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Background Diminishing volume of intracranial cerebrospinal fluid (CSF) in patients with space-occupying masses have been attributed to unfavorable outcome associated with reduction of cerebral perfusion pressure and subsequent brain ischemia. Objective The objective of this article is to employ a ratio of CSF volume to brain volume for longitudinal assessment of space-volume relationships in patients with extra-axial hematoma and to determine variability of the ratio among patients with different types and stages of hematoma. Patients and methods In our retrospective study, we reviewed 113 patients with surgical extra-axial hematomas. We included 28 patients (age 61.7 +/- 17.7 years; 19 males, nine females) with an acute epidural hematoma (EDH) ( n = 5) and subacute/chronic subdural hematoma (SDH) ( n = 23). We excluded 85 patients, in order, due to acute SDH ( n = 76), concurrent intraparenchymal pathology ( n = 6), and bilateral pathology ( n = 3). Noncontrast CT images of the head were obtained using a CT scanner (2004 GE LightSpeed VCT CT system, tube voltage 140 kVp, tube current 310 mA, 5 mm section thickness) preoperatively, postoperatively (3.8 ± 5.8 hours from surgery), and at follow-up clinic visit (48.2 ± 27.7 days after surgery). Each CT scan was loaded into an OsiriX (Pixmeo, Switzerland) workstation to segment pixels based on radiodensity properties measured in Hounsfield units (HU). Based on HU values from -30 to 100, brain, CSF spaces, vascular structures, hematoma, and/or postsurgical fluid were segregated from bony structures, and subsequently hematoma and/or postsurgical fluid were manually selected and removed from the images. The remaining images represented overall brain volume-containing only CSF spaces, vascular structures, and brain parenchyma. Thereafter, the ratio between the total number of voxels representing CSF volume (based on values between 0 and 15 HU) to the total number of voxels representing overall brain volume was calculated. Results CSF/brain volume ratio varied significantly during the course of the disease, being the lowest preoperatively, 0.051 ± 0.032; higher after surgical evacuation of hematoma, 0.067 ± 0.040; and highest at follow-up visit, 0.083 ± 0.040 ( p < 0.01). Using a repeated regression analysis, we found a significant association ( p < 0.01) of the ratio with age (odds ratio, 1.019; 95% CI, 1.009-1.029) and type of hematoma (odds ratio, 0.405; 95% CI, 0.303-0.540). Conclusion CSF/brain volume ratio calculated from CT images has potential to reflect dynamics of intracranial volume changes in patients with space-occupying mass.

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Pleomorphic xanthoastrocytoma (PXA) has been considered an astrocytic tumor with a relatively favorable prognosis. However, PXA cases having several recurrent patterns with poor prognosis have been reported in recent years, and a new concept of anaplastic PXA has been proposed. The present case was a 59-year-old woman who presented with tumor bleeding onset and cerebrospinal fluid dissemination. The patient had sudden-onset right hemiparesis, aphasia, and consciousness disturbance and was admitted to a local area hospital. After emergency surgery had removed the hematoma, postoperative contrast-enhanced CT scan revealed a left temporal tumor. A second surgery was therefore performed for initial tumor removal 2 months later. Histopathological findings showed that the tumor was typical PXA with strong pleomorphism and xanthomatous changes and contained an ependymoma-like component in the center area. However, endothelial proliferation and mitosis were more remarkable compared to ordinary PXA. The MIB-1 labeling index was 9.8% high. From these findings, the histopathological diagnosis was anaplastic PXA. The patient underwent surgery to remove recurrent tumors 5 and 16 months later. The patient died 36 months after the first onset, and CT revealed glioblastoma-like findings and cerebrospinal fluid dissemination. This case report is the first case in which PXA presented with tumor bleeding onset. Histopathological findings suggested anaplastic PXA from the first surgical specimens, and PXA recurred many times. We thus believe that the patient displayed primary anaplastic PXA rather than secondary anaplastic PXA that results in malignant transformation.

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OBJECTIVE: To determine whether a ratio of observed to predicted (O:P) cerebrospinal fluid (CSF) white blood cells (WBCs) after a traumatic lumbar puncture (LP) can be used to predict which patients do not have meningitis and can safely be discharged from the hospital. METHODS: A retrospective medical record review was performed on 2 cohorts of previously healthy children who had received an LP at Children's Memorial Hospital in Chicago, IL. All children were older than 1 month and had a red blood cell (RBC) count in the CSF >500/mm(3). Cohort 1 consisted of children who were examined in 1990 through 1999 and had CSF cultures positive for a bacterial pathogen. Cohort 2 consisted of children who were tested during January through December 1999 and had a CSF culture negative for any bacterial pathogen. Exclusion criteria included patients who received antibiotics within 72 hours before evaluation, patients with a previous neurosurgical procedure or CNS bleed, and patients whose complete blood count was not done within 6 hours of LP. The predicted CSF WBC count was calculated using the formula CSF WBC (predicted) = CSF RBC x (blood WBC/blood RBC). The O:P ratio was obtained by dividing the observed CSF WBC by the predicted CSF WBC. The simple ratio of WBCs to RBCs was also calculated. Sensitivity, specificity, positive predictive value, and negative predictive value were calculated to predict the absence of disease. Receiver operator characteristic curves were generated for the O:P ratio and the WBC:RBC ratio. Continuous variables were analyzed with Mann-Whitney U test. RESULTS: Among the 57 patients who fit all of the study criteria, 12 (21%) had positive CSF cultures for bacterial pathogens. The patients with meningitis were significantly older (median: 7.8 months; range: 1-106 months) than the patients without meningitis (median: 1.3 months; range: 1-139 months). The O:P ratio was significantly lower in the patients without meningitis (median: 0.064; range: 0.000054-1.09) as compared with patients with meningitis (median: 1.26; range: 0.045-4.72). The WBC:RBC ratio was significantly lower in the patients without meningitis (median: 0.001; range: 0-4.46) as compared with patients with meningitis (median: 1.98; range: 0.04-24.45). The specificity and positive predictive value of an O:P ratio

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Cerebral hematoma increases cerebrospinal fluid (CSF) endothelin-1 (ET-1). Inhibitors of ET-1 synthesis prevent this increment and hematoma-induced modification of cerebral arteriolar reactivity. We hypothesized that intrathecal ET-1 injection could 1) modify pial arteriolar reactivity similarly to hematoma; 2) increase CSF lysophosphatidic acid (LPA), a potential contributor to altered cerebrovascular reactivity; and 3) reduce the level of adenosine 3',5'-cyclic monophosphate (cAMP) in the CSF. Either ET-1 (10(-7) M) or artificial CSF was injected over the left parietal cortex of newborn pigs. Four days later, cranial windows were implanted. CSF ET was increased from a basal level of 11 fmol/ml to 18 fmol/ml 4 days after ET-1 injection, whereas CSF cAMP was reduced from 2,700 to 950 fmol/ml. The mean diameter of pial arterioles was reduced 31%. In control animals, 10(-12) M ET caused dilation, and higher concentrations induced vasoconstriction. Four days after ET-1 injection topical ET-1 caused constriction instead of dilation at 10(-12) M, and constrictions at higher doses were enhanced. Norepinephrine-induced constrictions were potentiated in the ET-1-injected group. Dilations to cAMP-dependent (but not independent) vasodilators were attenuated after ET-1. The concentration of the vasoconstrictor lipid mediator LPA increased approximately fourfold. Thus intrathecal injection of ET-1 mimics hematoma-induced modification of cerebral vascular reactivity and increase in LPA production. The mechanism(s) of ET-1- and hematoma-induced modifications may involve LPA, which is known to contribute to the loss of dilator responses by inhibition of cAMP product on. The present study further suggests that ET-1 together with LPA could be causing changes in cerebrovascular reactivity following cerebral hemorrhage. ET-1 stimulates the release of LPA from brain parenchyma independent of serum so that LPA could serve as a secondary mediator.

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Our purpose was to characterise the MRI appearances of clinically non-neoplastic chronic intracerebral haematomas (ICH). We examined 25 patients with a history of clinically non-neoplastic 0.5-to 1.5-year-old ICH who underwent prospective follow-up 1.0-T spin-echo MRI of the brain. On T1-weighted images most lesions gave lower signal than white matter and were isointense with cerebrospinal fluid (CSF). On T2-weighted images most were either totally low-signal and slit-like, or had a high-signal centre and a low-signal margin. The low-signal (haemosiderin) rim showed areas of discontinuity in 7 cases. Of 24 lesions, 4 showed small enhancing areas on contrast-enhanced images. In 10 cases the brain parenchyma surrounding the lesion showed high-signal on T2- and low signal on T1-weighted images, probably representing encephalomalacia. In 20 cases enlargement of a nearby CSF space was observed, and 14 cases showed atrophy of the brain stem ipsilateral to the lesion. We thus found more variation on MRI of clinically non-neoplastic chronic ICH than previously described.

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The analysis of intracranial pressure records in 95 cases of non-traumatic intracerebral haematoma is presented. In 74 cases continuous recording was done. No correlation was found between the values of this pressure and consciousness disturbances. Three types of pressure change patterns were demonstrated: type A - low or normal values unchanging in 43 cases, type B - high initial values with normalization during conservative treatment, type C - very high initial values which decreased after operation in only some patients.

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The results are presented of measurements of the intracranial pressure, pressure instability index and shifting of ventricular structures in 42 patients with non-traumatic intracerebral haematoma. Only the value of the instability index showed a correlation with the state of consciousness. For a more complete assessment of the state of sufficiency of the intracranial pressure compensation mechanism all these parameters should be analysed jointly.

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CSF nonspecific esterase (ANAE) activities of mononuclear phagocytes of 35 patients with intracerebral hematoma (ICH) with clear CSF and 25 with cerebral thrombosis and 17 normals were observed. The ANAE activities of ICH were much higher than those of thrombosis significantly (P less than 0.01). Furthermore, the distributions of ANAE activities of all cases suggested that there were few overlaps between both diseases. The CSF cytochemical detection was obviously superior to routine CSF cytological examination in differentiating strokes with clear CSF. The authors concluded that these results provided a simple inexpensive and relatively accurate method to differentiate hemorrhagic from ischemic cerebrovascular diseases in case of without CT.

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Using radioimmunoassay (RIA) concentrations of immunoreactive TRH (TRH-ir) in cerebrospinal fluid (CSF) and plasma were determined after acute head injury in 29 patients. The results showed that the concentrations of TRH-ir (pmol/L) in CSF and plasma on the days when injuries were sustained were 29.25 +/- 8.92 pg/ml and 30.29 +/- 8.26 (1 pg/ml = 2.8 pmol/L) in mildly (n = 12), 57.78 +/- 11.72 and 65.27 +/- 8.57 in moderately (n = 9), and 70.09 +/- 7.58 and 85.65 +/- 7.92 in severely (n = 8), head-injured patients. While the concentrations of TRH-ir in CSF and plasma were 25.11 +/- 11.85 and 27.90 +/- 11.39 in the control group (n = 10). Dynamic observations revealed that the contents of TRH-ir in CSF and plasma were gradually recovered to their control levels when improvement of the head-injured patients took place. But they were significantly decreased and became much lower than the control levels in patients with poor prognosis. These results suggest that the assay of TRH-ir in CSF and plasma has clinical significance in reflecting the severity and prognosis of acute head-injured patients.

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To evaluate the diagnostic value of lactate dehydrogenase (LD) isoenzymes in cerebrospinal fluid (CSF), 93 consecutive CSF specimens were analyzed. These specimens were from patients of four categories: tumors, infections, hemorrhages, and others. It was found that the isoenzyme patterns overlapped among different categories, but they differed within each category and were thus helpful in differential diagnosis. For instance, metastatic tumors showed prominent LD-5, whereas a primary brain tumor demonstrated an increase in all fractions. Viral encephalitis revealed an increase in the first three isoenzymes and bacterial meningitis, the last two. In acquired immune deficiency syndrome (AIDS) cases, however, LD isoenzyme changes were demonstrated in CSF when only cryptococcal meningitis and not when encephalitis was present. Both subdural and subarachnoid hemorrhages showed elevation of all fractions in our study. Elevation of the first three fractions was usually due to brain tissue damage or hemorrhage, as proven by our isoenzyme study of hemolysate mixed with CSF. The prominence of the last two fractions was related to anaerobic metabolism in the central nervous system or to granulocytic infiltration. In conclusion, LD isoenzyme analysis in CSF is helpful in differential diagnosis of various CNS disorders, although its sensitivity awaits further improvement.

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We tested the hypothesis that the concentration of atrial natriuretic factor in the cerebrospinal fluid is an indicator of brain injury in patients with intracranial disease. Atrial natriuretic factor concentration was measured in 72 samples of cerebrospinal fluid from 28 patients with intraventricular drains and in nine samples from outpatient controls undergoing diagnostic lumbar puncture. Levels were correlated with diagnosis; systemic fluid administration; concentration of atrial natriuretic factor in the plasma; intracranial pressure; sodium, glucose, and protein concentrations, osmolality, and cell count in the cerebrospinal fluid; sodium concentration in the serum; and hemodynamics. Atrial natriuretic factor concentration was highest in cerebrospinal fluid from patients with intracerebral hematoma, followed by those with obstructive hydrocephalus and subarachnoid hemorrhage (19 +/- 2, 13 +/- 3, and 8 +/- 2 pg/ml, respectively); atrial natriuretic factor concentration was less than 4 pg/ml in the controls. Patients treated with fluid restriction had significantly higher atrial natriuretic factor levels than those receiving maintenance or high-volume fluids (16 +/- 3, 8 +/- 2, 10 +/- 1 pg/ml, respectively). The concentration of atrial natriuretic factor in the plasma was significantly elevated in patients with intracerebral hematoma and subarachnoid hemorrhage (155 +/- 38 and 92 +/- 20 pg/ml, respectively) and did not correlate with fluid administration or the concentration of atrial natriuretic factor in the cerebrospinal fluid. Neither cerebrospinal fluid nor plasma concentrations of atrial natriuretic factor correlated with intracranial pressure; cerebrospinal fluid sodium, glucose, or protein concentrations, osmolality, or cell count; serum sodium concentration; or hemodynamics. We conclude that the concentration of atrial natriuretic factor in the cerebrospinal fluid is a nonspecific indicator of brain injury.(ABSTRACT TRUNCATED AT 250 WORDS)

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beta-endorphin-like immunoreactivity (beta-ELI) was measured in the cerebrospinal fluid (CSF) of 36 patients with acute head injury and 12 controls. The mean values of beta-ELI in CSF of controls and patients with moderate and severe acute head injury were 51.9 +/- 5.6 pg/ml, 110.5 pg/ml, and 173.8 +/- 20.1 pg/ml respectively, with significant difference between them (p less than 0.05). The results showed that beta-ELI increased in CSF of acute head injury patients.

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The authors examined 65 children with closed head trauma of varying severity and 68 children with other acute neurological diseases. A new method of the diagnosis and assessment of the severity of closed craniocerebral injury, namely, crystallographic examination of the patients' cerebrospinal fluid, was used in the study. The method helped to establish the clinical forms of closed head trauma and to determine its severity and the presence of complications.

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Therapeutical correction of intracranial pressure changes were conducted in 14 patients suffering from traumatic intracranial hematomas by endolumbar administration of physiological solution. The distinguishing feature of this method is the possibility of continuous control of the intracranial pressure level by means of long-term graphic recording of epidural pressure. This makes it possible to perform endolumbar administration of physiological solution in a dose which is determined by the initial level of epidural intracranial pressure. Therapeutic correction of intracranial pressure by endolumbar injection of physiological solution proved successful in the initial stages of dislocation of the brain and in stable intracranial hypotension.

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15 patients with psychosomatic disease, 26 patients with miscellaneous neurological diseases, and 16 patients with cerebrovascular disease were investigated with regard to concentrations of ferritin in serum and cerebrospinal fluid (CSF). The mean CSF ferritin concentration in the psychosomatic group was 6.2 micrograms/l +/- 2.4 (1 S.D.). Patients with recent cerebral infarction had similar values while 2 patients with intracerebral hematomas had very high CSF ferritin concentrations. There was a positive correlation between serum and CSF ferritin levels and between CSF total protein and ferritin in patients with a damaged blood-CSF barrier only. At present, the practical value of analysing ferritin in the CSF is very small.

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By means of a new technique (Particle Counting Immunoassay), we have determined the level of ferritin in 470 samples of cerebrospinal fluid of patients with various neurological disorders. The median value obtained in a control group was 2.3 ng/ml with an upper limit at 5.5 ng/ml. the concentrations in the serum and cerebrospinal fluid were independent, but that in cerebrospinal fluid correlated with its total protein content. High values of ferritin were found in infectious meningo-encephalitis, in vascular diseases of the central nervous system, and, unexpectedly, in several cases of dementia without obvious vascular pathology.

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Thirty-six patients with SAH were submitted to continuous ICP monitoring: in 33 cases a continuous ventricular fluid pressure recording was performed in acute stage. According to Hunt and Hess, 2 patients were graded I, one II, one III, 13 IV and 16 V. In the remaining 3 cases who developed a normal pressure hydrocephalus 15, 20 and 40 days from bleeding an extradural miniaturized transducer was applied. B and C waves were common findings in acutely recorded patients. Typical A waves accompanied base line recordings in patients with NPH. From analysis of data the authors evidenced that elevated ICP values have been registered not only in patients graded as III, IV and V but also in those graded I and II: as 89% of patients belong to grades IV and V it was impossible to correlate clinical status with ICP. In patients with spasm it was never noted ICP values higher than 20 mmHg during recording time (from 60 hours to 10 days). In order to reduce intracranial hypertension CSF drainage was performed in 33 patients acutely registered. In patients graded I and II this procedure was followed by an ICP reduction and an improvement of the clinical status. In none of the patients graded IV and V in spite of pressure maintained at 10 mmHg, CSF drainage affected clinical evolution.

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