Enzymes In Cerebrospinal Fluid Research Articles

Cyclic adenosine-3?,5?-monophosphate concentration and enzyme activities of cerebrospinal fluid in meningitis of children

The concentration of cyclic adenosine-3',5'-monophosphate (cAMP) and the activities of some enzymes of 29 children were measured from cerebrospinal fluid (CSF) and plasma at various stages of meningitis. The CSF cAMP values in acute untreated phase of aseptic and purulent meningitis were equal, but significantly higher than those of convalescent children with no pathological clinical or laboratory findings. During the whole course (up to 2 weeks) of antimicrobial treatment of the purulent meningitis CSF cAMP concentration was higher than in the convalescent phase. Of the CSF enzymes studied, the lactic dehydrogenase activity seemed to be the best indicator of changing stages of meningitis. It was clearly elevated in the acute, untreated phase of purulent meningitis then decreasing during the course of treatment. In aseptic meningitis this activity was at the normal level and the activities of creatine kinase and acid phosphatase behaved similarly. The plasma cAMP concentrations in the acute phase of purulent meningitis were in the same range as in the CSF. During the treatment no significant changes were seen. The enzyme activities in the plasma were normal. The CSF cAMP level seems to be a sensitive indicator of metabolic disturbances in meningitis and may serve as a diagnostic aid.

Lysosomal enzymes in motor neurone disease and multiple sclerosis

In nine patients with motor neurone disease the activity of acid phosphatase in cerebrospinal fluid (CSF) was higher ( P<0.005) than in nine controls. The activity of this enzyme in CSF from 18 patients with multiple sclerosis did not differ from control values. The activity of arylsulphatase in CSF was the same in the motor neurone, multiple sclerosis and control groups. In the serum, the activities of the two enzymes were similar in the three groups of patients.

Kinetic similarity of enzymes in human blood serum and cerebrospinal fluid: Aspartate aminotransferase and lactate dehydrogenase

Michaelis constants ( K m ) for l-aspartate and 2-oxoglutarate were calculated for aspartate aminotransferase of normal human blood serum and cerebrospinal fluid (CSF), and human brain supernatant and mitochondria. K m for pyruvate of lactate dehydrogenase from the same sources was also measured at a saturating concentration of NADH. The kinetic constants for enzymes from serum and CSF were similar, and differed significantly from those of brain enzymes, suggesting that CSF enzymes are derived from the blood stream by passage across the blood-CSF barrier.

Serum and cerebrospinal fluid enzymes in cerebrovascular disease. Creatine phosphokinase, aldolase, and lactic dehydrogenase.

THE clinical significance of enzymology in neurological disorders is as yet uncertain. A number of enzymes have been studied both in serum and in cerebrospinal fluid (CSF). In general, these studies have been limited to a single enzyme and have not included a comparison of the serum and CSF activities of the same enzymes. 1-12 Much more needs to be known about the levels of different enzymes in CSF, their relation with one another, and their relation to the serum levels of the same enzymes. In the present study, we compare the CSF and serum activities of the enzymes creatine phosphokinase (CPK), lactic dehydrogenase (LDH), and aldolase (ALD) in a series of patients suffering from acute vascular disorders of the brain. These enzymes are well-known in clinical enzymology and have been studied to some extent in the CSF. CPK in particular is an attractive enzyme because it is found

Enzymes in the Cerebrospinal Fluid

The clinical application of enzyme estimations in the cerebrospinal fluid (CSF) is reviewed. Relevant features of the physiology of the CSF in man, the precautions needed to obtain representative samples and valid controls, and the sources of enzyme in CSF are considered. Brief reference is made to the application of CSF enzyme assays in cerebrovascular disease and tumour diagnosis and in other neurological conditions including head injury and cerebral anoxia. Although at least 30 enzymes have been demonstrated in the CSF of man only glutamic-oxaloacetic transaminase (GOn and lactate dehydrogenase (LDH) have received much clinical attention. Lesser studies have been made on phosphohexose isomerase, isocitric dehydrogenase, phosphatases, ,B-glucuronidase, aldolase and creatine kinase. No comprehensive review has appeared in recent years. Green (1958) gives a fairly full account of papers up to that date and a few more recent works are quoted by Plum (1964). A review is in preparation for publication from this department. Attempts have been made to apply CSF enzyme estimations: (1) in cerebrovascular disease, to assess the presence, extent and progression of infarction and in efforts to distinguish thrombosis from haemorrhage, (2) to cerebral tumour suspects, as an aid to diagnosis and to differentiation of benign from malignant growths and tumours from infarcts, and to detect recurrence, (3) in cases of head injury, to assess severity and guide prognosis, and (4) in the assessment of perinatal hypoxia. In meningitis there is increased activity of several enzymes in CSF: correlation with the different types of meningitis has not been fully investigated. Enzyme changes have been reported in the CSF from cases of demyelinating diseases but no recent studies seem to have been made here. Sources of enzymes in the CSF are: (1) from the blood plasma via the choroid plexus, (2) from addition of whole blood in trauma and strokes and, more rarely, by haemorrhage into tumours and from bleeding secondary to coagulation defects, (3) from excess of white blood cells in meningitis and leucaemia, (4) from normal brain damaged by infarction, external trauma and internal compression, or rendered transiently more permeable by hypoxia

Exchange of albumin between blood, cerebrospinal fluid, and brain in the cat.

Exchange of albumin between blood, cerebrospinal fluid, and brain in the cat.

Glutamic oxaloacetic transaminase in serum and cerebrospinal fluid in parkinsonism.

INCREASED SERUM ENZYMES have been found in certain neuromuscular diseases, e.g. muscular dystrophy, and glutamic oxaloacetic transaminase (GOT) values of cerebrospinal fluid (CSF) have been found to be elevated in cerebral infarction following cerebrovascular accidents, in brain damage associated with head injury, as well as in some other conditions of nervous system disease. It has been noted that the blood-CSF barrier results in enzyme activities that are relatively independent for serum and cerebrospinal fluid. (A recent study using I 131 in puppies demonstrated the increased permeability of the blood-CSF barrier to GOT after prolonged hypoxia.) For this reason and because of the relative ease of acquiring blood, the clinical study of CSF enzymes and the knowledge of their alterations have been limited. Since this study was completed, increased CSF-GOT values have been found in children with acute paralytic poliomyelitis with no serum-glutamic oxaloacetic transaminase (S-GOT) correlation, and, an elevated S-GOT has

Effect of hyperoxia, hypercapnia, and hypoxia on blood-cerebrospinal fluid barrier.

The effect was evaluated in puppies and adult dogs by measuring the rate of passage of radioactive iodinated human serum albumin from plasma into the cerebrospinal fluid and by determining the plasma and cerebrospinal fluid glutamic oxalacetic transaminase and lactic dehydrogenase activities. Arterial O2 concentration and saturation, CO2, and pH determinations were obtained. In puppies, hypercapnia was associated with marked respiratory acidosis and produced a great increase in the rate of transfer of albumin I131 from plasma to cerebrospinal fluid. Prolonged hypoxia also produced a definite increase in permeability of the blood-cerebrospinal fluid barrier. Increased concentration ratios of cerebrospinal fluid enzyme activity/plasma enzyme activity were observed in both groups. Hypoxia alone did not cause significant changes. In adult dogs, hypercapnia or hypoxia did not result in comparable findings.

Cerebrospinal fluid enzymes as a function of age: its effect upon the significance of elevated values in various diseases of the nervous system.

In establishing control values of cerebrospinal fluid glutamic-oxalacetic transaminase, it was observed that the values for 5 of 25 control spinal fluids were considerably higher than the values for the remaining 20. It was not certain whether this indicated unrecognized cerebral disease, was merely a sampling error introduced by the relatively small number of control fluids, or was a true expression of the biological variation of the cerebrospinal fluid glutamic-oxalacetic transaminase levels. The clinical records of each of the five patients with high values were scrutinized for evidence of recent or old disease of the nervous system. In one of the five cases a diagnosis of chronic brain syndrome had been made on a previous hospital admission, and it seemed wise, therefore, to remove this case from the controls. In none of the remaining four cases was there present or past evidence of disease of the nervous system. It was

Receptor-destroying enzyme in cerebrospinal fluid of a case of pneumococcal meningitis.

Receptor-destroying enzyme in cerebrospinal fluid of a case of pneumococcal meningitis.

ACTIVITY OF GLUTAMIC-OXALACETIC TRANSAMINASE AND LACTIC DEHYDROGENASE IN CEREBROSPINAL FLUID AND PLASMA OF NORMAL AND ABNORMAL NEWBORN INFANTS

The activity of the enzymes, glutamic-oxalacetic transaminase and lactic dehydrogenase, in the cerebrospinal fluid and plasma was studied in 54 normal full-term newborn infants from 2½ to 240 hours of age, and in 20 newborn infants suspected to have intracranial pathology. The normal range of activities of these enzymes in cerebrospinal fluid and plasma are described. In the infants with suspected intracranial pathology, the average glutamic-oxalacetic transaminase activity of cerebrospinal fluid was 82% higher than in the normal newborn infant, and plasma glutamic-oxalacetic transaminase activity, had an 18% mean increase over normal. In the cerebrospinal fluid of the abnormal infants, lactic dehydrogenase activity had a mean increase of 309% over normal, and plasma lactic dehydrogenase activity revealed an increase of 11% over normal. Enzyme determinations in cerebrospinal fluid, particularly lactic dehydrogenase, may be useful in the study of newborn infants suspected of intracranial pathology.

Cerebrospinal fluid enzymes in central nervous system lipidoses (with particular reference to amaurotic family idiocy).

Summary1) Simultaneous determinations of glutamic oxalacetic transaminase (GOT), aldolase and lactic dehydrogenase (LD) were estimated of sera and cerebrospinal fluid (CSF) derived from 9 cases of infantile Amaurotic Family Idiocy (IAFI), 2 cases of Niemann-Pick's Disease (NPD) and 33 control patients with other neurologic disorders. 2) Parallel values of GOT and LD were invariably elevated in IAFI, while only the serum and CSF GOT were increased in NPD. The CSF aldolase was usually elevated in all cases of CNS lipidosis, while serum aldolase levels were but slightly increased. Significant CSF enzyme rises were also noted in occasional control patients with actively progressive cerebral degeneration. 3) The data suggest that nervous system necrosis incident to the lipidoses may be biochemically distinguished from other forms of neural degeneration by the analysis of multiple enzyme levels in serum and CSF.

Cholinesterases of cerebrospinal fluid; data for normal fluids and fluids from patients with syphilis, meningitis, or poliomyelitis.

In confirmation of the work of others it has been shown that the principal enzyme in human cerebrospinal fluid that can hydrolyze acetylcholine is true cholinesterase. There is in addition a lesser quantity of pseudocholinesterase. The true cholinesterase, but not the pseudocholinesterase, was found to be significantly increased in the spinal fluids of patients with syphilis, while the pseudocholinesterase, and not the true cholinesterase, was increased in the fluids of patients with either meningitis or poliomyelitis. The true cholinesterase activity was correlated neither with the protein concentration nor with the cell count, while the pseudocholinesterase was correlated with the protein concentration and less significantly with the cell count. When correction was made for the correlation between cell count and protein concentration, the correlation between pseudocholinesterase activity and protein concentration remained statistically significant, but that between pseudocholinesterase and cell count became of dubious significance. In pathological conditions it appears unlikely that either true cholinesterase or pseudocholinesterase is derived from the white cells in the fluid. It is possible that the increased pseudocholinesterase comes from the blood plasma as a result of an increase in the permeability of the "plasma–spinal fluid barrier" and that the increased true cholinesterase comes from the substance of the brain or spinal cord. For the pathological conditions studied, the determination of true and pseudocholinesterase activity of the spinal fluid would be of little value as a diagnostic aid.