Cerebrospinal fluid cytology after subarachnoid hemorrhage

1979 ◽  
Vol 51 (3) ◽  
pp. 352-354 ◽  
Author(s):  
Umeo Ito ◽  
Yutaka Inaba
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
False Negative ◽  
Content Type ◽  
Cerebrospinal Fluid Cytology ◽  
Csf Cells ◽  
Fine Print ◽  
Fluid Cytology

✓ A method is described which has been found capable of detecting subarachnoid hemorrhage (SAH) up to 15 to 17 weeks after its occurrence. The episode of SAH was confirmed by bloody and/or xanthochromic cerebrospinal fluid (CSF) at the time of SAH onset. In this study, 47 samples of lumbar CSF from diagnostically confirmed SAH patients were used. The CSF cells were collected onto slides and stained with May-Gruenwald-Giemsa or Perl's reagent. Iron-positive cells were detected at 1 week, increased by 4 to 6 weeks to 8.5% of total nucleated cells, and decreased to 1% by 15 to 17 weeks. All 27 samples obtained at 2 to 9 weeks after SAH showed iron-positive cells. No iron-positive cells (false-negative samples) were noted in 25% (one of four) of samples obtained during the first week, and in 33% (one of three) of samples obtained 10 to 12 weeks and 15 to 17 weeks after SAH. Of the total samples (37) obtained within 17 weeks after SAH, 8.1% (three of 37) were false negative. No iron-positive cells were detected in samples obtained later than 21 weeks after the SAH episode (10 samples).

Free fatty acids in human cerebrospinal fluid following subarachnoid hemorrhage and their potential role in vasospasm: a preliminary observation

2002 ◽  
Vol 97 (2) ◽  
pp. 272-279 ◽  
Author(s):  
Julie G. Pilitsis ◽  
William M. Coplin ◽  
Michael H. O'Regan ◽  
Jody M. Wellwood ◽  
Fernando G. Diaz ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Cerebrospinal Fluid ◽  
Linoleic Acid ◽  
Subarachnoid Hemorrhage ◽  
Palmitic Acid ◽  
Free Fatty Acids ◽  
Potential Role ◽  
The Other ◽  
Content Type ◽  
Fine Print

Object. The mechanisms leading to vasospasm following subarachnoid hemorrhage (SAH) remain unclear. Accumulation in cerebrospinal fluid (CSF) of free fatty acids (FFAs) may play a role in the development of vasospasm; however, in no previous study have concentrations of FFAs in CSF been examined after SAH. Methods. We collected samples of CSF from 20 patients with SAH (18 cases of aneurysmal SAH and two cases of spontaneous cryptogenic SAH) and used a high-performance liquid chromatography assay to determine the FFA concentrations in these samples. We then compared these findings with FFA concentrations in the CSF of control patients. All FFA concentrations measured 24 hours after SAH were significantly greater than control concentrations (p < 0.01 for palmitic acid and < 0.001 for all other FFAs). All measured FFAs remained elevated for the first 48 hours after SAH (p < 0.05 for linoleic acid, p < 0.01 for palmitic acid, and p < 0.001 for the other FFAs). After 7 days, a second elevation in all FFAs was observed (p < 0.05 for linoleic acid, p < 0.01 for palmitic acid, and p < 0.001 for the other FFAs). Samples of CSF collected within 48 hours after SAH from patients in whom angiography and clinical examination confirmed the development of vasospasm after SAH were found to have significantly higher concentrations of arachidonic, linoleic, and palmitic acids than samples collected from patients in whom vasospasm did not develop (p < 0.05). Conclusions. Following SAH, all FFAs are initially elevated. A secondary elevation occurs between 8 and 10 days after SAH. This study provides preliminary evidence of FFA elevation following SAH and of a potential role for FFAs in SAH-induced vasospasm. A prospective study is warranted to determine if CSF concentrations of FFAs are predictive of vasospasm.

Detection of soluble E-selectin, ICAM-1, VCAM-1, and L-selectin in the cerebrospinal fluid of patients after subarachnoid hemorrhage

1998 ◽  
Vol 89 (4) ◽  
pp. 559-567 ◽  
Author(s):  
Richard S. Polin ◽  
Murad Bavbek ◽  
Mark E. Shaffrey ◽  
Kevin Billups ◽  
Christopher A. Bogaev ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Content Type ◽  
Vascular Adhesion Molecules ◽  
And Migration ◽  
Vascular Adhesion ◽  
Fine Print

Object. The goal of this study was to explore whether the levels of soluble adhesion molecules were elevated in cerebrospinal fluid (CSF) after subarachnoid hemorrhage (SAH). This association was suggested by the known inflammatory response in vasospasm and the role of vascular adhesion molecules in regulating leukocytic adhesion to, and migration across, vascular endothelium. Methods. A prospective analysis was performed on CSF samples obtained in 17 patients who had suffered a recent aneurysmal SAH and in 16 control patients by using quantitative enzyme-linked immunosorbent assays for E-selectin, intercellular adhesion molecule—1 (ICAM—1), vascular adhesion molecule—1 (VCAM-1), and L-selectin. Levels of soluble forms of E-selectin (p = 0.0013), ICAM-1 (p = 0.0001), and VCAM-1 (p = 0.048) were found to be elevated in the CSF of patients after SAH compared with levels in the CSF of normal controls, patients with unruptured aneurysms, and patients tested months after SAH occurred. In addition, individual patients tested at the time of their initial ictus demonstrated a fall in adhesion molecule levels over time. Levels of E-selectin (p = 0.044) were highest in patients who later developed moderate or severe vasospasm. Conclusions. Adhesion molecules are known to be involved in white cell adherence to the endothelium and subsequent diapedesis and migration in which a role in initiation of tissue damage is postulated. The authors have demonstrated the elevation of three adhesion molecules, with severely elevated levels of E-selectin seen in patients who later develop vasospasm. A correlation with a role of vascular adhesion molecules in the pathogenesis of cerebral vasospasm is suggested.

Value of cerebrospinal fluid cytology for the diagnosis of malignancies in the central nervous system

1978 ◽  
Vol 48 (5) ◽  
pp. 747-753 ◽  
Author(s):  
J. Chris Balhuizen ◽  
Gerard Th. A. M. Bots ◽  
Aart Schaberg ◽  
Fré T. Bosman
Keyword(s):  
Central Nervous System ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Retrospective Analysis ◽  
Content Type ◽  
Secondary Tumors ◽  
Cerebral Tumors ◽  
The Central Nervous System ◽  
Fine Print ◽  
Fluid Cytology

✓ The authors present a retrospective analysis of the results of the cytological examinations of cerebrospinal fluid (CSF) samples and tumor-cyst aspirates deriving from 262 patients treated for malignant intracranial primary and secondary tumors, and vertebral and peridural metastastic processes. Positive preoperative CSF samples were found in 15.3% of all cases of primary cerebral malignancies (13.9% of all gliomas) and positive postoperative CSF samples were found in 40% (91% of the medulloblastoma cases). In all cases of single or multiple secondary cerebral tumors, positive preoperative CSF samples were found in 20%.

A membrane filter technique for cerebrospinal fluid cytology

1972 ◽  
Vol 36 (5) ◽  
pp. 661-666 ◽  
Author(s):  
J. Ronald Rich
Keyword(s):  
Cerebrospinal Fluid ◽  
Membrane Filter ◽  
Intracranial Tumor ◽  
Content Type ◽  
Filter Technique ◽  
Abnormal Cells ◽  
Excellent Preservation ◽  
Concentration Methods ◽  
Fine Print ◽  
Fluid Cytology

✓ A simple membrane filter technique is described for the collection and demonstration of exfoliated neoplastic cells in the cerebrospinal fluid (CSF). Abnormal cells were demonstrated in 30 cases: in four of these the diagnosis of a benign intracranial tumor was possible. Using this technique, it appears that cells from the majority of neoplasms in contact with the CSF will be demonstrable. This new technique is superior in many ways to the conventional concentration methods of centrifugation, flocculation, sedimentation, or filtration now used. The primary advantages are the simplicity, the bedside availability, the ability to reuse the filtered fluid for additional studies, the preservation of the cells for later analysis should a cytological laboratory not be immediately available, and, of primary importance, the excellent preservation of cellular morphology.

Source and cause of endothelin-1 release into cerebrospinal fluid after subarachnoid hemorrhage

1997 ◽  
Vol 87 (2) ◽  
pp. 287-293 ◽  
Author(s):  
Ryszard M. Pluta ◽  
Robert J. Boock ◽  
John K. Afshar ◽  
Kathleen Clouse ◽  
Mima Bacic ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Cerebral Vasospasm ◽  
Plasma Levels ◽  
Transient Cerebral Ischemia ◽  
Content Type ◽  
Endothelin 1 ◽  
Fine Print

✓ Despite years of research, delayed cerebral vasospasm remains a serious complication of subarachnoid hemorrhage (SAH). Recently, it has been proposed that endothelin-1 (ET-1) mediates vasospasm. The authors examined this hypothesis in a series of experiments. In a primate model of SAH, serial ET-1 levels were measured in samples from the perivascular space by using a microdialysis technique and in cerebrospinal fluid (CSF) and plasma during the development and resolution of delayed vasospasm. To determine whether elevated ET-1 production was a direct cause of vasospasm or acted secondary to ischemia, the authors also measured ET-1 levels in plasma and CSF after transient cerebral ischemia. To elucidate the source of ET-1, they measured its production in cultures of endothelial cells and astrocytes exposed to oxyhemoglobin (10 µM), methemoglobin (10 µM), or hypoxia (11% oxygen). There was no correlation between the perivascular levels of ET-1 and the development of vasospasm or its resolution. Cerebrospinal fluid and plasma levels of ET-1 were not affected by vasospasm (CSF ET-1 levels were 9.3 ± 2.2 pg/ml and ET-1 plasma levels were 1.2 ± 0.6 pg/ml) before SAH and remained unchanged when vasospasm developed (7.1 ± 1.7 pg/ml in CSF and 2.7 ± 1.5 pg/ml in plasma). Transient cerebral ischemia evoked an increase of ET-1 levels in CSF (1 ± 0.4 pg/ml at the occlusion vs. 3.1 ± 0.6 pg/ml 4 hours after reperfusion; p < 0.05), which returned to normal (0.7 ± 0.3 pg/ml) after 24 hours. Endothelial cells and astrocytes in culture showed inhibition of ET-1 production 6 hours after exposure to hemoglobins. Hypoxia inhibited ET-1 release by endothelial cells at 24 hours (6.4 ± 0.8 pg/ml vs. 0.1 ± 0.1 pg/ml, control vs. hypoxic endothelial cells; p < 0.05) and at 48 hours (6.4 ± 0.6 pg/ml vs. 0 ± 0.1 pg/ml, control vs. hypoxic endothelial cells; p < 0.05), but in astrocytes hypoxia induced an increase of ET-1 at 6 hours (1.5 ± 0.6 vs. 6.4 ± 1.1 pg/ml, control vs. hypoxic astrocytes; p < 0.05). Endothelin-1 is released from astrocytes, but not endothelial cells, during hypoxia and is released from the brain after transient ischemia. There is no relationship between ET-1 and vasospasm in vivo or between ET-1 and oxyhemoglobin, a putative agent of vasospasm, in vitro. The increase in ET-1 levels in CSF after SAH from a ruptured intracranial aneurysm appears to be the result of cerebral ischemia rather than reflecting the cause of cerebral vasospasm.

Potassium and the pathogenesis of cerebral arterial spasm in dog and man

1971 ◽  
Vol 35 (1) ◽  
pp. 45-50 ◽  
Author(s):  
Robert H. Wilkins ◽  
Philip Levitt
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Arteries ◽  
Arterial Spasm ◽  
Content Type ◽  
Blood Clots ◽  
The Individual ◽  
Fine Print

✓ This study investigates the possibility that the intracranial arterial spasm occurring in patients with subarachnoid hemorrhage might be due to potassium released from blood clots surrounding the involved cerebral arteries. Although cerebral arterial spasm could be induced in the dog by the injection of potassium into the chiasmatic cistern, it only occurred with potassium concentrations higher than those expected to result from hemolysis of subarachnoid clots. Furthermore, the potassium concentrations were not elevated in the cerebrospinal fluid of human patients with subarachnoid hemorrhage, and the individual potassium values could not be correlated with the presence or degree of spasm encountered in these patients.

Bilirubin as a cerebrospinal fluid marker of sentinel subarachnoid hemorrhage: a preliminary report in pigs

2004 ◽  
Vol 101 (6) ◽  
pp. 1026-1029 ◽  
Author(s):  
Chad J. Morgan ◽  
Gail J. Pyne-Geithman ◽  
Edward C. Jauch ◽  
Rakesh Shukla ◽  
Kenneth R. Wagner ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Time Course ◽  
Isotonic Saline ◽  
Bilirubin Concentration ◽  
Content Type ◽  
Arterial Blood ◽  
Potential Marker ◽  
Yorkshire Pigs ◽  
Fine Print

Object. A model of subarachnoid hemorrhage (SAH) in pigs was developed to investigate bilirubin concentration in cerebrospinal fluid (CSF) as a potential marker of sentinel SAH. Methods. Seven male Yorkshire pigs received a 250-µl injection of either whole autologous arterial blood (four animals) or isotonic saline (three animals) into the cisternae magna in an effort to produce volumetrically a model of sentinel SAH and a control injection model, respectively. Cerebrospinal fluid volumes of 100 µl were then collected from both the lumbar cistern and cisternae magna at 1 to 2-hour intervals for a total of 24 hours postinjection. The CSF was then tested for bilirubin. Mean concentrations of bilirubin (± standard deviation [SD]) obtained from the lumbar cistern 24 hours following the injection of blood or saline were 4.38 ± 1.04 µM in the SAH animals and 1.02 ± 0.05 µM in the controls. At 24 hours postinjection, mean concentrations (± SD) of cisternae magna bilirubin were 7.29 ± 1.33 ÉM and 1.33 ± 0.14 µM in the SAH animals and controls, respectively. In the SAH group, both the lumbar cistern and cisternae magna bilirubin concentrations differed significantly from baseline values 12 hours following SAH. Conclusions. Elevated concentrations of CSF bilirubin can be detected following a low-volume SAH, and the production of bilirubin occurred over a predictable time course. Twelve hours after hemorrhage, an elevated CSF bilirubin concentration was an indicator of hemolysis occurring in the subarachnoid spaces. The presence of bilirubin in CSF is a potential marker for differentiating SAHs from traumatic lumbar punctures in humans.

Cerebral arterial spasm

1974 ◽  
Vol 40 (4) ◽  
pp. 442-450 ◽  
Author(s):  
George S. Allen ◽  
Lavell M. Henderson ◽  
Shelley N. Chou ◽  
Lyle A. French
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Human Serum ◽  
Basilar Artery ◽  
Contractile Activity ◽  
Arterial Spasm ◽  
Content Type ◽  
Canine Basilar Artery ◽  
Fine Print

✓ In vitro experiments were performed to determine the contractile activity of human serum and cerebrospinal fluid on the canine basilar artery. The majority of contractile activity in these CSF samples, which were collected 2 to 7 days following a subarachnoid hemorrhage, was proven to be due to serotonin. Serotonin was capable of producing a prolonged contraction of the artery depending on its activity. Methylsergide reversibly blocked the artery's response to serotonin and caused a contraction of the basilar artery. Phenoxybenzamine irreversibly blocked the basilar artery's response to serotonin, serum, and CSF.

Increased CSF neopterin levels in subarachnoid hemorrhage

1990 ◽  
Vol 73 (1) ◽  
pp. 69-71 ◽  
Author(s):  
Tiit Mathiesen ◽  
Dietmar Fuchs ◽  
Helmut Wachter ◽  
Hans von Holst
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
T Cell ◽  
Cerebral Ischemia ◽  
T Cell Activation ◽  
Macrophage Activation ◽  
Cell Activation ◽  
Delayed Cerebral Ischemia ◽  
Content Type ◽  
Fine Print

✓ Neopterin concentrations, reflecting T-cell macrophage activation, were analyzed in serum and cerebrospinal fluid (CSF) obtained from 14 patients with subarachnoid hemorrhage (SAH). Neopterin concentrations were elevated in both the serum and CSF. The increase in neopterin concentrations was most marked in the CSF, rising from Days 1 to 3 through Days 6 to 9; levels were highest in patient suffering from delayed cerebral ischemia. The present data were interpreted as signs of an ongoing T cell activation both systemically and in the CSF compartment following SAH.

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