Vascular endothelial growth factor in CSF: a biological marker for carcinomatous meningitis

OBJECTIVE: To determine the value of vascular endothelial growth factor (VEGF) in CSF as a marker for carcinomatous meningitis (CM). METHODS: The concentration of VEGF was measured by ELISA in matched samples of CSF and serum collected from 162 patients. These included patients with solid tumors with CM (n = 11) or brain metastases without concomitant CM (n = 12), paraneoplastic neurologic syndromes (n = 4), viral (n = 15) and bacterial (n = 20) meningitis, and a variety of non-neoplastic and noninfectious neurologic diseases (n = 100). Using CSF/serum albumin ratios, the VEGF index was calculated to estimate the proportion of intrathecally produced VEGF. Immunohistochemical staining for VEGF was performed in a brain metastasis from a mammary carcinoma associated with CM. RESULTS: High VEGF levels (median 6,794.8 pg/mL) were found in CSF of all patients with CM, whereas VEGF levels in matched sera were comparable to other disease groups. In patients with CM, the concentration of VEGF in CSF decreased significantly following antineoplastic treatment. In CSF samples from patients with brain metastases without concomitant CM, VEGF was not detectable. Median VEGF concentration in CSF from patients with acute bacterial meningitis was 38.6 pg/mL, with only 9 of these 17 patients showing detectable VEGF levels in CSF. The VEGF indices in patients with bacterial meningitis were significantly lower than in tumor patients with CM (<22.8 versus >62.3), suggesting that the proportion of intrathecally produced VEGF is much higher in patients with CM as compared with patients with bacterial meningitis. Patients without neoplastic or infectious neurologic disorders consistently showed VEGF levels in CSF below the assay detection limit of 25 pg/mL. Immunohistochemistry revealed strong cytoplasmic staining for VEGF in a metastatic lesion from breast cancer infiltrating the meninges. CONCLUSION: In patients with carcinomatous meningitis, significant amounts of VEGF are released into CSF. This study yields preliminary evidence that VEGF in CSF may be a useful biologic marker for both the diagnosis and evaluation of treatment response in carcinomatous meningitis.     

NF-kappaB activation in cerebrospinal fluid cells from patients with meningitis

We examined whether or not NF-kappaB, a factor that regulates expression of the genes that code for pro-inflammatory cytokines, is activated in cerebrospinal fluid (CSF) cells to investigate the production of pro-inflammatory cytokines by CSF cells in patients with meningitis. Western blotting demonstrated that NF-kappaB was more activated in CSF cells of patients with bacterial meningitis than in those of patients with aseptic meningitis. NF-kappaB was hardly activated in carcinomatous meningitis. The NF-kappaB activation in CSF cells of patients with meningitis tended to be correlated with the CSF interleukin-6 concentration. Our data suggested that CSF cells produce pro-inflammatory cytokines through NF-kappaB activation in meningitis, and that increased NF-kappaB activation in CSF cells indicate infectious meningitis rather than carcinomatous meningitis.     

Sequential analyses of neurobiochemical markers of cerebral damage in cerebrospinal fluid and serum in CNS infections

OBJECTIVE: To elucidate the relation between release patterns and cerebrospinal fluid/serum concentrations of neurobiochemical markers of cerebral damage and their potential value as monitoring parameters in central nervous system infections. METHODS: We investigated protein S-100B and neuron-specific enolase (NSE) in 102 sequential cerebrospinal fluid (CSF)-serum-pairs in patients with bacterial (n = 11) or viral (n = 13) meningitis/meningoencephalitis and neuroborreliosis (n = 8) in comparison with controls (n = 13). RESULTS: Highest S-100B values in CSF and serum were found on admission and showed a significant decrease afterwards. Comparison between disease groups revealed significant differences between bacterial and viral meningitis and neuroborreliosis for S-100B and also when compared with controls. NSE was not significantly elevated. CONCLUSIONS: S-100B is altered in CNS infection but does not provide additional benefit in the differential diagnosis when compared with standard CSF parameters. Nevertheless, S-100B values might be used as an additional monitoring parameter especially when sequential lumbar punctures are contraindicated.     

Soluble CD40 and soluble CD40L concentrations in the serum and the cerebrospinal fluid of patients with tick borne encephalitis and neuroborreliosis

BACKGROUND AND PURPOSE: The interaction between CD40 and CD40L is essential in generating of an immunological response also intrathecally. The aim of the study was estimation of a concentration soluble form of CD40, CD40L (CD154) in the bacterial and viral inflammation of the central nervous system in two compartments - blood circulation and intrathecally, before and after the treatment. MATERIAL AND METHODS: sCD40 and sCD40L were tested twice before and after treatment in pairs serum and CSF of 40 patients treated in the Dept. of Infectious Diseases and Neuroinfections. Patients were divided in two groups: (n=20) patients with tick borne encephalitis (TBE) (group I, n=20) and patients with neuroborreliosis in the form of lymphocytic meningitis (group II, n=20). ELISA assays were performed. RESULTS: Significantly increased concentrations of sCD40, sCD40L in CSF (higher in neuroborreliosis) were measured. We found also an increased concentration of sCD40L in inflammatory CSF in both tested groups (in neuroboreliosis lasting also after 4 weeks of treatment), compared with the control group (below the detection limit in normal CSF). CONCLUSIONS: Results of estimation of the sCD40 and sCD40L concentrations indicate their role in the intrathecal inflammation process of bacterial and viral etiology. The increased serum concentration of sCD40L in TBE and CD40 in neuroborreliosis indicate that peripheral activation of the immunological system persists after cessation of treatment and after the clinical recovery. The defense mechanisms are more pronounced in neuroborreliosis than in tick borne encephalitis.     

Soluble urokinase receptor (uPAR,CD 87) is present in serum and cerebrospinal fluid in patients with neurologic diseases

BACKGROUND: The receptor for urokinase plasminogen activator (uPAR) promotes invasion by neoplastic or inflammatory cells by focusing proteolysis of urokinase to the cell surface. In pathologic conditions, soluble forms of the receptor (suPAR) are released, and activate cell receptors to promote chemotaxis. In the CNS, suPAR and other components of the plasminogen activation system (PAS) could be associated with an increase of the blood-brain barrier (BBB) permeability and subsequent neural damage. OBJECTIVE: To detect suPAR in the serum and cerebrospinal fluid (CSF) of patients with diverse neurologic conditions. PATIENTS AND METHODS: Serum and CSF from 121 patients with cancer, bacterial and viral infection, stroke, demyelinating disease and peripheral neuropathy were examined for the presence of suPAR. RESULTS: suPAR was elevated in the serum of patients with paraneoplastic syndromes, and carcinomatous meningitis and infections, but less in stroke and demyelinating disease patients. CSF suPAR was present in the cancer and CNS infection groups, but not in the other groups. The levels of serum and CSF suPAR were correlated, and CSF suPAR correlated with the albumin index. CONCLUSIONS: suPAR is present in serum and CSF of patients with carcinomatous meningitis, paraneoplastic disorders and bacterial and viral infection of the CNS. suPAR could be associated with BBB disruption and with promotion of CNS invasion by chemotactically active cells, macromolecules, and microbes.     

NF-κB activation in cerebrospinal fluid cells from patients with meningitis

Abstract

We examined whether or not NF-κB, a factor that regulates expression of the genes that code for pro-inflammatory cytokines, is activated in cerebrospinal fluid (CSF) cells to investigate the production of pro-inflammatory cytokines by CSF cells in patients with meningitis. Western blotting demonstrated that NF-κB was more activated in CSF cells of patients with bacterial meningitis than in those of patients with aseptic meningitis. NF-κB was hardly activated in carcinomatous meningitis. The NF-κB activation in CSF cells of patients with meningitis tended to be correlated with the CSF interleukin-6 concentration. Our data suggested that CSF cells produce pro-inflammatory cytokines through NF-κB activation in meningitis, and that increased NF-κB activation in CSF cells indicate infectious meningitis rather than carcinomatous meningitis.     

Role of the urokinase plasminogen activator system in patients with bacterial meningitis

BACKGROUND: The urokinase plasminogen activator system has the potency to promote leukocyte recruitment and blood-CSF barrier breakdown, and thus may play an important pathophysiologic role in bacterial meningitis. METHODS: CSF and serum concentrations of urokinase-plasminogen activator (urokinase [uPA]), uPA receptor (uPAR), and PA inhibitor-1 (PAI-1) were quantified by ELISA in 12 patients with bacterial meningitis, control patients (n = 10) with noninflammatory neurologic diseases, and 10 patients with Guillain-Barré syndrome (GBS), a disease in which blood-CSF barrier disruption occurs without CSF pleocytosis. Casein zymography was used to determine PA-dependent plasminogen activation in the CSF. RESULTS: A marked increase in uPA-dependent plasminogen activation was detected in the CSF of patients with bacterial meningitis vs CSF of patients with GBS and controls. Accordingly, ELISA analysis of CSF revealed intrathecal upregulation of uPA protein in patients with bacterial meningitis. CSF concentrations of uPAR and PAI-1 were also elevated in these patients. The serum of patients with bacterial meningitis showed elevated protein levels of uPA, but not uPAR or PAI-1. Positive correlations were found between blood-CSF barrier breakdown and CSF uPA concentrations, and between CSF pleocytosis and CSF/serum ratios of the potent chemokine uPAR in patients with bacterial meningitis. Furthermore, an adverse clinical outcome in these patients correlated with serum uPA concentrations. CONCLUSION: In bacterial meningitis, the urokinase plasminogen activator system is involved in leukocyte recruitment and breaching of the blood-CSF barrier, and this may contribute to an unfavorable clinical outcome.     

Free amino acid pattern of cerebrospinal fluid in meningeal pathology

Free amino acid concentrations of CSF were measured in bacterial meningitis, aseptic meningitis, meningoradiculitis Garin-Bujadoux-Bannwarth, multiple sclerosis, carcinomatous meningitis, and controls. Almost all CSF amino acids were highly elevated in bacterial but not in aseptic meningitis, meningoradiculitis Garin-Bujadoux-Bannwarth or carcinomatous meningitis thus providing a laboratory tool for their differential diagnosis. In carcinomatous meningitis the amino acid pattern indicates metabolic activity of tumor cells. Minimal alterations were found in multiple sclerosis which have no diagnostic value.     

New and old diagnostic markers of meningitis in cerebrospinal fluid (CSF)

Five new markers (tumor necrosis factor TNF-alpha, interleukin IL-1 beta, IL-6, IL-8, lipopolysaccharide binding protein (LBP)) and 11 old classical markers were evaluated in 180 cerebrospinal fluid (CSF) and serum pairs to discriminate acute bacterial meningitis (BM) on admission from aseptic (viral) meningitis (AM), bacterial meningitis treated with antibiotics (TM) from AM, and AM from multiple sclerosis (MS). Statistical tests were computed which classified correctly > or =90% of the patients with BM, TM, AM at a sum minimum of false positive plus false negative results, and which reached additionally > or =90% sensitivity and specificity. To discriminate BM from AM, CSF IL-6 test > or =500 ng/l and CSF IL-1 beta test > or =8 ng/l besides CSF lactate test > or =3.5mM/l and CSF granulocyte test > or =150 M/l were revealed. CSF lactate test > or =3.2 mmol/l discriminated TM from AM. CSF leukocyte test > or =35 M/l discriminated AM from MS. Tests with the new markers were more laborious, expensive, and time consuming compared to CSF lactate test. Test candidates, detecting > or =80% of patients with > or =80% sensitivity and specificity, were evaluated with CSF TNF-alpha, IL-8 and LBP, serum IL-6, CSF leukocytes, lymphocytes and monocytes, Qglucose, CSF total protein, albumin, and Qalbumin. All tests should be reviewed in context of clinical findings to diagnose BM reliably.     

Concentration of the beta-chemokine CCL5 (RANTES) in cerebrospinal fluid in patients with tick-borne encephalitis

BACKGROUND AND PURPOSE: In tick-borne encephalitis (TBE), perivascular infiltrates are formed within the central nervous system (CNS) and are accompanied by pleocytosis with a predominance of T CD4+ lymphocytes in cerebrospinal fluid (CSF). Factors responsible for leukocyte flow into CNS in TBE have not been investigated. We evaluated the concentration of the chemotactic factor for lymphocytes, chemokine CCL5 (RANTES, Regulated upon Activation, Normal T cell Expressed and Secreted) in CSF and serum of patients with TBE and assessed its correlation with CSF pleocytosis. MATERIAL AND METHODS: Group I consisted of 10 patients with TBE virus infection presenting as meningitis; group II included 11 patients with TBE presenting as encephalomeningitis or myeloencephalomeningitis. The control group consisted of 8 patients, in whom neuroinfection and infection with TBE virus was excluded. The concentration of CCL5 was measured by ELISA in CSF and serum samples taken within 24 hours after hospitalization (examination 1) and in the convalescence period, on average after 16 days (examination 2). RESULTS: Mean CCL5 concentration in serum did not differ between the groups, while in CSF it was significantly increased in group I (64.3+/-75.5 pg/ml in examination 1 and 44.4+/-39.5 pg/ml in examination 2) and in group II (38.4+/-17.0 pg/ml in examination 1 and 48.8+/-24.7 pg/ml in examination 2) in comparison with controls (3.7+/-5.3 pg/ml). There was no significant difference regarding CCL5 concentration between groups I and II and between the examination 1 and 2. There was no correlation between the concentration of CCL5 and CSF parameters. CONCLUSIONS: The concentration of CCL5 is increased in CSF, but not in serum of patients with TBE. This increase does not depend on the clinical form of the disease and is sustained after the disappearance of the symptoms of acute infection. Further studies are necessary to determine the source of CCL5, and its role in the pathogenesis of TBE and its sequelae.     

Diagnostic value of elastase-α1-proteinase inhibitor in cerebrospinal fluid

In this report we introduce CSF Elastase-alpha 1-Proteinase inhibitor as a valuable indicator for differentiating bacterial meningitis from aseptic meningitis and other neurological disorders. All patients (n = 26) with bacterial meningitis had increased CSF concentrations of E-alpha 1-PI above the range of normal (range of reference values: 0.0-2.3 micrograms/l, n = 79; bacterial meningitis: 30-3490 micrograms/l, n = 26). Concentrations of E-alpha 1-PI in bacterial meningitis were significantly elevated when compared with those in aseptic meningitis (0.0-194 micrograms/l, n = 37), polyneuropathy (0-23 micrograms/l, n = 24) and cerebrovascular attack (0-23.2 micrograms/l, n = 17).     

Chemokines CXCL10 and CXCL11 in the cerebrospinal fluid of patients with tick-borne encephalitis

OBJECTIVES: The aim of our study was to determine whether cerebrospinal fluid (CSF) of patients with tick-borne encephalitis (TBE) contains CXCL10, CXCL11, p40 subunit of interleukin-12 (IL-12)/IL-23, IL-18 and IL-15. We compared serum and CSF concentrations of CXCL10 and analysed the possible concentration gradient of this chemokine between the periphery and central nervous system. MATERIALS AND METHODS: The study enrolled 19 TBE patients and 10 patients with non-inflammatory neurological diseases. RESULTS: CSF of TBE patients contained CXCL10 (median 217 pg/ml), CXCL11 (8.3 pg/ml), p40 subunit of IL-12/IL-23 (38.9 pg/ml), IL-18 (30.1 pg/ml) and IL-15 (5.9 pg/ml). CXCL10 in the CSF of TBE patients was higher compared with serum (median 62 pg/ml, P < 0.001). CONCLUSION: CSF of TBE patients contains CXCL10, CXCL11, p40 subunit of IL-12/IL-23, IL-18 and IL-15. Increased CXCL10 concentration in CSF suggests a role for this chemokine in the recruitment of CXCR3-expressing T-cells into the CSF of TBE patients.     

Beta-2-microglobulin and ferritin in cerebrospinal fluid for evaluation of patients with meningitis of different etiologies.

To determine whether or not the beta-2-microglobulin (beta2-m) and/or ferritin levels in cerebrospinal fluid (CSF) can be used as markers for the differential diagnosis of meningitis and determination of the response to treatment, 122 subjects with etiologically well-characterized diagnoses were classified into three groups: bacterial meningitis (n = 5; mean age +/- SD. 1.0+/-1.0 year), viral meningitis (n = 39; 5.9+/-3.8 years), and a non-meningitis group (n = 78; 5.2+/-4.9 years). The levels of beta2-m and ferritin in CSF were determined by means of a latex photometric immunoassay. The statistical significance of the data was analyzed with the Mann Whitney U-test. A receiver operating characteristic curve was used to evaluate the diagnostic accuracy of each prediction marker. This study indicated that (1) the levels of beta2-m and ferritin in CSF were related with age in the non-meningitis group: subjects of up to 5 months of age exhibited higher concentrations of these proteins than ones of above 6 months of age (beta2-m, 1.89+/-1.13 vs. 0.84+/-0.65 mg/l. P < 0.01; ferritin, 2.97+/-2.04 vs. 1.81+/-1.34 microg/l, P = 0.09); (2) the beta2-m level was significantly higher in the CSF of patients with viral meningitis than in ones without meningitis (2.41+/-1.23 vs. 0.84+/-0.65 mg/l, P < 0.01): the best cut-off value was 1.2 mg/l (3) the ferritin level was significantly higher in the CSF of patients with bacterial meningitis than in ones with viral meningitis (43.24+/-39.49 vs. 6.81+/-7.41 microg/l, P < (.01): the best cut-off value was 7.5 microg/l; and (4) sequential measurement of the CSF ferritin level was of value for determination of the response to antibiotic treatment for bacterial meningitis. These results only apply to patients of greater than 6 months of age. beta2-m and ferritin in the CSF can be used as an ancillary tool for diagnostic guidance in the acute phase of meningitis and determination of the response to treatment for bacterial meningitis.     

Interleukin-1β and tumor necrosis factor-α in cerebrospinal fluid of children with bacterial meningitis

Certain cytokines may contribute to the sequence of events that lead to meningeal inflammation in bacterial meningitis. The purpose of this study was to determine the levels of cytokines in the cerebrospinal fluid (CSF) of children with bacterial meningitis and aseptic meningitis of different etiologies. We determined the concentrations of interleukin-1beta (IL-1beta) and tumor necrosis factor (TNF-alpha) in the CSF of 171 specimens of 144 patients whose cases were classified as follow: bacterial meningitis (n=23), aseptic meningitis (n=26) and non-meningitis (n=95). The detectable IL-1beta concentration (> or =20 pg/ml) in the bacterial meningitis, aseptic meningitis and non-meningitis groups were observed with 78.3%, 3.8%, and 8.4%, respectively. Significantly higher serum IL-1beta concentrations were detected in those with bacterial meningitis than those with aseptic meningitis (538.93+/-605.32 pg/ml vs 2.52+/-11.57 pg/ml; P<0.001) or among non-meningitis subjects (2.90+/-11.91 pg/ml; P<0.001). The mean TNF-alpha concentration was 148.74+/-338.77 pg/ml. There was significantly more TNF-alpha than aseptic meningitis (6.85+/-17.93 pg/ml; P<0.001) or non-meningitis (7.67+/-16.07 pg/ml; P<0.001). With regard to diagnosis, measurement of IL-1beta and TNF-alpha levels showed sensitivities of 78% and 74%, respectively; specificities of 96% and 81%, respectively. It is suggested that the levels of these cytokines, especially IL-1beta and TNF-alpha, are useful markers for distinguishing bacterial meningitis from aseptic meningitis.     

Dexamethasone decreases cerebrospinal fluid soluble tumor necrosis factor receptor 1 levels in bacterial meningitis

It is known that the use of adjunctive dexamethasone in bacterial meningitis reduces audiologic and neurologic sequelae. The cerebrospinal fluid (CSF) level of soluble tumor necrosis factor 1 (sTNFR1) is an important indicator of neurologic sequelae in bacterial meningitis. We measured the CSF levels of IL-6 and sTNFR1 before administration of antibiotics (CSF1) and 1-3 days after administration of antibiotics (CSF2) in nine patients with bacterial meningitis who received dexamethasone sodium and five without dexamethasone. The CSF2 IL-6 levels of patients with/without dexamethasone were significantly lower than for CSF1 IL-6 levels (p = 0.0077, and p = 0.0431, respectively). There were no significant differences of the ratio of CSF2/CSF1 IL-6 levels between patients with dexamethasone and those without dexamethasone. CSF2 sTNFR1 levels of patients with dexamethasone were significantly lower than for CSF1 sTNFR1 levels (p = 0.0208). However, CSF2 sTNFR1 levels of patients without dexamethasone were significantly higher than for CSF1 sTNFR1 levels (p = 0.0422). The ratio of CSF2/CSF1 sTNFR1 levels of patients with dexamethasone was significantly lower than that without dexamethasone (p = 0.0063). Our present study suggests that dexamethasone inhibits increase of CSF sTNFR1 levels after antibiotics therapy in bacterial meningitis.     

Immunoglobulin abnormalities in the cerebrospinal fluid during bacterial meningitis

11 patients with bacterial meningitis, examined during the course of the disease for immunoglobulin (Ig) abnormalities in the cerebrospinal fluid (CSF), all had an increased CSF IgM index equal to (CSF/serum IgM):(CSF/serum albumin), indicating intrathecal IgM production. Seven patients had a slightly increased CSF IgG index, and 7 a slightly increased IgA index. Six of the 11 patients had an increased IgM index in the presence of normal indices for IgG and IgA. Follow-up revealed the return of these values to normal. Four patients had identical oligoclonal IgG bands in the CSF and serum, probably representing a systemic immune response, but in only one case were oligoclonal bands suggestive of intrathecal IgG production found. No oligoclonal IgA response was demonstrable in the 4 patients examined. Antigen-immunofixation or antigen-absorption studies revealed evidence of a specific, intrathecal IgG antibody response in only 2 patients, while a search for IgG antibodies against aetiologically unrelated bacterial and viral antigens was negative. With the exception of IgM production, therefore, a humoral intrathecal immune response is less common in bacterial than in aseptic meningitis.     

Level of transforming growth factor beta 1 is elevated in cerebrospinal fluid of children with acute bacterial meningitis

We investigated the levels of transforming growth factor beta 1 (TGF-β1) in cerebrospinal fluid (CSF) in children with meningitis, with a view to prognostic relevance. CSF TGF-β1 levels on admission were measured by a sandwich enzyme immunoassay in children with bacterial meningitis (n = 16), aseptic meningitis (n = 12), and control subjects without evidence of central nervous system (CNS) infection (n = 16). Patients were followed up for a mean duration of 13 months, and neurodevelopmental sequelae was determined for those with bacterial meningitis. On admission, CSF TGF-β1 levels were significantly higher in children with bacterial meningitis (mean, standard error, 32.92, 2.36 pg/ml) as opposed to those with aseptic meningitis (25.26, 1.72 pg/ml) (P = 0.0155), or control subjects (20.53, 1.05 pg/ml) (P < 0.0001). The CSF TGF-β1 levels in children with aseptic meningitis were higher than those in the control group, but without significance (P = 0.02). No apparent correlation existed between CSF TGF-β1 levels and CSF protein or cell counts in patients with bacterial meningitis. No significant difference in CSF TGF-β1 levels was found between patients with or without major sequelae following bacterial meningitis. Received: 19 March 1997 Received in revised form: 24 June 1997 Accepted: 20 August 1997     

C-reactive protein in serum and cerebrospinal fluid in various neurological disorders: Apparent local consumption during bacterial meningitis

The level of C-reactive protein (CRP) was determined in the cerebrospinal fluid (CSF) by particle counting immunoassay. In non-neurological patients (N = 24), CRP was detectable only in 10 samples at concentrations ranging from 1.5 to 37 μg/l. The multiple sclerosis group did not differ from the controls. The highest CRP levels were found in viral and bacterial, including tuberculous, infections of the nervous system, with overlapping results for the various types of infections. However, in serum, the levels of CRP were much higher in pyogenic than in viral meningitis. We compared the CSF CRP/serum CRP ratio to the same ratio for albumin and found a significant correlation between the two ratios in viral, but not in bacterial, infections. These results suggest a local consumption of CRP during bacterial meningitis.     

LDH isoenzymes in cerebrospinal fluid in various brain tumours.

This study examined the isoenzymatic pattern of LDH in the cerebrospinal fluid (CSF) as well as the ratio between the five fractions of LDH among patients with various brain tumours, carcinomatous meningitis and control groups. LDH 1/LDH 2 less than 1 was found significant for carcinomatous meningitis (p less than 0.001) and brain metastases (p less than 0.001). LDH 1/LDH 2 ratio was found to be significantly lower in carcinomatous meningitis than in brain metastases (p less than 0.05). No LDH 1/LDH 2 ratios smaller than 1 were found in the other groups. The LDH 1/LDH 2 ratio smaller than 1 was found in the early stage of carcinomatous meningitis without other evidences of the involvement of the leptomeninges. Examination of LDH 1/LDH 2 can be found as an adjunctive method to identify brain metastases and carcinomatous meningitis at the initial stage.     

Does lumbar cerebrospinal fluid reflect ventricular cerebrospinal fluid? A prospective study in patients with external ventricular drainage

Ventriculitis may sometimes occur after an external ventricular drain has been removed, and diagnosis has to be made by lumbar puncture. But are the lumbar findings comparable to previously obtained ventricular results? In a prospective study, sample pairs of ventricular and lumbar cerebrospinal fluid (CSF) were obtained at an interval of <30 min in 25 patients with increased intracranial pressure suffering from cerebral hemorrhage (n = 15), meningitis/encephalitis (n = 6), cerebral infarction (n = 3), and meningeosis carcinomatosa (n = 1). CSF was analyzed for protein, albumin, IgG, IgA, IgM, glucose, lactate, and leukocytes including cytological differentiation. A significant ventriculo-lumbar increase was observed for protein, albumin, and the immunoglobulins. Lactate was distributed equally in ventricular and lumbar CSF, as well as glucose in the cerebral hemorrhage subgroup (n = 15). Cell count failed to show a clear ventriculo-lumbar ratio. Cytological distribution was comparable in lumbar and ventricular CSF, except for macrophages showing a significant rostrocaudal decrease. In conclusion, in cases of clinically suspected bacterial central nervous system infection after removal of an external ventricular drain, lumbar CSF lactate, glucose, and cytology are comparable to previously determined ventricular values, and thus may help physicians to choose the best treatment.