Cerebrospinal fluid ferritin in brain necrosis: evidence for local synthesis.

Ferritin was measured in cerebrospinal fluid (CSF) and serum of an unselected neurological population. An increase in CSF ferritin was found to be associated with pathological processes in which there was either necrosis or haemorrhage involving the brain. There was no correlation between the CSF and serum concentrations of ferritin in the reference population. Neither was there any correlation between CSF ferritin and CSF albumin in the reference population. After subarachnoid haemorrhage, intrathecal production of ferritin was found to occur since in some patients the concentration of ferritin in CSF was higher than that of homologous serum. Even in the reference population the concentration of ferritin found in the CSF was much higher than could be explained by passive transfer across the blood-CSF barrier. Therefore local synthesis of ferritin by brain cells occurs even under normal circumstances.

Xanthochromia after subarachnoid haemorrhage needs no revisitation.

Recently it was contended that it is bloodstained cerebrospinal fluid (CSF) that is important in the diagnosis of subarachnoid haemorrhage (SAH) and not xanthochromia, and also that a normal CT scan and the absence of xanthochromia in the CSF do not exclude a ruptured intracranial aneurysm. The CSF findings were therefore reviewed of 111 patients with a proven SAH. All patients had xanthochromia of the CSF. Lumbar punctures were performed between 12 hours and one week after the ictus. Xanthochromia was still present in all (41) patients after 1 week, in all (32) patients after 2 weeks, in 20 of 22 patients after three weeks and in 10 of 14 patients after four weeks. In six years we identified only 12 patients with sudden headache, normal CT, bloodstained CSF, and no xanthochromia. Angiography was carried out in three and was negative. All 12 patients survived without disability and were not re-admitted with a SAH (mean follow up 4 years). It is concluded that it is still xanthochromia that is important in the diagnosis of SAH and not bloodstained CSF. Furthermore a normal CT scan and the absence of xanthochromia do exclude a ruptured aneurysm, provided xanthochromia is investigated by spectrophotometry and lumbar puncture is carried out between 12 hours and 2 weeks after the ictus.

Lipid peroxidation products and antioxidant proteins in plasma and cerebrospinal fluid from multiple sclerosis patients.

Lipid peroxidation (LPx) products were measured as thiobarbituric acid-reactive substances (TS) and lipid-soluble fluorescent pigments (FP) in both plasma and CSF from MS patients and controls. Although no significant changes were found in MS plasma, we report here for the first time increases in both TS and FP in MS CSF (p less than 0.05 and p less than 0.01, respectively, compared with patients with other neurological diseases), indicating that increased LPx in CNS may be a feature of MS. Levels of transferrin were normal but caeruloplasmin (CP), a major antioxidant plasma protein, was significantly raised in MS patients (p less than 0.01) and this may represent an adaptive response to increased oxidative challenge. Neither of these proteins was detectable in CSF using radial immunodiffusion. There was no significant correlation between the severity or duration of the disease nor the period since the last relapse and either LPx products or CP suggesting that the changes observed in this work are not simply the direct result of demyelination and tissue damage.

Cerebrospinal fluid as a diagnostic body fluid.

The cerebrospinal fluid is a dynamic, metabolically active substance that has many important functions. It is invaluable as a diagnostic aid in the evaluation of inflammatory conditions, infectious or noninfectious, involving the brain, spinal cord, and meninges. The cerebrospinal fluid may be obtained with relative ease with the use of lumbar puncture, but failing this, alternative techniques are available. With the judicious use of the computerized axial tomographic scan, the removal of cerebrospinal fluid has little attendant risk. Age-related and compartmental variations in chemical and cellular composition are important considerations in the interpretation of results. Alterations in cerebrospinal fluid constituents from different pathologic processes may be similar in certain circumstances and cause interpretation difficulties.