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.

Cerebral microdialysis monitoring: determination of normal and ischemic cerebral metabolisms in patients with aneurysmal subarachnoid hemorrhage

2000 ◽  
Vol 93 (5) ◽  
pp. 808-814 ◽  
Author(s):  
Mette K. Schulz ◽  
Lars Peter Wang ◽  
Mogens Tange ◽  
Per Bjerre
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Delayed Cerebral Ischemia ◽  
Neuronal Injury ◽  
Low Flow ◽  
Cerebral Microdialysis ◽  
Intracerebral Microdialysis ◽  
Content Type ◽  
Wide Range ◽  
Fine Print

Object. The success of treatment for delayed cerebral ischemia is time dependent, and neuronal monitoring methods that can detect early subclinical levels of cerebral ischemia may improve overall treatment results. Cerebral microdialysis may represent such a method. The authors' goal was to characterize patterns of markers of energy metabolism (glucose, pyruvate, and lactate) and neuronal injury (glutamate and glycerol) in patients with subarachnoid hemorrhage (SAH), in whom ischemia was or was not suspected.Methods. By using low-flow intracerebral microdialysis monitoring, central nervous system extracellular fluid concentrations of glucose, pyruvate, lactate, glutamate, and glycerol were determined in 46 patients suffering from poor-grade SAH. The results in two subgroups were analyzed: those patients with no clinical or radiological signs of cerebral ischemia (14 patients) and those who succumbed to brain death (five patients).Significantly lower levels of energy substrates and significantly higher levels of lactate and neuronal injury markers were observed in patients with severe and complete ischemia when compared with patients without symptoms of ischemia (glucose 0 compared with 2.12 ± 0.15 mmol/L; pyruvate 0 compared with 151 ± 11.5 µmol; lactate 6.57 ± 1.07 compared with 3.06 ± 0.32 mmol/L; glycerol 639 ± 91 compared with 81.6 ± 12.4 µmol; and glutamate 339 ± 53.4 compared with 14 ± 3.33 µmol). Immediately after catheter placement, glutamate concentrations declined over the first 4 to 6 hours to reach stable values. The remaining parameters exhibited stable values after 1 to 2 hours.Conclusions. The results confirm that intracerebral microdialysis monitoring of patients with SAH can be used to detect patterns of cerebral ischemia. The wide range from normal to severe ischemic values calls for additional studies to characterize further incomplete and possible subclinical levels of ischemia.

Cerebral hemodynamic impairment after aneurysmal subarachnoid hemorrhage as evaluated using transcranial Doppler ultrasonography: relationship to delayed cerebral ischemia and clinical outcome

2001 ◽  
Vol 95 (3) ◽  
pp. 393-401 ◽  
Author(s):  
Tõnu Rätsep ◽  
Toomas Asser
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Clinical Outcome ◽  
Transcranial Doppler ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Content Type ◽  
Unfavorable Clinical Outcome ◽  
Hemodynamic Impairment ◽  
Fine Print

Object. In this study the authors evaluated the relative role of cerebral hemodynamic impairment (HDI) in the pathogenesis of delayed cerebral ischemia and poor clinical outcome after aneurysmal subarachnoid hemorrhage (SAH). Methods. Cerebral hemodynamics were assessed daily with transcranial Doppler (TCD) ultrasonography in 55 consecutive patients with verified SAH. Hemodynamic impairment was defined as blood flow velocity (BFV) values consistent with vasospasm in conjunction with impaired autoregulatory vasodilation as evaluated using the transient hyperemic response tests in the middle cerebral arteries. A total of 1344 TCD examinations were performed, in which the evaluation of HDI was feasible during 80.9% and HDI was registered during 12% of the examinations. It was found that HDI occurred in 60% of patients and was frequently recorded in conjunction with severe vasospasm (p < 0.05) and a rapid increase of BFV values (p < 0.05). Detection of HDI was closely associated with the development of delayed ischemic brain damage after SAH (p < 0.05). Furthermore, because delayed ischemia was never observed in cases in which vasospasm had not led to the development of HDI, its occurrence increased significantly the likelihood of subsequent cerebral ischemia among the patients with vasospasm (p < 0.05). Detection of HDI was independently related to unfavorable clinical outcome according to Glasgow Outcome Scale at 6 months after SAH (p < 0.05). Conclusions. The results showed that HDI is common after SAH and can be evaluated with TCD ultrasonography in routine clinical practice. Detection of HDI could be useful for identifying patients at high or low risk for delayed ischemic complications and unfavorable clinical outcome after SAH.

Aspirin and delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage

1995 ◽  
Vol 82 (6) ◽  
pp. 945-952 ◽  
Author(s):  
Seppo Juvela
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Cerebral Infarction ◽  
Platelet Function ◽  
Delayed Cerebral Ischemia ◽  
Aneurysm Rupture ◽  
Content Type ◽  
Reduced Risk ◽  
Fine Print

✓ This follow-up study was designed to evaluate whether the use of aspirin either before or after aneurysm rupture affects the occurrence of delayed cerebral ischemia. Aspirin inhibits platelet function and thromboxane production and has been shown to reduce the risk of various cardiovascular and cerebrovascular ischemic diseases. Following admission, the patients in this study were interviewed regarding their use of aspirin and other medicines prior to and after hemorrhage, and their urine was screened qualitatively for salicylates. Patient outcome and the occurrence of hypodense lesions consistent with cerebral infarction on follow-up computerized tomography (CT) were studied prospectively up to 1 year after hemorrhage. Of 291 patients, 31 (11%) died because of the initial hemorrhage and 18 (6%) died due to rebleeding within 4 days after hemorrhage. Of the remaining 242 patients, 90 (37%) had delayed cerebral ischemia, which caused a permanent neurological deficit or death in 54 patients (22%). Of 195 patients undergoing follow-up CT, 85 (44%) had cerebral infarction that was not seen on the CT scan obtained on admission. Those who had salicylates in the urine on admission had a relative risk of 0.40 (95% confidence interval (CI), 0.15 to 1.10) of delayed ischemia with fixed deficit and a risk of 0.40 (95% CI, 0.18 to 0.93) of cerebral infarction compared with patients who did not have salicylates in their urine. This reduced risk of ischemic complications with aspirin use was restricted to those patients who used aspirin before hemorrhage, when the risk of ischemia was 0.21 (95% CI, 0.03 to 1.63) and the risk of infarct was 0.18 (95% CI, 0.04 to 0.84) compared with those who had not used aspirin. The reduced risk of cerebral infarction remained significant after adjustment for several potential confounding factors (adjusted risk 0.19; 95% CI, 0.04 to 0.89). These observations suggest that platelet function at the time of subarachnoid hemorrhage may be associated with delayed cerebral ischemia after aneurysm rupture.

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.

Plasma endothelin concentrations after aneurysmal subarachnoid hemorrhage

2000 ◽  
Vol 92 (3) ◽  
pp. 390-400 ◽  
Author(s):  
Seppo Juvela
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Healthy Volunteers ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Plasma Concentrations ◽  
Delayed Cerebral Ischemia ◽  
Neurological Deficits ◽  
Content Type ◽  
History Of ◽  
Fine Print

Object. The pathogenesis of cerebral vasospasm and delayed ischemia after subarachnoid hemorrhage (SAH) seems to be complex. An important mediator of chronic vasospasm may be endothelin (ET), with its powerful and long-lasting vasoconstricting activity. In this study the author investigated the correlation between serial plasma concentrations of ET and ischemic symptoms, angiographically demonstrated evidence of vasospasm, and computerized tomography (CT) findings after aneurysmal SAH.Methods. Endothelin-1 immunoreactivity in plasma was studied in 70 patients with aneurysmal SAH and in 25 healthy volunteers by using a double-antibody sandwich-enzyme immunoassay (immunometric) technique.On the whole, mean plasma ET concentrations in patients with SAH (mean ± standard error of mean, 2.1 ± 0.1 pg/ml) did not differ from those of healthy volunteers (1.9 ± 0.2 pg/ml). Endothelin concentrations were significantly higher (p < 0.05) in patients who experienced delayed cerebral ischemia with fixed neurological deficits compared with those in other patients (post-SAH Days 0–5, 3.1 ± 0.8 pg/ml compared with 2.1 ± 0.2 pg/ml; post-SAH Days 6–14, 2.5 ± 0.4 pg/ml compared with 1.9 ± 0.2 pg/ml). Patients with angiographic evidence of severe vasospasm also had significantly (p < 0.05) elevated ET concentrations (post-SAH Days 0–5, 3.2 ± 0.8 pg/ml; post-SAH Days 6–14, 2.7 ± 0.5 pg/ml) as did those with a cerebral infarction larger than a lacuna on the follow-up CT scan (post-SAH Days 0–5, 3.1 ± 0.8 pg/ml; post-SAH Days 6–14, 2.5 ± 0.4 pg/ml) compared with other patients. Patients in whom angiography revealed diffuse moderate-to-severe vasospasm had significantly (p < 0.05) higher ET levels than other patients within 24 hours before or after angiography (2.6 ± 0.3 compared with 1.9 ± 0.2 pg/ml). In addition, patients with a history of hypertension or cigarette smoking experienced cerebral infarctions significantly more often than other patients, although angiography did not demonstrate severe or diffuse vasospasm more often in these patients than in others.Conclusions. Endothelin concentrations seem to correlate with delayed cerebral ischemia and vasospasm after SAH. The highest levels of ET are predictive of the symptoms of cerebral ischemia and vasospasm, and ET may also worsen ischemia in patients with a history of hypertension. Thus, ET may be an important causal or contributing factor to vasospasm, but its significance in the pathogenesis of vasospasm remains unknown.

Plasma endothelin and big endothelin concentrations and serum endothelin-converting enzyme activity following aneurysmal subarachnoid hemorrhage

2002 ◽  
Vol 97 (6) ◽  
pp. 1287-1293 ◽  
Author(s):  
Seppo Juvela
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Plasma Concentrations ◽  
Delayed Cerebral Ischemia ◽  
Magnetic Resonance Images ◽  
Converting Enzyme ◽  
Content Type ◽  
Endothelin Converting Enzyme ◽  
Fine Print

Object. Pathogenesis of delayed ischemia after aneurysmal subarachnoid hemorrhage (SAH) seems to be complex. An important mediator of chronic vasospasm may be endothelin (ET)-1 with its powerful and long-lasting vasoconstricting activity. In this prospective study the author investigated the correlations between serial plasma concentrations of ET-1 and big ET-1 as well as the ET-1/big ET-1 molar concentration ratio and serum endothelin-converting enzyme (ECE)-1 activity, and ischemic complications after SAH. Methods. To measure plasma ET-1 (51 patients), big ET-1 immunoreactivity (22 patients), and serum ECE-1 activity (13 patients), blood samples were obtained on admission, in the morning after aneurysm surgery, and during the 2nd week after hemorrhage in 51 consecutive patients (28 men and 23 women, with a mean age of 50.8 years) with aneurysmal SAH. Mean plasma concentrations of ET-1 in patients with SAH (mean ± standard deviation: on admission, 4.2 ± 2 pg/ml; after surgery, 4.3 ± 2.2 pg/ml; and during the 2nd week after SAH, 3.7 ± 1.9 pg/ml) differed from those in healthy volunteers (2.9 ± 1.2 pg/ml; p < 0.01). Plasma concentrations of ET-1 and big ET-1 as well as the ET-1/big ET-1 ratio did not change significantly with elapsed time following SAH; however, serum ECE-1 activity during the 2nd week after SAH was higher in patients with SAH than that in controls (162 ± 43 compared with 121 ± 56 pg/ml, respectively; p = 0.028). Plasma ET-1 concentrations (p < 0.05) and the ET-1/big ET-1 ratios (p = 0.063) were higher but plasma big ET-1 concentrations were lower (p < 0.05) in patients who experienced symptomatic delayed cerebral ischemia, compared with other patients with SAH. In addition, in cases in which follow-up computerized tomography scans or magnetic resonance images demonstrated permanent ischemic lesions attributable to vasospasm, patients had higher ET-1 concentrations than did other patients with SAH. Conclusions. The plasma ET-1 concentration correlates with delayed cerebral ischemia after SAH, suggesting that an increased ET conversion rate in the endothelium predicts ischemic symptoms. Increased serum ECE-1 activity during the 2nd week may reflect the severity of endothelial injury to cerebral arteries.

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.

Subarachnoid hemorrhage of unknown origin: prognosis and prognostic factors

1985 ◽  
Vol 63 (3) ◽  
pp. 349-354 ◽  
Author(s):  
Jan Brismar ◽  
Göran Sundbärg
Keyword(s):  
Prognostic Factors ◽  
Subarachnoid Hemorrhage ◽  
Prognostic Significance ◽  
Delayed Cerebral Ischemia ◽  
Content Type ◽  
Full Activity ◽  
Time Work ◽  
Part Time ◽  
Part Time Work ◽  
Fine Print

✓ The cases of 127 consecutive patients with subarachnoid hemorrhage (SAH), in whom cerebral panangiography revealed no cause for the bleeding nor any sign of an intraparenchymatous hemorrhage, were reviewed in a study of the long-term prognosis and the possible prognostic factors in this condition. Data for all 127 patients in the study were obtained, with an average follow-up period of 5.4 years. After the 1st week post-SAH, only three rebleeds had occurred. In all, 80% of the patients had returned to full activity, 91% to at least part-time work; if the patients with hypertension were excluded, these figures rose to 86% and 95%, respectively. Decreased wakefulness on admission related to a slightly poorer prognosis, whereas age and red blood cell count in the cerebrospinal fluid had no prognostic significance. Of those patients who, at the end of the 2nd week following the SAH, were fully awake and had not developed any symptoms of delayed cerebral ischemia (87% of all patients admitted), 88% returned to full activity, 97% to at least part-time work. The survival rate for this group, as well as causes of death, seem to be within the range for normal individuals. It should thus be possible to inform these patients (at least the normotensive ones) of the benignity of their condition, directly after normal angiography. Even among the patients who were able to return to full activity, symptoms attributable to the SAH were common: 22% experienced problems such as frequent headaches, vertigo, irritability, and increased fatigability.

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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