Cerebrospinal Fluid Lactic Acid Research Articles

Survival outcomes and treatment experience of 124patients with primary central nervous system lymphoma.

Primary central nervous system lymphoma (PCNSL) is arare malignancy of the central nervous system with high invasiveness. There is little consensus on the treatment of PCNSL. This study retrospectively studied data from PCNSL patients in asingle center to summarize treatment experience and explore prognostic factors. Survival curves were drawn using the Kaplan-Meier method and prognostic factors were analyzed using Cox's hazards model. In multivariate analysis, cerebrospinal fluid lactic acid dehydrogenase (CSF LDH; p = 0.005 and p = 0.002), neutrophil to lymphocyte ratio (NLR; p = 0.014 and p = 0.038), and completion of four cycles of induction therapy (p < 0.001and p < 0.001) were significant and independent predictors of overall survival (OS) and progression-free survival (PFS), respectively. On the basis of this study, we propose that PCNSL patients should receive early induction therapy with sufficient cycles. Subsequent consolidation therapy can prevent relapses and improve survival. In patients with PCNSL, the independent prognostic factors for OS and PFS were CSF LDH level, NLR, and full cycles of induction therapy.

Correlation between cerebrospinal fluid abnormalities before ventriculoperitoneal shunt and postoperative intracranial infection in adult patients with hydrocephalus: A clinical study.

To identify the relationship between preoperative cerebrospinal fluid (CSF) leukocyte, chloride, glucose, aspartate aminotransferase, lactate dehydrogenase, adenosine deaminase, lactic acid and protein levels and ventriculoperitoneal shunt infection. Records of 671 consecutive adult patients who underwent ventriculoperitoneal shunt surgery for the treatment of hydrocephalus at Zhujiang Hospital affiliated with Southern Medical University from January 2011 to March 2022 were reviewed. The patients were divided into infection and non-infection groups based on the presence of postoperative infection. For all patients, we analyzed age; sex; primary disease; preoperative CSF leukocyte, chloride, glucose, aspartate aminotransferase, lactate dehydrogenase, adenosine deaminase, lactic acid and protein levels; postoperative temperature; and postoperative infection. A total of 397 patients were included, 28 (7.05%) of whom had an infection within 6 months of the operation and the remaining had no infection. There was no significant difference in age, sex, primary disease, leukocyte, chloride ion, aspartate aminotransferase, lactate dehydrogenase, adenosine deaminase and protein levels in CSF between infection group and non-infection group (p > 0.05). The postoperative infection rate of patients with CSF glucose < 2.8 mmol/L (x 2 = 11.650, p = 0.001) and CSF lactic acid >2.8 mmol/L (x 2 = 12.455, p < 0.001) was higher than that of patients with CSF glucose level ≥2.8 mmol/L and CSF lactic acid level in the range of (1-2.8) mmol/L, respectively, with statistical difference. Compared with the non-infection group, the level of CSF glucose (t = 4.113, p < 0.001) was significantly lower, and the level of CSF lactic acid (t = 6.651, p < 0.001) was significantly higher in the infection group. Multivariate logistic regression analysis showed that preoperative cerebrospinal fluid glucose < 2.8 mmol/L (OR = 3.911, 95% CI: 1.653~9.253, p = 0.002) and cerebrospinal fluid lactate >2.8 mmol/L (OR = 4.712, 95% CI: 1.892~11.734, p = 0.001) are risk factors for infection after ventriculoperitoneal shunt. ROC analysis revealed that the area under the curve (AUC) for CSF glucose and lactic acid level were 0.602 (95% CI: 0.492-0.713) and 0.818 (95% CI: 0.738-0.898), respectively. The infection group had higher rates of fever and body temperature on postoperative day 3-7 (p < 0.05). For adult hydrocephalus patients without clinical manifestations of intracranial infection but only with simple abnormality of cerebrospinal fluid, when the content of glucose in cerebrospinal fluid is < 2.8 mmol/L, and the content of lactic acid is >2.8 mmol/L, it is recommended to perform ventriculoperitoneal shunt after further improvement of cerebrospinal fluid indicators, otherwise, hasty operation will increase the postoperative infection rate. The postoperative fever rate of ventriculoperitoneal shunt surgery is high and the body temperature drops rapidly. If there is still fever after day 3 after surgery, whether there is intracranial infection should be considered.

Lactic acid, neuron-specific enolase, and blood–brain barrier index after a severe traumatic brain injury: a prospective study

Objective To explore the clinical significance of dynamic monitoring of cerebrospinal fluid (CSF) and serum Lactic acid（Lac), neuron-specific enolase (NSE), and the blood–brain barrier (BBB) index in evaluating the condition and prognosis after a severe traumatic brain injury (TBI). Methods A total of 52 severe TBI patients admitted to the Department of Neurosurgery within 24 hours after injury were dynamically monitored. CSF and serum samples were collected on the 1st, 3rd, and 7th day after a severe TBI to monitor the changes in Lac, NSE, and the BBB index. Intracranial pressure (ICP), Glasgow coma scale (GCS), and 6-month Glasgow outcome scale-extended (GOS-E) were tested. According to the results of GOS-E, the patients were divided into two groups (i.e. the poor prognosis group and good prognosis group). Statistical analysis was conducted to investigate the clinical significance of dynamic monitoring of CSF and serum Lac, NSE, and BBB index after a severe TBI. Results After a severe TBI, the levels of Lac, NSE, and BBB in CSF and serum were significantly higher than those in the normal range. Lac, NSE, and the BBB index did not correlate with ICP (except serum Lac) but had correlations with GCS and post-injury 6 months post-injury (except serum Lac). Moreover, the correlations between Lac, NSE, and BBB index were statistically significant (p < 0.05): CSF Lac and CSF NSE; CSF Lac and serum NSE; Lac and BBB index of CSF; Lac and BBB index of CSF; NSE and CSE of serum; CSF NSE and BBB index; and serum NSE and BBB index. Additionally, serum NSE is correlated with NSE in CSF (p < 0.05). Conclusion After a severe TBI, dynamic monitoring of CSF and serum Lac, NSE, and BBB index has the potential to assess the condition, predict the prognosis, and have clinical significance.

Systemic lupus erythematosus (SLE) cerebritis versus Listeria monocytogenes meningoencephalitis in a patient with systemic lupus erythematosus on chronic corticosteroid therapy: The diagnostic importance of cerebrospinal fluid (CSF) of lactic acid levels

BackgroundListeria monocytogenes is a motile, aerobic, Gram-positive intracellular bacillus that causes enteritis, meningitis, meningoencephalitis, or subacute bacterial endocarditis. Patients with impaired T-lymphocyte function/cell-mediated immunity are predisposed to intracellular pathogens, e.g., L. monocytogenes. In adults, infection by L. monocytogenes of the central nervous system (CNS) clinically manifests as either acute bacterial meningitis or meningoencephalitis. In patients with systemic lupus erythematosus (SLE) presenting with headache and fever, SLE cerebritis must be differentiated from acute bacterial meningitis by lumbar puncture and cerebrospinal fluid (CSF) analysis. Neuropathogenic viruses are the most common causes of meningoencephalitis. The most rapid and accurate way to differentiate bacterial meningoencephalitis from nonbacterial meningoencephalitis is CSF lactic acid levels. MethodsWe present a patient receiving chronic corticosteroid therapy and manifesting SLE and severe L. monocytogenes meningoencephalitis. An early diagnosis of L. meningoencephalitis was achieved by demonstrating a very highly elevated level of lactic acid in his CSF, days before CSF and blood cultures tested positive for L. monocytogenes. Results and ConclusionIn this patient, the highly elevated levels of lactic acid in his CSF ruled out both viral meningoencephalitis and SLE cerebritis. The case was complicated by communicating hydrocephalus, and the patient later underwent placement of a shunt. He completed 6 weeks of meningeal dosed ampicillin.

Cerebrospinal fluid lactic acid levels: Accurate, fast, and inexpensive

Cerebrospinal fluid lactic acid levels: Accurate, fast, and inexpensive

Cerebrospinal fluid lactic acid levels: Accurate, fast, and inexpensive

Cerebrospinal fluid lactic acid levels: Accurate, fast, and inexpensive

Non Invasive Microwave Sensor for the Detection of Lactic Acid in Cerebrospinal Fluid (CSF)

This research involves the use of a low power microwave sensor for analysis of lactic acid in cerebrospinal fluid (CSF), an indicator of neurological impairment during aortic aneurysm surgery which could provide the basis for improved treatment regimes and better quality of care with more efficient use of resources. This paper presents initial work using standard lactate curves in water followed by lactate in "synthetic CSF". A multi-modal spectral signature has been defined for lactate, forming the basis for subsequent development of microwave sensor platform that is able to detect concentrations of lactic acid in CSF of volumes less than 1ml.

New Technique uses to Evaluate Cerebrospinal Fluid Lactic Acid as an Aid Differential Diagnosis of Bacterial and Viral Meningitis

The level of lactic acid in cerebrospinal fluid has been suggested as useful diagnostic. Parameter to differentiate between bacterial and viral meningitis,especially in patients partially treated before admission to hospital. A concentration of&gt; (35 mgm/dl) determined by an enzymatic methods has been considered in several studies to provide definite evidence of meningitis of bacterial origin,whereas lower level indicates no bacterial involvement, over past (20) months we had analyzed by the enzymatic methods, the lactate level in (302) cerebrospinal fluids submitted from adults patients with various conditionsinvolving in central nervous system. Fifty fluids had lactate levels of&gt; (35 mg/dl) of which (162) were cases of infective meningitis of varying etiology.In this adults study the lactate level in the cerebrospinal fluid did provide equivocal evidence of bacterial infection and provide assistance to any greater degree than the standard parameters of leucocytes counts, protein and glucose contents in the differential diagnosis of bacterial meningitis from that of any other etiology.

Quantification of cerebrospinal fluid lactic acid in the differential diagnosis between HIV chronic meningitis and opportunistic meningitis

Approximately 40% of HIV infected patients have chronic meningitis at various stages during the infection, 59% are asymptomatic. This is a diagnosis of exclusion and a confounding factor in cerebrospinal fluid (CSF) analysis, any other causes of chronic meningitis by opportunistic or co-infection must be ruled out. The aim of this study was to analyze CSF lactic acid (LA) as an adjuvant biomarker in chronic meningitis due to HIV. CSF LA was quantified in 223 CSF samples by the Dimension AR (Dade Behring, Deerfield, IL, USA), distributed into nine groups: 1) HIV positive with an increase in CSF WBCs (n=17); 2) HIV positive with normal CSF (n=20); 3) enterovirus meningitis (n=33); 4) Herpesviridae meningoencephalitis (n=30); 5) fungal meningitis (n=25); 6) tuberculosis (TB) meningitis (n=17); 7) toxoplasmosis (n=18); 8) neurosyphilis (n=6); 9) control group (n=57). CSF LA (median; IQR) was higher in samples with TB meningitis (5.5; 2.9-7.5 mmol/L) and Cryptococcus neoformans meningitis (3.9; 2.7-5.8 mmol/L) compated with samples with HIV chronic meningitis (1.7; 1.4-1.9 mmol/L) and other groups (p ≤ 0.0001). For the diagnosis of HIV chronic meningitis, using a cut-off of 3.5 mmol/L, CSF LA showed high sensitivity and negative predictive value, although low specificity. CSF LA helps to discriminate between C. neoformans or TB meningitis and HIV chronic meningitis: CSF LA can be included with the methods currently used to identify these specific pathogens, though it does not replace them. It is rapid, inexpensive and easy to perform, and can be used in developing countries.

Facial herpes zoster complicated by varicella zoster virus (VZV) encephalitis: The diagnostic significance of atypical lymphocytes in cerebrospinal fluid (CSF)

Background In general, viral infections of the central nervous system (CNS) manifest as encephalitis and, less commonly, as meningoencephalitis or aseptic meningitis. Varicella zoster virus (VZV) is an uncommon cause of encephalitis. Methods Herpes zoster (shingles) is a cutaneous reactivation of previous chickenpox infection due to VZV. Herpes zoster may be dermatomal (ie, <3 dermatomes) or disseminated (ie, >3 dermatomes). Decreased cell-mediated immunity from stress, steroids, or immunosuppressive drugs often precede dermatomal/disseminated herpes zoster. With herpes zoster, the closer the dermatomal involvement is to the CNS (ie, head/neck shingles), the more likely a patient will have symptomatic CNS involvement (eg, encephalitis). Except for the association of the herpes zoster rash and the simultaneous/subsequent encephalitis, there are few clinical features that distinguish VZV encephalitis from that due to other viruses. The cerebrospinal fluid (CSF) profile of VZV encephalitis is usually clinically indistinguishable from that due to of other causes of viral encephalitis. In VZV meningoencephalitis or encephalitis, the CSF typically shows a modest lymphocytic pleocytosis with normal CSF glucose levels, variably elevated CSF protein levels, and normal CSF lactic acid levels. Atypical lymphocytes are rare in the CSF with VZV encephalitis. Results We present the case of a 75-year-old woman who developed VZV encephalitis after having herpes zoster on her forehead. Except for facial herpes zoster, there were no clinically distinguishing features to determine the cause of her encephalitis. Her CSF had 800 white blood cells/high power field with 26% lymphocytes (17% atypical lymphocytes). The patient’s CSF glucose and CSF lactate dehydrogenase levels were normal, and her CSF protein was elevated. The CSF lactic acid was minimally elevated secondary to red blood cells in the CSF. Electroencephalogram showed general background slowing bilaterally, typical of viral encephalitis. The absence of unilateral focal frontotemporal/parietal lobe focus on electroencephalogram argued against the diagnosis of herpes simplex encephalitis. CSF atypical lymphocytes provided the key clue to the etiology of her encephalitis. CSF atypical lymphocytes are not uncommon in Epstein–Barr virus or cytomegalovirus encephalitis. Less commonly, atypical lymphocytes may be present in the CSF with enteroviruses, West Nile encephalitis, and Japanese encephalitis. VZV is a rare cause of atypical lymphocytes in the CSF but was the clue to the diagnosis before CSF polymerase chain reaction results for VZV were available. Her CSF polymerase chain reaction was negative for Mycobacterium tuberculosis, herpes simplex virus, human herpesvirus-6, cytomegalovirus, enteroviruses, and West Nile virus, but was positive for VZV. She made an uneventful recovery with acyclovir. Conclusion CSF atypical lymphocytes, if present, are an important diagnostic clue in some causes of viral encephalitis. The most common cause of nonseasonal viral encephalitis is herpes simplex virus, which is not associated with CSF atypical lymphocytes. Patients with Epstein–Barr virus, cytomegalovirus, West Nile encephalitis, and enteroviruses usually have extra-CNS signs and symptoms which should suggest the cause of the patient’s encephalitis. CSF atypical lymphocytes limit the differential diagnostic possibilities in patients with viral encephalitis and may be the key clue to the diagnosis, as in the case presented.

Eosinophilic meningitis — an immunophenotyping recording of a very rare clinical entity — Brief Report

A very rare clinical entity, so-called eosinophilic meningitis, classified by prevalence of eosinophils in cerebrospinal fluid (CSF), with the presence of pleiocytosis, has been recorded in our laboratory four times only in the last 24 years. A low glucose level, elevation of total protein and lactic acid in CSF were detected in all the clinical cases. The last two cases were made possible by using flow cytometry method; surprisingly, the presence was found in mature T-cells in CSF, predominantly helpers (CD3+, CD4+) and, practically, none is B-cells (CD19+), plasma cells (CD138+) and NK-cells.

Quantitation of cerebrospinal fluid lactic acid in infectious and non-infectious neurological diseases

The differential diagnosis between bacterial and viral meningitis is not easy in some cases. Cerebrospinal fluid (CSF) analysis is essential for establishing this diagnosis. The objectives were to quantitate lactic acid (LA) concentrations in bacterial and viral meningitis, and other central nervous system (CNS) diseases in order to evaluate the diagnostic utility of CSF LA for discriminating bacterial from viral meningitis. CSF LA was measured in 139 CSF samples from seven groups: viral meningitis with classic CSF; suspicion of viral meningitis with neutrophils in CSF; bacterial meningitis; non-infectious neurological diseases; chronic meningitis; traumatic lumbar puncture (LP) and normal CSF. CSF LA was higher in bacterial meningitis 8.7 + 5.4 mmol/L compared with viral meningitis (1.9 + 0.6) and the other groups (p < 0.0001). CSF LA in the groups with viral meningitis was not different compared to groups with non-infectious CNS diseases and chronic meningitis. The ability of CSF LA to discriminate bacterial from viral meningitis showed a sensitivity of 80% and specificity of 97%, positive predictive value (PPV) of 94%, and negative predictive value (NPV) of 89%. CSF LA is a powerful test to discriminate bacterial from viral meningitis with high sensitivity, specificity and predictive values. CSF LA can help in the cases with diagnostic uncertainty.

Quantification of lactic acid in cerebrospinal fluid samples of infectious and noninfectious neurological diseases

Background The differential diagnosis between bacterial and viral meningitis is based on the cerebrospinal fluid (CSF) cellular and biochemistries characteristics, it is important for the adequate treatment and prognosis. CSF lactic acid determination is considered the best biomarker for this differential diagnosis. The objectives of this study were to quantify CSF lactic acid levels in bacterial and viral meningitis comparing with other infectious and noninfectious central nervous system diseases; and to calculate the CSF acid lactic operational characteristics as a biomarker for the differential diagnosis between bacterial and viral meningitis.

Listeria monocytogenes encephalitis mimicking Herpes Simplex virus encephalitis: The differential diagnostic importance of cerebrospinal fluid lactic acid levels

Listeria monocytogenes is a common cause of bacterial meningitis in elderly patients and in those with impaired cellular immunity. The most common central nervous system infection caused by L. monocytogenes is acute bacterial meningitis; meningoencephalitis is uncommon and encephalitis is rare. Early diagnosis of L. monocytogenes meningitis is difficult because only 50% of cerebrospinal fluid (CSF) Gram stains are negative. L. monocytogenes is one of the few central nervous system pathogens associated with red blood cells in the CSF. When L. monocytogenes presents as encephalitis with red blood cells in the CSF, the clinical presentation mimics most closely herpes simplex virus (HSV)-1 encephalitis. Because the therapies for L. monocytogenes and HSV-1 are different, early diagnostic differentiation is clinically important. The CSF lactic acid is the best way to rapidly differentiate between these two entities; the CSF lactic acid level is elevated in L. monocytogenes but is not elevated in HSV-1 encephalitis. The case presented is an elderly man with chronic lymphocytic leukemia who presented with encephalitis. Advanced age and chronic lymphocytic leukemia predispose him to a wide variety of pathogens, but the rapidity and severity of his clinical presentation made L. monocytogenes and HSV-1 encephalitis the most likely diagnostic possibilities. The CSF Gram stain was negative, but the elevated CSF lactic acid levels with encephalitis and red blood cells in the CSF indicated L. monocytogenes as the most likely pathogen. We present a case of L. monocytogenes encephalitis mimicking HSV-1 encephalitis. While receiving ampicillin therapy, the patient remained unresponsive for more than 1 week and then suddenly regained consciousness and recovered without neurologic sequelae.

Liver transplantation in mitochondrial respiratory chain disorders.

Mitochondrial respiratory chain disease may lead to neonatal or late onset liver failure, requiring liver transplantation. In rare cases, the disease is restricted to the liver and the patient is cured after surgery. More frequently, other organs are simultaneously involved and neuromuscular or other extra-hepatic symptoms may pre-exist, or appear in the post-transplant follow up. Pre-transplant evaluation should aim to rule out neurological disease, which may be difficult to differentiate from signs accompanying liver insufficiency. Cerebrospinal fluid lactic acid levels, compared to blood lactate, may be suggestive of central nervous system involvement. Of 11 cases with respiratory chain disorders who had liver transplantation in various centres, 4 are alive and well on follow up, and 6 died, three of them having developed neurological disease post orthotopic liver transplantation. All three patients with initial liver and gastro-intestinal disease died early after transplantation, indicating that these may be poor candidates for this procedure. Liver transplantation is feasible in hepatic respiratory chain disorders, but extra-hepatic disease should be ruled out before transplantation. Extra-hepatic manifestations may, however, appear and cause patient death despite successful transplantation.

Nitric oxide concentrations and cerebrospinal fluid parameters in an experimental animal model of Streptococcus pneumoniae meningitis.

Streptococcus pneumoniae is a common cause of meningitis. Nitric oxide (NO) has been implicated in causing cerebral edema. Modulating NO production in cerebrospinal fluid (CSF) may have a role in the treatment of bacterial meningitis. Experimental S. pneumoniae meningitis was induced in a rabbit model to determine CSF parameters and NO concentrations. An electrochemical probe in the CSF throughout the 7-hour experiment monitored NO concentrations. The animals had S. pneumoniae (10(5)) injected intracisternally and incubated for 1 hour. Cerebrospinal fluid 200-300 microl was obtained by intracisternal puncture at zero, 2, 4, and 7 hours after drug administration to measure glucose, protein, and lactic acid by standard chemical methods. White blood cell count was measured by hemocytometry. Three groups of five animals were used-control (C), ceftriaxone (CTX), and ceftriaxone plus dexamethasone (CTX+D). Ceftriaxone concentrations in CSF were obtained by microdialysis and analyzed by high-performance liquid chromatography. Mean (+/- SEM) CSF white blood cell count was significantly higher at 2 hours in the C group than in the other two groups (C 7307 +/- 1302, CTX 605 +/- 345, CTX+D 730 +/- 43/mm3, p<0.002). Ceftriaxone induced a significant rise in protein at 4 hours compared with the other groups (C 364 +/- 107, CTX 1158 +/- 797, CTX+D 365 +/- 100 mg/dl, p<0.02). Cerebrospinal fluid lactic acid was significantly different at 4 and 7 hours between C and CTX+D groups (4-hr C 8.0 +/- 2.2, CTX+D 2.0 +/- 0.4 mmol/L, p<0.05; 7-hr C 10.2 +/- 2.4, CTX+D 2.8 +/- 0.8 mmol/L, p<0.01). Median NO concentrations were significantly elevated in the control group compared with the other two groups (C 11.7, CTX 6.8, CTX+D 6.5 micro, p<0.02 C vs CTX, p<0.01 C vs CTX+D). Average (+/- SEM) NO concentrations were significantly higher in the C group at 4 hours (18.1 +/- 0.4, CTX 5.8 +/- 1.8 microM, p<0.05; CTX+D 11.5 +/- 4.0 microM, p>0.05), whereas they did not rise significantly until 7 hours in the CTX group (CTX 18.7 +/- 0.7, C 8.9 +/- 0.4 microM, p=0.055; CTX+D 8.1 +/- 2.2 microM, p<0.05). These results indicate that ceftriaxone with or without dexamethasone significantly decreases lactic acid concentrations and white cell penetration into the CSF in an experimental model of S. pneumoniae meningitis. In addition, ceftriaxone induced a significant elevation in CSF protein. Median NO production in the CSF was significantly attenuated by ceftriaxone.

Cerebrospinal fluid/serum lactic acid in Nigerian children with febrile convulsions.

Cerebrospinal fluid (CSF) and serum lactic acid levels were prospectively assayed in 42 children less than 5 years old with febrile convulsions who were divided into two groups for analytical purposes, irrespective of aetiology of pyrexia. One group (24 children) had brief febrile seizures and the remaining 18 children had prolonged febrile seizures. CSF and serum lactic acid values were obtained for brief and prolonged seizures. On admission, the mean CSF lactic acid was significantly higher (p < 0.05) in children with prolonged than with brief seizures, but the mean serum lactic acid was not significantly different between the two groups. Twelve of the 18 children (67%) with prolonged seizures and elevated CSF lactate had seizure recurrence. There were no recurrences of seizures in children with a brief initial seizure and low CSF lactate. CSF lactic acid is elevated in children with prolonged seizures and this may be useful in detecting those with a prolonged seizure where the history of the duration of the seizure is not clear. Prolonged seizure has been associated with the risk of recurrence and therefore such children with elevated CSF lactic acid levels might benefit from long-term anticonvulsant therapy.

The rett syndrome and CSF lactic acid patterns

We investigated both blood and cerebrospinal fluid (CSF) lactate and pyruvate levels in seven girls with the Rett syndrome (RS) and evaluated the relationship between CSF lactate and pyruvate levels and the clinical manifestations, particularly seizures, anticonvulsant medication, and breathing dysfunction including breath holding, apnea and hyperventilation. Elevated lactate and pyruvate levels in CSF with normal serum lactate were found in two RS patients. Elevated CSF lactate correlated significantly with the clinical occurrence of hyperventilation (P0 = 0.048, Fisher exact probability). We measured native and dichloroacetate (DCA)-activated pyruvate dehydrogenase (PDH) complex activities in two patients (#1 and 2) using cultured lymphoblastoid cell lines which were transformed by EB virus and the results were normal. We also analyzed CSF citric acid intermediates from 7 RS patients including citric acid, cis-aconitate, alpha-ketoglutarate, succinate, fumarate, malate and oxaloacetate. These concentrations were not significantly different from those control patients (N = 21). An elevated lactate level may be a clue to clarify the etiology of RS.

CSF monoamine metabolites, cholinesterases and lactate in the adult hydrocephalus syndrome (normal pressure hydrocephalus) related to CSF hydrodynamic parameters.

Monoamine metabolites, cholinesterases and lactic acid in lumbar cerebrospinal fluid (CSF) were investigated on patients with the adult hydrocephalus syndrome (idiopathic normal pressure syndrome; AHS, n = 15), Alzheimer's disease (AD, n = 14), multi-infarct dementia (MID, n = 13) and controls (n = 21). Patients had clinical and CSF hydrodynamic investigations. Monoamine concentrations were determined by reversed-phase liquid chromatography, cholinesterases and lactate were determined photometrically. In the AHS patients, CSF monoamine concentrations were not significantly different compared with controls, AD or MID patients. AHS and AD patients showed a similar reduction of CSF acetylcholinesterase activity compared with controls. Positive correlations were found in concentrations of CSF homovanillic acid, CSF 5-hydroxyindoleacetic acid and CSF lactic acid versus CSF outflow conductance (that is, resistance against CSF outflow) in the AHS patients. A similar pattern was observed in a subgroup of MID patients characterised by dilated ventricles and disturbed CSF hydrodynamics. These data suggest that a low CSF outflow conductance may facilitate the clearance of acidic substances from the arachnoid space at the probenecid sensitive active transport site. Alternative explanations would be that a pathologically low CSF outflow conductance is accompanied by an inverse caudorostral flow of CSF or a compromised trans-ependymal diffusion.

Spinal angiomas: The meaning of cerebrospinal fluid lactic acid in the etiology and differential diagnosis of transverse myelopathy

We report five out of eleven patients with transverse myelopathy due to spinal angiomas. Transverse myelopathy can be caused by a number of disorders. The formation of lactic acid points to ischaemia within the spinal cord, due to altered haemodynamics as in spinal angiomas. The meaning of cerebrospinal fluid lactic acid is discussed with respect to etiology and differential diagnosis of transverse myelopathy. The combined finding of CSF lactic acid and protein elevation in the absence of cell count and immunological and/or serological abnormalities points to an isolated vascular cause of the transverse myelopathy.