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.

The role of endothelin-1 in the origin of cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage

1992 ◽  
Vol 77 (1) ◽  
pp. 96-100 ◽  
Author(s):  
Ryuta Suzuki ◽  
Hiroyuki Masaoka ◽  
Yukio Hirata ◽  
Fumiaki Marumo ◽  
Eiji Isotani ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Time Course ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Normal Range ◽  
Content Type ◽  
Patient Groups ◽  
Group 3 ◽  
Fine Print

✓ Plasma and cerebrospinal fluid (CSF) endothelin (ET)-1-like immunoactivity in 27 patients with aneurysmal subarachnoid hemorrhage (SAH) was measured serially by radioimmunoassay for 2 weeks after SAH onset. Mean ET-1-like immunoactivity levels in plasma of patients with SAH were highly elevated during the whole study period, while the levels in CSF of the same patients were not. Plasma ET-1-like immunoactivity levels in patients with SAH classified as Fisher computerized tomography (CT) Group 3 were higher than those in patients with SAH classified as Fisher CT Groups 1 and 2. There were no significant differences in plasma ET-1-like immunoactivity levels between the patient groups stratified by Hunt and Kosnik grade. In this series, plasma ET-1-like immunoactivity levels in the 12 patients with vasospasm were higher than those in the 15 patients without vasospasm during the 1st week; CSF ET-1-like immunoactivity levels in patients with vasospasm were in the normal range on Days 0 to 3 after SAH onset, then became elevated on Days 5 to 7 and remained high until the end of the 2nd week. In contrast, CSF ET-1-like immunoactivity levels in patients without vasospasm were within the normal range during the entire period of study. The time course of the occurrence of vasospasm and that of the increase in CSF ET-1-like immunoactivity coincided precisely. The possible role of endogenous ET-1 in the pathogenesis of vasospasm due to SAH is discussed.

Evaluation of a method for noninvasive intracranial pressure assessment during infusion studies in patients with hydrocephalus

2000 ◽  
Vol 92 (5) ◽  
pp. 793-800 ◽  
Author(s):  
Bernhard Schmidt ◽  
Marek Czosnyka ◽  
Jens Jürgen Schwarze ◽  
Dirk Sander ◽  
Werner Gerstner ◽  
...  
Keyword(s):  
Mathematical Model ◽  
Intracranial Pressure ◽  
Time Course ◽  
Cerebral Blood Flow Velocity ◽  
Absolute Error ◽  
Content Type ◽  
Arterial Blood ◽  
Potential Clinical Benefit ◽  
The Mean ◽  
Fine Print

Object. A mathematical model previously introduced by the authors allowed noninvasive intracranial pressure (nICP) assessment. In the present study the authors investigated this model as an aid in predicting the time course of raised ICP during infusion tests in patients with hydrocephalus and its suitability for estimating the resistance to outflow of cerebrospinal fluid (Rcsf).Methods. Twenty-one patients with hydrocephalus were studied. The nICP was calculated from the arterial blood pressure (ABP) waveform by using a linear signal transformation, which was dynamically modified by the relationship between ABP and cerebral blood flow velocity. This model was verified by comparison of nICP with “real” ICP measured during lumbar infusion tests. In all simulations, parallel increases in real ICP and nICP were evident. The simulated Rcsf was computed using nICP and then compared with Rcsf computed from real ICP. The mean absolute error between real and simulated Rcsf was 4.1 ± 2.2 mm Hg minute/ml. By the construction of simulations specific to different subtypes of hydrocephalus arising from various causes, the mean error decreased to 2.7 ± 1.7 mm Hg minute/ml, whereas the correlation between real and simulated Rcsf increased from R = 0.73 to R = 0.89 (p < 0.001).Conclusions. The validity of the mathematical model was confirmed in this study. The creation of type-specific simulations resulted in substantial improvements in the accuracy of ICP assessment. Improvement strategies could be important because of a potential clinical benefit from this method.

Acute cerebral blood flow response to dopamine-induced hypertension after subarachnoid hemorrhage

1994 ◽  
Vol 80 (5) ◽  
pp. 857-864 ◽  
Author(s):  
Joseph M. Darby ◽  
Howard Yonas ◽  
Elizabeth C. Marks ◽  
Susan Durham ◽  
Robert W. Snyder ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Systemic Blood Pressure ◽  
Content Type ◽  
Arterial Blood ◽  
Induced Hypertension ◽  
Fine Print

✓ The effects of dopamine-induced hypertension on local cerebral blood flow (CBF) were investigated in 13 patients suspected of suffering clinical vasospasm after aneurysmal subarachnoid hemorrhage (SAH). The CBF was measured in multiple vascular territories using xenon-enhanced computerized tomography (CT) with and without dopamine-induced hypertension. A territorial local CBF of 25 ml/100 gm/min or less was used to define ischemia and was identified in nine of the 13 patients. Raising mean arterial blood pressure from 90 ± 11 mm Hg to 111 ± 13 mm Hg (p < 0.05) via dopamine administration increased territorial local CBF above the ischemic range in more than 90% of the uninfarcted territories identified on CT while decreasing local CBF in one-third of the nonischemic territories. Overall, the change in local CBF after dopamine-induced hypertension was correlated with resting local CBF at normotension and was unrelated to the change in blood pressure. Of the 13 patients initially suspected of suffering clinical vasospasm, only 54% had identifiable reversible ischemia. The authors conclude that dopamine-induced hypertension is associated with an increase in flow in patients with ischemia after SAH. However, flow changes associated with dopamine-induced hypertension may not be entirely dependent on changes in systemic blood pressure. The direct cerebrovascular effects of dopamine may have important, yet unpredictable, effects on CBF under clinical pathological conditions. Because there is a potential risk of dopamine-induced ischemia, treatment may be best guided by local CBF measurements.

Time course of vasospasm in man

1978 ◽  
Vol 48 (2) ◽  
pp. 173-178 ◽  
Author(s):  
Bryce Weir ◽  
Michael Grace ◽  
John Hansen ◽  
Charles Rothberg
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Subarachnoid Space ◽  
Time Course ◽  
Content Type ◽  
Base Of Skull ◽  
Fine Print

✓ Measurements were made at eight predetermined positions on 627 sets of angiograms from 293 patients with aneurysms. A ratio between the sum of the vessel diameters in the subarachnoid space to the sum in the base of skull and neck was calculated and plotted against time. Vasospasm has its onset in man about Day 3 after subarachnoid hemorrhage, is maximal at Days 6 to 8, and is gone by Day 12. There is a tendency for patients in poor clinical grades to have more vasospasm. The patients with most vasospasm have a significantly higher mortality than those with the least.

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).

Changes of neuropeptide immunoreactivity in cerebrovascular nerve fibers after experimentally produced SAH

1987 ◽  
Vol 66 (5) ◽  
pp. 741-747 ◽  
Author(s):  
Yoshihiko Uemura ◽  
Tetsuo Sugimoto ◽  
Shinichiro Okamoto ◽  
Hajime Handa ◽  
Noboru Mizuno
Keyword(s):  
Body Weight ◽  
Subarachnoid Hemorrhage ◽  
Substance P ◽  
Unit Area ◽  
Single Injection ◽  
Nerve Fibers ◽  
The Other ◽  
Content Type ◽  
Arterial Blood ◽  
Fine Print

✓ The immunoreactivity of vasoactive intestinal polypeptide (VIP)-, substance P (SP)-, and neuropeptide Y (NPY)-containing nerve fibers in the basilar artery (BA) and proximal portion of the middle cerebral artery (M1) was immunohistochemically examined in the dog after experimentally produced subarachnoid hemorrhage (SAH). The SAH was produced by a single injection of fresh autologous arterial blood (1 ml/kg body weight) into the cisterna magna. The density (the averaged number of nerve fibers in a unit area) of VIP-, SP-, and NPY-immunoreactive perivascular nerve fibers in the M1 segment and the BA was markedly decreased (5% to 40% of the normal value) immediately after the injection. The density of VIP- and SP-immunoreactive perivascular fibers increased 2 or 3 weeks after SAH and became normal by the 63rd day after injection. On the other hand, no substantial recovery was observed in the density of NPY-immunoreactive perivascular fibers by 63 days after injection.

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.

Subarachnoid hemorrhage—induced upregulation of the 5-HT1B receptor in cerebral arteries in rats

2003 ◽  
Vol 99 (1) ◽  
pp. 115-120 ◽  
Author(s):  
Jacob Hansen-Schwartz ◽  
Natalie Løvland Hoel ◽  
Cang-Bao Xu ◽  
Niels-Aage Svendgaard ◽  
Lars Edvinsson
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Real Time ◽  
Cerebral Vasospasm ◽  
Cerebral Arteries ◽  
Specific Treatment ◽  
Content Type ◽  
Sequence Of Events ◽  
Arterial Blood ◽  
Receptor Phenotype ◽  
Fine Print

Object. Cerebral vasospasm following subarachnoid hemorrhage (SAH) leads to reduced blood flow in the brain. Inspired by organ culture—induced changes in the receptor phenotype of cerebral arteries, the authors investigated possible changes in the 5-hydroxytryptamine (HT) receptor phenotype after experimental SAH. Methods. Experimental SAH was induced in rats by using an autologous prechiasmatic injection of arterial blood. Two days later, the middle cerebral artery (MCA), posterior communicating artery (PCoA), and basilar artery (BA) were harvested and examined functionally with the aid of a sensitive in vitro pharmacological method and molecularly by performing quantitative real-time reverse transcription—polymerase chain reaction (PCR). In the MCA and BA the 5-HT1B receptor was upregulated, as determined through both functional and molecular analysis. In response to selective 5-HT1 receptor agonists both the negative logarithm of the 50% effective concentration was increased (one log unit in the MCA and one half unit in the BA), as was the agonist's potency (increased by 50% in the MCA and doubled in the BA). In addition, the authors found an approximately fourfold increase in the number of copies of messenger RNA coding for the 5-HT1B receptor as determined by quantitative real-time PCR. In the PCoA no upregulation of the 5-HT1B receptor was observed. Conclusions. Changes in the receptor phenotype in favor of contractile receptors may well represent the end stage in a sequence of events leading from SAH to the actual development of cerebral vasospasm. Insight into the mechanism of upregulation may provide new targets for developing specific treatment against cerebral vasospasm.

Transcranial Doppler ultrasound studies of cerebral autoregulation and subarachnoid hemorrhage in the rabbit

1990 ◽  
Vol 73 (4) ◽  
pp. 601-610 ◽  
Author(s):  
Richard J. Nelson ◽  
Sheila Perry ◽  
Tony K. Hames ◽  
John D. Pickard
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Flow Velocity ◽  
Doppler Ultrasound ◽  
Transcranial Doppler ◽  
Cerebral Autoregulation ◽  
Time Course ◽  
Cerebrovascular Reactivity ◽  
Waveform Analysis ◽  
Content Type ◽  
Fine Print

✓ The authors describe a method for Doppler ultrasound recording of flow velocity in the basilar artery of normal rabbits and rabbits with experimental subarachnoid hemorrhage (SAH). With this transcranial Doppler (TCD) model, clinical assumptions regarding flow velocity/cerebral blood flow (CBF) relationships, autoregulatory responses, and Doppler spectral waveform analysis can be tested under controlled conditions and compared with established methods of CBF measurement (hydrogen clearance). The time course of changes in flow velocity following SAH (cerebral vasospasm) is successfully demonstrated using the experimental TCD method. There are significant differences in the flow velocity and CBF responses to hypercapnia, hypocapnia, and trimethaphan-induced hypotension which indicate that TCD cannot be considered a simple alternative to CBF measurement for the study of cerebrovascular reactivity and cerebral autoregulation.

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.

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