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Thirtynine (39) patients with subarachnoid haemorrhage (SAH) were studied with computed tomography (CT). The amount of blood in the cerebrospinal fluid (CSF) and the degree of hydrocephalus were evaluated. These two parameters were correlated with the clinical condition on admission and at discharge and against CSF concentration of a series of CSF substances. These included the major monoamine metabolites homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA) and 3-methoxy-4-hydroxyphenylethyleneglycol (MOPEG) and in addition the concentrations of hypoxanthine, aspartate and somatomedins. The amount of blood and the degree of hydrocephalus on admission did not seem to influence the concentration of these substances over time. It was found that patients with large amounts of blood in the CSF had a worse clinical outcome (p<0.05) compared to patients with no or moderate amount of blood. In addition, patients with enlargement of the temporal horns showed a worse clinical condition on admission (p<0.01) than did patients without such enlargement. Despite a significant (p<0.01) vasoconstriction there was no correlation between vascular calibre and concentration of the substances in the CSF. It is speculated whether or not the increased levels of these substances were the result of cell lysis per se, a disturbance of the CSF circulation or to the toxic effect of blood resulting in deranged metabolism in both the CSF and brain tissue after SAH. [ABSTRACT FROM AUTHOR]

The somatomedins, multitargit growth-promoting peptide hormones, were measured with radio receptor assay in cerebrospinal fluid (CSF) after subarachnoid haemorrhage (SAH) in 21 patients and after head injury in 2 patients. In the first group of 10 patients, lumbar (n=8) or central (n=2) CSF was collected on days three, six and nine after SAH. 6 of the 8 patients with SAH showed an increase in somatomedin concentrations ranging between 0.52-1.26 U/ml while 2 patients fell within the normal range between 0.19-0.48 U/ml. In the 2 patients with head injury, the somatomedin concentrations were scarcely detectable. In the second group of 13 patients with SAH, CSF was collected peroperatively during surgical clipping of an aneurysm. These patients fell into two groups: 6 patients who had CSF somatomedin levels within the normal range and 7 patients with pathologically increased somatomedin concentrations ranging between 0.38-1.26 U/ml. Neither the neurological condition nor the cerebral vascular diameter correlated with the somatomedin concentrations. It is suggested that the increased somatomedin levels in CSF after SAH could be a compensatory response in order to stimulate cerebral anabolism after injury. [ABSTRACT FROM AUTHOR]

Twenty amino acids were determined chromatographically in cerebrospinal fluid (CSF) from 26 patients and in plasma from 13 of the patients with subarachnoid haemorrhage (SAH). In the first group of 13 patients, from which lumbar CSF and plasma were collected on days three, six and nine after SAH, there was a significantly increased CSF concentration from day three to six and/or nine in all amino acids except for taurine which was within the normal range. In the second group of 13 patients, from which CSF was collected during peroperative clipping of aneurysms, there was an increased concentration in lumbar and central CSF in all amino acids except for taurine compared to controls. There was no correlation between any of the amino acids and cerebral vascular diameter as assessed by angiography. It is suggested that the increased levels in lumbar and central CSF amino acids result from proteolysis due to catabolic processes and from impaired clearance of the amino acids from CSF after SAH. [ABSTRACT FROM AUTHOR]

The concentrations of the dopamine metabolite homovanillic acid (HVA), the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) and the norepinephrine metabolite 3-methoxy-4-hydroxyphenylglycol (MOPEG) were determined in cerebrospinal fluid (CSF) from patients with subarachnoid haemorrhage (SAH) using a mass fragmentographic method. In a first group of 24 patients lumbar CSF was collected during the first 10 days after SAH. The concentrations of HVA and 5-HIAA showed a several-fold increase in the majority of subjects while that for MOPEG was less pronounced in comparison to controls. In a second group of 12 SAH-patients, CSF was collected in 10 ml fractions during surgical clipping of aneurysms. The mean concentrations of HVA, 5-HIAA and MOPEG in lumbar CSF was 469,275 and 39 pmol/l, respectively, whereas central CSF concentrations were 1,212, 499 and 48 pmol/ml, respectively. Compared to healthy controls, both HVA and 5-HIAA showed increased levels (pl 0,01) but MOPEG was within the normal range. No correlation between the concentrations of the monoamine metabolites, the neurological condition or the cerebral vascular diameter was observed in neither of the two groups. It is suggested that the accumulation of HVA and 5-HIAA in SAH patients is explained by a disturbance of the active transport mechanism. [ABSTRACT FROM AUTHOR]

The adenine nucleotide metabolites hypoxanthine, xanthine and uric acid were determined by high performance liquid chromatography in cerebrospinal fluid (CSF) from 25 patients with subarachnoid haemorrhage (SAH) and from 26 control subjects. In addition, the haemoglobin and protein levels in the CSF of the patients were determined. In 13 subjects, from which lumbar CSF was collected three, six and nine days after SAH, there was a gradual increase in 8 patients for hypoxanthine and in 3 of the 13 patients for xanthine and uric acid. The mean concentrations were not significantly higher than the controls. In 12 SAH patients, consecutive CSF fractions of 10 ml were collected peroperatively during surgical clipping of aneurysms. The hypoxanthine concentrations increased continously from lumbar to central CSF samples. Hypoxanthine levels were 6.5±1.0 μM in lumbar CSF compared to 11.8±2.3 μM in central CSF (p<0.001), while xanthine, uric acid, haemoglobin and protein levels were equally distributed. Furthermore, the SAH patients showed about 3 times higher concentrations of central CSF hypoxanthine (p<0.01) and xanthine (p<0.05) while that for uric acid was similar compared to all control subjects. Also, an in vitro study showed that the increased concentrations of the adenine nucleotide metabolites could not be caused by degradation of blood components in the subarachnoid space. It is presumed that the increased central CSF concentrations of hypoxanthine that were demonstrated in patients after SAH could be a sensitive marker for brain tissue ischaemia. However, since there was no correlation between the hypoxanthine levels, clinical condition or cerebral vascular diameter, other factors have to be excluded before ischaemia alone could explain the elevated central hypoxanthine levels in patients without major clinical dysfunction after SAH. [ABSTRACT FROM AUTHOR]