Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CEREBROSPINAL FLUID”

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.

At least 685 records · Page 38Linked to original sources
PubMed2003

Evaluation of ventriculo-cisternal perfusion model as a method to study cerebrospinal fluid formation.

AIM: To evaluate ventriculo-cisternal perfusion as a method for measuring cerebrospinal fluid formation rate, calculated by means of the Heisey et al equation. Method. All experiments were carried out on anesthetized domestic cats fixed in the sphinx position in a stereotaxic frame. Ventriculo-cisternal perfusion was used at an intracranial pressure of -10 cm H2O at different perfusion rates (32.0, 65.5, 125.0, and 252.0 microL/min). Dextran blue was applied as an indicator substance and the concentration of the indicator was measured with a spectrophotometer at a wavelength of 635 nm. Cerebrospinal fluid formation rate was calculated with the equation of Heisey et al. Results. The indicator substance was less diluted at a higher perfusion rate, and the calculated cerebrospinal fluid formation rate was lower. The increase in perfusion rate from 65.5 to 125.0 to 252.0 microL/min increased the concentration of indicator substance from 0.75 to 0.89 to 0.97 mg/mL and decreased calculated cerebrospinal fluid formation rate from 21.8 to 15.4 to 7.8 microL/min. This reduction was linear and an increase in the perfusion rate by 1.0 microL/min decreased the cerebrospinal formation rate by 0.05 microL/min. Conclusion. The calculated cerebrospinal fluid formation rate depends on different perfusion rates. The increase in the perfusion rate diminishes the calculated formation rate. Ventriculo-cisternal perfusion may not be a suitable method to calculate the cerebrospinal fluid formation rate according to the equation of Heisey et al.

Animals↗
PubMed1985

24-hour cerebrospinal fluid levels of vasopressin in hydrocephalic patients.

The variation in vasopressin concentrations of ventricular cerebrospinal fluid and plasma throughout a 24-h period was studied in 10 patients with hydrocephalus. In 6 control patients, the diurnal variation in plasma vasopressin concentrations was studied. Vasopressin concentrations were determined by radioimmunoassay in plasma and in extracted and unextracted cerebrospinal fluid. Cortisol and osmolality in plasma were also measured. Vasopressin concentrations measured in extracted cerebrospinal fluid showed only small intra- and interindividual variation, while the corresponding values for unextracted cerebrospinal fluid were 2-5-fold higher and showed more variation. Plasma vasopressin concentrations varied considerably throughout the 24-h period in the individual hydrocephalic patient and between the patients. The pattern of variation was inconstant with no circadian rhythm, and the variation was not related to any changes in plasma osmolality, blood pressure or intracranial pressure. In some of the patients, the normal diurnal pattern of variation in plasma cortisol was broken, however, without a relation to the observed fluctuations in vasopressin concentrations. The abnormal variation of plasma vasopressin and cortisol was considered to reflect stress in connection with the intracranial pressure monitoring procedure. In the control patients, plasma vasopressin showed only small variations and plasma cortisol showed a normal diurnal rhythm. It is concluded that cerebrospinal fluid vasopressin concentration in patients with hydrocephalus is very constant throughout the day, even when plasma vasopressin concentrations show marked episodic increases. Thus, a circadian rhythm in the cerebrospinal fluid vasopressin concentration, as reported in several animal species, could not be confirmed in these patients.

Adult↗
PubMed1986

Peripheral sympathectomy and adrenal medullectomy do not alter cerebrospinal fluid norepinephrine.

Despite a blood-brain barrier for norepinephrine, the concentration of norepinephrine in plasma and cerebrospinal fluid has been observed to be similar. This relationship between plasma and cerebrospinal fluid norepinephrine levels suggest that peripheral sympathetic neurons innervating blood vessels to brain and spinal cord may contribute significantly to cerebrospinal fluid norepinephrine levels, and questions the validity of cerebrospinal fluid norepinephrine as an index of central nervous system noradrenergic activity. We demonstrate that extensive destruction of the peripheral sympathetic nervous system and the adrenal medulla has no effect on rat cerebrospinal fluid norepinephrine. It is therefore unlikely that peripheral sources of norepinephrine contribute significantly to cerebrospinal fluid norepinephrine levels.

Adrenal Glands↗
PubMed1994

Cerebral blood flow and effects of cerebrospinal fluid on calcium transport in patients with cerebral infarction.

BACKGROUND AND PURPOSE: In this study we investigated whether cerebrospinal fluid in patients with brain infarction possesses an activity that contributes to the evolution of brain ischemia. As a test, the effect of cerebrospinal fluid on Ca2+ influx into the intracellular space was chosen because this process is a mechanism for vasospasm, platelet aggregation as thrombi, and neuron damage. METHODS: Effects of cerebrospinal fluid taken from 48 patients with cerebral hemispheric infarction on the concentration of cytosolic free Ca2+ in platelets were studied using the fluorescent probe quin-2. Hemispheric cerebral blood flow was measured using 133Xe intravenous injection. RESULTS: Cerebrospinal fluid in 19 of 48 patients with cerebral hemispheric infarction increased the level of cytosolic free Ca2+ in platelets. The course of the disease in the patients who showed a positive effect of cerebrospinal fluid on Ca2+, when compared with that of patients who showed a negative effect, was characterized by a more severe clinical manifestation and mortality. The decrease in hemispheric cerebral blood flow was more marked in both ischemic and contralateral hemispheres in patients with positive effects of cerebrospinal fluid on the level of Ca2+. CONCLUSIONS: These data suggest that the ability of cerebrospinal fluid to evoke Ca2+ influx into the intracellular space in patients with brain infarction is a factor that aggravates ischemic brain damage.

Biological Transport↗
PubMed1993

Vasopressin in cerebrospinal fluid of newborns with hypoxic-ischemic encephalopathy. Preliminary report.

Vasopressin in cerebrospinal fluid has been measured in 27 fullterm newborns with hypoxic-ischemic encephalopathy. These newborns were divided into three groups according to the degree of neurological involvement, and they have been compared with a control group of 10 newborns. Determinations of vasopressin in cerebrospinal fluid and plasma were done by RIA. The cerebrospinal fluid vasopressin in asphyxiated newborns was higher than in the control group (p < 0.001); the mean concentration in the group of newborns classified as moderate or severe hypoxic-ischemic encephalopathy was higher than in the control group (18.7 pg/ml vs 4.66 pg/ml), and also higher than in the group classified as mild (14.2 pg/ml). Cerebrospinal fluid vasopressin values have a direct relationship to the plasmatic values at 12 hours of life (r = 0.76; p < 0.001). We concluded that vasopressin values in cerebrospinal fluid at 12 hours increase according to the clinical severity of the neonatal hypoxic-ischemic encephalopathy and that they have a strong relationship with plasmatic vasopressin.

Asphyxia Neonatorum↗
PubMed1985

Cytopathogenic cerebrospinal fluid from neurological and psychiatric patients.

Cerebrospinal fluids (CSFs) were examined for the presence of a cytopathogenic component by an in vitro assay. No abnormal proteins were detected in CSF which produced cytopathic effects. The cytopathic effect was associated with high-molecular-weight material which was resistant to enzyme treatment. The effect persisted after extensive ultraviolet irradiation. The presence of the cytopathic effect was associated with increased CSF enolase levels.

Cells, Cultured↗
PubMedDate not supplied

[Studies of alanine and aspartate transaminases, lactate dehydrogenase and phosphocreatine kinase levels in the cerebrospinal fluid and serum in multiple sclerosis].

In the cerebrospinal fluid and serum the activity was determined of phosphocreatine kinase (CPK), lactic dehydrogenase (LDH), aspartate transaminase (AspAT) and alanine transaminase (AlAT) in 107 cases of multiple sclerosis. The results were compared with those in a control group of neurosis and a highly significant (three times) increase was observed in the activity of CPK and LDH in the cerebrospinal fluid as a result of organic damage to the brain tissue. By chromatographic method direct data were obtained indicating that increased CPK activity in the cerebrospinal fluid was connected with the CK-BB isoenzyme, that is with the cerebral fraction of the enzyme.

Adult↗
PubMed1990

[Typical CT findings with the intrathecal infusion test in post-traumatic disorders of cerebrospinal fluid dynamics].

Simultaneous computer tomographic and cerebrospinal fluid dynamics examinations in patients with high-pressure hydrocephalus, normal pressure hydrocephalus and cerebral atrophic processes are presented and discussed. Exclusive CT and MR examinations do not allow a differentiation of patients with normal pressure hydrocephalus and patients with cerebral atrophy. In the simultaneous examinations the morphological substrate during the intrathecal infusion test is represented.

Adult↗
PubMed2004

Cerebrospinal fluid biomarkers in experimental spinal nerve root injury.

STUDY DESIGN: Cerebrospinal fluid biomarkers were evaluated in a setup using established pig models to mimic clinical disc herniation. OBJECTIVES: To investigate biomarkers for nerve tissue injury, inflammation, and pain in cerebrospinal fluid after mechanical compression and/or nucleus pulposus application to spinal nerve roots. SUMMARY OF BACKGROUND DATA: The association between mechanical compression, biochemical effects of nucleus pulposus, and nerve root injury in degenerative disc disorders is incompletely investigated. METHODS: The unilateral S1 nerve root was exposed in 20 pigs. The animals were divided into four groups (n = 5 each): 1) slow-onset mechanical compression with an ameroid constrictor; 2) autologous nucleus pulposus application; 3) mechanical compression plus nucleus pulposus; and 4) sham operation. After 1 week, 6 mL of cerebrospinal fluid was collected, and four structural nerve proteins, neurofilaments, S-100, glial fibrillary acidic protein, neuron-specific enolase, the proinflammatory cytokine interleukin-8, the neurotransmitter nociceptin, and substance P endopeptidase activity were analyzed using immunoassays. RESULTS: The concentration of neurofilament was increased in the mechanical compression group (17.0 microg/L +/- 5.0) and in the mechanical compression plus nucleus pulposus group (19.8 +/- 12.1 microg/L) compared with the sham group (0.9 +/- 0.9 microg/L) and the nucleus pulposus group (0.4 +/- 0.1 microg/L) (P < 0.01 for both). The concentration of nociceptin was increased significantly in the mechanical compression group (24.0 +/- 8.6 fm/mL) and in the mechanical compression plus nucleus pulposus group (31.2 +/- 6.6 fm/mL) compared with the sham group (7.0 +/- 1.3 fm/mL) (P < 0.05 and P < 0.01, respectively). A correlation was found between concentrations of neurofilament and nociceptin (r = 0.50, P < 0.05). There were no intergroup differences regarding glial fibrillary acidic protein, neuron-specific enolase, S-100, interleukin-8, or substance P endopeptidase activity. CONCLUSIONS: The present study demonstrates increased concentrations of neurofilament and nociceptin in cerebrospinal fluid after nerve root compression. A simultaneous application of nucleus pulposus did not increase the response.

Animals↗
PubMed2003

Elevated cerebrospinal fluid levels of glutamate in children with bacterial meningitis as a predictor of the development of seizures or other adverse outcomes.

OBJECTIVE: Evaluation of elevated cerebrospinal fluid levels of glutamate in children with bacterial meningitis as a predictor of seizures or other adverse outcomes. DESIGN: Prospective cohort study with controls. SETTING: A 36-bed pediatric intensive care unit and primary pediatric referral center. PATIENTS: From 1999 to 2001, a total of 55 patients, between the ages of 0 and 18 yrs, with lumbar punctures performed for suspected meningitis. MEASUREMENTS AND MAIN RESULTS: A total of 23 patients had bacterial meningitis confirmed by cerebrospinal fluid/blood culture and elevated cerebrospinal fluid white blood cell counts, and 32 patients, who tested negative, were included as controls. The median age for the patients with meningitis was 1.0 yr (range, 0.0-15.2 yrs), and in the culture-negative group (control group), the median age was 0.3 yrs (range, 0.0-17.0 yrs). The average cerebrospinal fluid white blood cell count was 2707 +/- 3897 in the group with bacterial infection, whereas in the control group, the average was 148 +/- 259 (p < .01). Patients with bacterial meningitis had a mean cerebrospinal fluid glutamate level of 60.5 +/- 88.4 mol/L, whereas the mean cerebrospinal fluid glutamate level in the control group was 4.9 +/- 11.0 mol/L (p < .01). However, only 10 of 23 children with bacterial meningitis had a second lumbar puncture performed during the study. There was no correlation between the cerebrospinal fluid white blood cell count and cerebrospinal fluid glutamate levels in either the study or control patients. None of the control patients developed seizures or neurologic deficits, despite some patients having elevated glutamate levels. However, four patients with bacterial meningitis developed seizures after admission to the hospital, and ten were discharged with at least some neurologic sequelae attributable to their infection. Two out of the three who developed seizures and had a repeat lumbar puncture demonstrated persistent elevation of cerebrospinal fluid glutamate levels. In addition, 70% of patients (7 of 10) with Streptococcus pneumoniae meningitis developed neurologic complications (p = .04). CONCLUSIONS: Bacterial meningitis in children causes an increase in cerebrospinal fluid glutamate that in many cases persists over time. However, in this limited study, neither higher nor persistent elevation of cerebrospinal fluid glutamate levels is predictive of which patients might develop seizures or other apparent immediate adverse outcomes after invasive infection. The responsible organism seems to have far more significance in predicting the development of adverse sequelae.

Adolescent↗
PubMed1991

Cerebrospinal fluid leaks and meningitis in acoustic neuroma surgery.

Cerebrospinal fluid leaks and associated meningitis are the most common life-threatening complications of surgery for acoustic neuromas. This retrospective study reviews 319 patients who had surgery for 321 acoustic tumors at the Sunnybrook Health Sciences Center, University of Toronto, from April 1975 to March 1990. Cerebrospinal fluid leaks occurred after 13.4% of primary tumor operations. Surgical repair was required in 6.2% of all patients; 4.4% needed more than one operation. Meningitis occurred in 5.3% of all patients. These complications were more common in larger tumors and after the combined translabyrinthine middle fossa approach. Transnasopharyngeal eustachian tube obliteration was used to stop recurrent cerebrospinal fluid leaks in two patients.

Adolescent↗
PubMed1981

[Myelopathies: behavior of cerebrospinal fluid cells and proteins].

Data on cerebrospinal fluid (CSF) cells and proteins (total proteins and gamma globulins content) are reviewed in 287 patients with myelopathies. Clinical data on these patients were reported. Results obtained are distributed according to diagnoses and to time of disease (tables 1 and 2). Informations obtained through the study show that signalization of CSF system is related to the episode responsible by the disease, when the episode is singular. Repeated episodes or a progressive evolution are more apt to produce a maintained signalization of CSF cyto-protein dual. In this way data on infectious myelopathies, multiple sclerosis and neuromyelitis optica are compared to those found in post-vaccination, post-infection and post-intoxication myelopathies, as well as to those found in B-12 deficiency and myelopathies of vascular origin. Primary myelitis are evaluated in report to this comparison. It is shown that changes in the CSF cyto-protein dual are more related to those found in multiple sclerosis and neuromyelitis optica when chronic primary myelitis is considered. In acute and sub-acute primary myelitis they are related to those found in post-vaccination, post-infection and post-intoxication myelopathies.

Cerebrospinal Fluid↗
PubMed1996

Spontaneous spinal cerebrospinal fluid leaks and intracranial hypotension.

Spinal cerebrospinal fluid (CSF) leaks are often implicated as the cause of the syndrome of spontaneous intracranial hypotension, but they have rarely been demonstrated radiographically or surgically. The authors reviewed their experience with documented cases of spinal CSF leaks of spontaneous onset in 11 patients including their surgical observations in four of the patients. The mean age of the six women and five men included in the study was 38 years (range 22-51 years). All patients presented with a postural headache; however, most had additional symptoms, including nausea, emesis, sixth cranial-nerve paresis, or local back pain at the level of the CSF leak. All patients underwent indium-111 radionucleotide cisternography or computerized tomographic (CT) myelography. The location of the spontaneous CSF leak was in the cervical spine in two patients, the cervicothoracic junction in three patients, the thoracic spine in five patients, and the lumbar spine in one patient. The false negative rate for radionucleotide cisternography was high (30%). Subdural fluid collections, meningeal enhancement, and downward displacement of the cerebellum, resembling a Chiari I malformation, were commonly found on cranial imaging studies. In most patients, the symptoms resolved in response to supportive measures or an epidural blood patch. Leaking meningeal diverticula were found to be the cause of the CSF leak in four patients who underwent surgery. In three patients these diverticula could be ligated with good result but in one patient an extensive complex of meningeal diverticula was found to be inoperable. Two patients had an unusual body habitus and joint hypermobility, and two other patients had suffered a spontaneous retinal detachment at a young age. In conclusion, spontaneous spinal CSF leaks are uncommon, but they are increasingly recognized as a cause of spontaneous intracranial hypotension. Most spinal CSF leaks are located at the cervicothoracic junction or in the thoracic spine, and they may be associated with meningeal diverticula. The radiographic study of choice is CT myelography. The disease is usually self-limiting, but in selected cases our experience with surgical ligation of leaking meningeal diverticula has been satisfactory. An underlying connective tissue disorder may be present in some patients with a spontaneous spinal CSF leak.

Adult↗
PubMedDate not supplied

[Disorders of acid-base equilibrium in the cerebrospinal fluid after intracranial operations].

The authors collected 27 patients after intracranial operations in whom the cerebrospinal fluid was investigated at least 3 times during 10 days. The patients were divided into 2 groups--a group of 16 patients with favourable outcome, and a group of 11 patients who died. On the basis of arithmetical means of pCO2 and HCO3 values hypothetical curves of the course of acid-base equilibrium in the blood and cerebrospinal fluid were plotted in both groups during 10 days. In the initial period metabolic acidosis was found in the cerebrospinal fluid and respiratory alkalosis in the blood in both groups. After several days metabolic alkalosis developed in the group of patients with favourable outcome while the metabolic acidosis in the cerebrospinal fluid was balanced. In the group with unfavourable outcome metabolic alkalosis in the blood was less evident and metabolic acidosis in the cerebrospinal fluid was increased. The authors think that metabolic alkalosis in the blood has a compensatory effect on metabolic acidosis in the cerebrospinal fluid and brain.

Acid-Base Equilibrium↗
PubMed1979

[Cerebrospinal fluid in cysticercosis of the brain].

Cerebrospinal fluid (CSF) changes in brain cysticercosis have long been known. Its characteristic features are a mild or moderate pleocytosis with eosinophils, a slight or moderate protein increase with an elevated gammaglobulin concentration, and a positive complement fixation test. Unfortunately all these abnormalities are not always present together and difficulties may be encountered in the diagnosis. This paper presents a study based on the experience acquired in the CSF Laboratory of the Neurological Department of Escola Paulista de Medicina (São Paulo, Brasil) after 35 years' work, and 120.000 CSF specimens examined. The material consists of 147 cases of brain cysticercosis confirmed by necropsy, surgery, subcutaneous or intraocular cysticercus, x ray of the skull, and of 509 clinical observation with suggestive CSF changes. It is the purpose of this paper to appreciate the importance of each of the CSF tests and to observe the CSF abnormalities during the course of this disease. The results of the study of the 79 cases varified by necropsy or surgery showed that the characteristic CSF changes that make the diagnosis of brain cysticercosis were observed in 54 percent of the cases. The eosinophils were present in 82 percent, protein changes in 78 percent, complement fixation test in 70 per cent, hypertension in 55 per cent, and decreased sugar content in 27 per cent of the cases. In two cases the CSF was normal. As the eosinophils and the protein abnormalities may be seen in several other diseases, the complement fixation test for cysticercus should be regarded as the most important CSF test in the diagnosis of brain cysticercosis. The successive CSF specimens withdrawn of 40 patients during the course of this disease have shown that the abnormalities went on for 4 to 18 years observation, suggesting that the parasites were alive. On the contrary, in 11 other cases it was varified the final CSF normalization after 5 to 14 years, suggesting that the parasites were dead. The CSF was normal in 31 out of 42 patients with opaque nodules visible in skull films (calcified cysticercus). In the remaining 11 cases, the characteristic CSF findings were observed in 3, but in 8 cases the only abnormalities were positive complement fixation test or eosinophils. In 14 out of 26 patients with subcutaneous or introacular cysticercus there were the usual CSF changes but in the other remaining cases the CSF was normal. The absence of treatment for brain cysticercosis is consistent with the persistence of CSF abnormalities in the specimens examined during the course of this disease. This calls for an integrated prophylactic to all Latin-American countries in order to exterminate this serious disease for the well-being of the next generation.

Brain Diseases↗
PubMed1990

Cerebrospinal fluid values in the very low birth weight infant.

The cerebrospinal fluid values obtained in the first 12 weeks of life from 43 infants with birth weights of 1500 gm or less were analyzed to determine the ranges for leukocyte count and chemistry values. All these neonates had birth weights appropriate for gestational age, negative cerebrospinal fluid culture for bacteria, and no evidence of intracranial bleeding by head ultrasound examination. The mean birth weight was 1002 gm (range 550 to 1500 gm), and mean gestational age was 27 weeks (range 24 to 33 weeks). The mean cerebrospinal fluid leukocyte count was 5 cells/mm3 (range 0 to 44 cells/mm3); leukocyte differential was 7% polymorphonuclear leukocytes (range up to 66%) and 85% mononuclear leukocytes (range 13% to 100%). Additional values included protein concentration, 142 mg/dl (range 45 to 370 mg/dl); and glucose, 60 mg/dl (range 29 to 217 mg/dl). Knowledge of these measurements should help in the interpretation of the cerebrospinal fluid values of the very low birth weight infant undergoing examination of a central nervous system disorder.

Birth Weight↗
PubMed1992

The effect of chronic and acute changes in plasma composition on vasopressin secretion and cerebrospinal fluid in the rat.

The effects of chronic and acute changes in plasma composition on the osmolality and sodium concentration of cerebrospinal fluid and plasma vasopressin (AVP) concentration have been examined. Chronic elevation of plasma osmolality in three strains of genetically AVP-deficient rats (Brattleboro and New Zealand hypertensive and normotensive Brattleboro) was associated with increased cerebrospinal fluid osmolality by comparison with AVP-replete controls (Long Evans and New Zealand genetically hypertensive and normotensive rats). The linear correlation between plasma and cerebrospinal fluid osmolality did not reflect a similar relationship between plasma and cerebrospinal fluid sodium concentration. Hypertensive animals exhibited a threefold higher plasma AVP concentration in association with significantly elevated cerebrospinal fluid osmolality by comparison with normotensive controls. Although ip hypertonic saline injection elicited parallel increases in plasma and cerebrospinal fluid osmolality and sodium concentration in both hypertensive and normotensive rats, only in the normotensives did this result in an increase in plasma AVP concentration. These results indicate that cerebrospinal fluid is subject to modest chronic and acute changes in osmolality and sodium concentration which may contribute to the osmotic control of AVP secretion. The disturbed control of vasopressin secretion in hypertensive rats may in part be related to the abnormal cerebrospinal fluid composition in these animals.

Animals↗
PubMed1985

Changes in the surface fine structure of ependyma of the rat third ventricle following operative leakage of cerebrospinal fluid.

The role of the ventricular ependyma in the elaboration of cerebrospinal fluid under resting conditions is well documented. In an attempt to elucidate its response to cerebrospinal fluid leakage, male young adult Wistar rats were subjected to lumbar spinal transection under intraperitoneal Nembutal anaesthesia. Control animals received a sham operation, involving opening up the cerebrospinal fluid space and its closure. A scanning electron microscopical study of the third ventricular ependyma on the seventh postoperative day revealed pronounced surface modifications in the experimental animal which included (i) bulbous dilatations in the ciliary shafts with frequent apical blebbing, and an overall turgid appearance of most cilia; (ii) a profusion of tall and stout microvilli in the non-ciliated zones; (iii) an increase in the size and number of blebs; and (iv) a greater number of supraependymal cells especially on the ventricular floor. The significance of these changes is discussed in the light of available studies. The results, considered collectively, seem to reflect an augmented activity of the ventricular ependyma as a compensatory measure to counteract the effects of cerebrospinal fluid leakage caused by surgical trauma. Such activity may be both absorptive and secretory in nature.

Animals↗