ACID MONOAMINE METABOLITES OF CEREBROSPINAL FLUID IN MENINGITIS AND ENCEPHALITIS

The concentrations of the acid monoamine metabolites homovanillic acid (HVA) and 5-hydroxyindolcacetic acid (5-HIAA) were measured by spectrophotofluorometric techniques in lumbar cerebrospinal fluid obtained from patients with meningitis and encephalitis. Very high concentrations of HVA were found in 4 patients with bacterial meningitis in the acute stage and a marked fall was observed after treatment. The levels found in 3 patients with aseptic meningitis and in 2 out of 4 patients with encephalitis were also above the control values. Interference with the active transport mechanism for acid monoamine metabolites from cerebrospinal fluid to blood may account for the high concentrations of HVA found in patients with meningitis. In a limited material investigated there was no obvious difference between the levels of 5-HIAA found in cerebrospinal fluid obtained from meningitic patients as compared to controls.     

PURINE METABOLITES AND PYRIMIDINE BASES IN CEREBROSPINAL FLUID OF CHILDREN WITH SIMPLE FEBRILE SEIZURES

Adenosine monophosphate, inosine monophosphate, inosine, adenosine, guanosine, adenine, guanine, hypoxanthine, xanthine, uric acid and pyrimidine bases were determined in the CSF of 18 children after simple febrile seizures and in a control group. There was no statistically significant difference between the two groups for any of these metabolites. This suggests that simple febrile seizures neither significantly disturb the metabolism of nucleotides, nucleosides or bases, nor significantly deplete neuron adenosine triphosphate ATP levels.     

GAS CHROMATOGRAPHIC SEPARATION AND MASS SPECTROMETRIC IDENTIFICATION OF POLYOLS IN HUMAN CEREBROSPINAL FLUID AND PLASMA

Seven polyols, erythritol, arabinitol, anhydroflucitol, mannitol, sorbitol, myoinositol and possibly ribitol were identified in human cerebrospinal fluid by means of gas-liquid chromatography and mass spectrometry. Quantitative data were obtained for five polyols, arabinitol, anhydroglucitol, mannitol, sorbitol and myoinositol, by screening of 205 CSF samples. These five polyols represented 90–95 per cent of the polyol-concentration which was 340 ± 105 μmol/l in the total series. The concentration of polyols in the CSF was two times higher than that in the plasma (148 ± 30 μmol/l), where only anhydroglucitol and myoinositol could be quantitated. The variations noted were not associated with age, sex or the plasma concentrations of polyols. The polyols of the CSF most likely originate from brain tissue and/or spinal cord since penetration from the plasma against a gradient seems unlikely.     

CEREBROSPINAL FLUID NUCLEOTIDE METABOLITES FOLLOWING SHORT FEBRILE CONVULSIONS

Cerebrospinal fluid (CSF) markers of cerebral energy depletion were measured in 32 infants and children following short (less than 10 minutes) febrile convulsions, and in 19 controls. Specific and sensitive indices of high-energy phosphate compound depletion (hypoxanthine, xanthine and uridine) showed no marked changes. Values for patients and febrile controls were significantly higher than for afebrile controls, which is consistent with increased cerebral metabolism in febrile patients. There were no differences in pH, lactate or creatine kinase levels in the CSF of patients and controls. The results suggest that short febrile convulsions are benign and that in the absence of risk factors for the subsequent development of epilepsy, prophylactic anticonvulsant treatment is not indicated.     

CHANGES IN THE ELECTROPHORETIC PATTERN OF THE LUMBAR CEREBROSPINAL FLUID DURING FRACTIONAL GAS ENCEPHALOGRAPHY

The changes occurring in the electrophoretic pattern of the lumbar cerebrospinal fluid during GEG were studied in 144 mental defectives. The first sample was taken immediately after lumbar puncture prior to removal of CSF and injection of contrast gas. The last of the three samples was withdrawn approximately 25 min after the first, the patient being still seated. Altogether, 316 electrophoretic analyses were made with the cellulose acetate method. The factors possibly influencing the changes in the electrophoretic pattern were investigated statistically with the aid of a computer. The following changes in the mean proportions of the CSF protein electrophoretic fractions during GEG were found, with the χ²-test, to be significant: decrease in albumin and increase in α₂-globulin and in β-globulin. The grade of cortical gas filling seemed to be positively correlated with the magnitude of the electrophoretic changes. Thus, for example in cases of macroventriculy, where the cortical gas filling was generally poor, the electrophoretic changes were slight. The changes seem to be mainly attributable to changes in membrane permeability due to irritation by the GEG procedure in accordance with physico-chemical laws. The admixture of CSF from the more cranial spaces with the lumbar samples seems to be only of secondary importance, as the primary differences are also due to permeability. It is important that the clinician should be aware of these changes in behaviour of the CSF electrophoretic pattern during GEG, so as to avoid unnecessary additional work and erroneous diagnoses and conclusions. Even statistically non-significant changes may be of clinical importance if the only sample available for CSF electrophoresis is influenced by the irritating effect of GEG.     

CEREBROSPINAL FLUID NUCLEOTIDE METABOLITES FOLLOWING NON-CONVULSIVE STATUS EPILEPTICU

The authors studied specific and sensitive indicators of neuronal adenosine triphosphate (ATP) depletion--hypoxanthine, xanthine and uridine levels--in the cerebrospinal fluid (CSF) of nine children during non-convulsive status epilepticus. No evidence of ATP depletion was found and CSF pH and creatine kinase levels were similar to those of controls. Hypoxanthine, xanthine and uridine had a tendency to be low, but this was significant only for xanthine. The authors speculatively link this reduction to a reduction in neuronal protein synthesis. This might be a mechanism whereby non-convulsive status epilepticus could lead to intellectual deterioration and dementia.