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The workup of patients with suspected subarachnoid hemorrhage (SAH) presenting late is complicated by a loss of diagnostic sensitivity of computed tomography (CT) brain imaging and cerebrospinal fluid (CSF) bilirubin levels. In this prospective longitudinal study of CSF ferritin levels in SAH, serial CSF samples from 14 patients with aneurysmal SAH requiring extraventricular drainage (EVD) were collected. The control group comprised 44 patients presenting with headache suspicious of SAH. Nine patients underwent a traumatic spinal tap. CSF ferritin levels were significantly higher in the patients with SAH compared with controls (P < .0001). The upper reference range of CSF ferritin is 12 ng/mL, and there was no significant difference between the traumatic and normal spinal taps (mean, 9.0 ng/mL vs 3.9 ng/mL; P = .59). CSF ferritin levels increased after SAH, from an average of 65 ng/mL on day 1 to 1750 ng/mL on day 11 (P < .01). Both the Fisher and Columbia CT scores were significantly correlated with CSF ferritin level. The increase in CSF ferritin level after SAH and possibly may provide additional diagnostic information in patients with suspected SAH who present late to the clinic., (Copyright © 2011 National Stroke Association. All rights reserved.)

Intracellular calcium (Ca++) regulation of cerebral vessels is impaired after subarachnoid hemorrhage (SAH), making secondary pathways, such as that involving apolipoprotein E, potentially more influential. To evaluate cerebrospinal fluid (CSF) apolipoprotein E and Ca++ levels as biomarkers of cerebral vasospasm, we examined changes in levels over time and apolipoprotein E (APOE) epsilon4 allele presence after SAH in individuals with and without vasospasm. We hypothesized that individuals with low apolipoprotein E levels, increased Ca++ levels and/or at least one copy of the APOE epsilon4 allele would have vasospasm. Daily samples from 50 participants, aged 18-75, with SAH were used to quantify apolipoprotein E and Ca++ levels. Vasospasm was verified using cerebral angiogram and/or elevated transcranial Dopplers in combination with clinical neurologic deterioration. Overall apolipoprotein E levels were higher in individuals with the APOE epsilon4 allele (p = .02) or angiographic vasospasm (p = .01), but there were no differences between individuals with and without symptomatic vasospasm. There were no significant changes in apolipoprotein E levels over time. Individuals with the epsilon4 allele had lower Ca++ levels (p = .02) with trends suggesting a different pattern of change over time (p = .07). CSF Ca++ levels were lower in individuals with symptomatic vasospasm (p < .01). Change in apolipoprotein E and Ca++ levels (p = .006) correlated over time regardless of genotype or vasospasm status. These findings suggest that apolipoprotein E and Ca++ may be interacting after SAH, but this interaction does not appear to influence vasospasm.

Object: Despite the application of current standard therapies, vasospasm continues to result in death or major disability in patients treated for ruptured aneurysms. The authors investigated the effectiveness of continous MgSO4 infusion for vasospasm prophylaxis., Methods: Seventy-six adults (mean age 54.6 years; 71% women; 92% Caucasian) were included in this comparative matched-cohort study of patients with aneurysmal subarachnoid hemorrhage on the basis of computed tomography (CT) findings. Thirty-eight patients who received continuous MgSO4 infusion were matched for age, race, sex, treatment option, Fisher grade, and Hunt and Hess grade to 38 historical control individuals who did not receive MgSO4infusion. Twelve grams of MgSO4 in 500 ml normal saline was given intravenously daily for 12 days if the patient presented within 48 hours of aneurysm rupture. Vasospasm was diagnosed on the basis of digital substraction angiography, CT angiography, and transcranial Doppler ultrasonography, and evidence of neurological deterioration. Symptomatic vasospasm was present at a significantly lower frequency in patients who received MgSO4 infusion (18%) compared with patients who did not receive MgSO4 (42%) (p = 0.025). There was no significant difference in mortality rate at discharge (p = 0.328). A trend toward improved outcome as measured by the modifed Rankin Scale (p = 0.084), but not the Glasgow Outcome Scale (p = 1.0), was seen in the MgSO4 treated group., Conclusions: Analysis of the results suggests that MgSO4 infusion may have a role in cerebral vasospasm prophylaxis if therapy is initiated within 48 hours of aneurysm rupture.

Purpose: The monohydroxylated metabolite of arachidonic acid, 20-hydroxyeicosatetraenoic acid (20-HETE), is a potent vasoconstrictor of cerebral microvessels. 20-HETE formation is substantially elevated in the cerebral spinal fluid (CSF) in the rat subarachnoid hemorrhage (SAH) model. The presence of 20-HETE in human CSF has not been demonstrated. Therefore, it was the purpose of this study to determine if HETE metabolites are present in human CSF after SAH., Methods: CSF samples were collected daily from four SAH patients over 15 days. HETE metabolites were separated by HPLC with identification by ion-trap MS/MS and quantification via single quadrupole MS operating in negative single ion monitoring mode., Results: Two major metabolites were identified as 12-HETE and 20-HETE. 20-HETE maximal concentrations were 2.9 and 0.7 ng/ml at approximately 70 h in the two patients with symptomatic cerebral vasospasm (SV) after SAH. Concentrations of 12-HETE in these patients peaked at 21.9 ng/ml and 2.8 ng/ml. Concentrations of 20-HETE and 12-HETE were non-detectible in the majority of the samples obtained from two matched SAH patients without SV., Conclusions: This study is the first to demonstrate that 20-HETE and 12-HETE are present in the CSF of SAH patients at physiologically relevant concentrations. Based on this information future prospective studies will allow for the delineation of the role of these metabolites in the pathogenesis of SAH.

Patients experiencing subarachnoid hemorrhage (SAH) symptoms may delay seeking medical attention, not realizing the severity of these symptoms. The purposes of this study were to determine (a) the length of time between the development of SAH symptoms in patients and when treatment was initially sought and (b) whether the delay in hospital admission had an effect on patient outcomes. Inclusion criteria were age (18-75 years) and diagnosis of severe SAH. Consent was obtained on 90 eligible patients admitted to the neurovascular intensive care unit. Outcomes were assessed at 3 months using the Glasgow Outcome Scale (GOS) and Modified Rankin Scale (MRS). Initial time delay, calculated by subtracting the time of initial symptom development from the time of admission to the emergency department (ED), ranged from 0.08 to 103 hours. There was no relationship between the initial time delay and GOS or MRS scores. There was a significant difference between the time to initial ED admission to a trauma ED and to a community ED; patients were admitted within 2.7 hours to a trauma ED admission, compared to 7 hours for a community ED admission. There was a significant relationship between the Hunt and Hess Scale and GOS and between the Hunt and Hess and MRS. There was a significant relationship between the Fisher Grade and GOS and between the Fisher Grade and MRS. This study shows that patients may delay treatment for nearly 7 hours after initial symptoms develop. This suggests that laypersons are not aware of SAH symptoms, thereby delaying ED admission and care. The study also suggests that more severe symptoms upon admission to the ED were related to poorer outcomes. Initial clinical presentation is a useful predictor for SAH outcomes. This study supports the idea that the general public needs to be educated on the symptoms of SAH.

The purpose of this study was to compare functional outcomes at 6 months post-subarachnoid hemorrhage (SAH) secondary to cerebral aneurysm rupture in subjects who were either surgically clipped or endovascularly coiled while controlling for aneurysm site.A retrospective chart review of 228 subjects was performed. The sample included subjects (ages 18 to 75) with the diagnosis of SAH from a ruptured cerebral aneurysm verified by angiography or computed tomographic angiography with a Hunt and Hess score >2 and/or a Fisher grade >1. Aneurysm site was determined by the neurosurgeon then categorized into posterior or anterior circulation. The sample was stratified into 2 groups by treatment. Functional outcome was evaluated at 6 months post-SAH using the Glasgow Outcome Scale and Modified Rankin Scale.There were no significant differences in age, race, sex, or Fisher grade between treatment groups. There were significant differences in Hunt and Hess scores (P=0.02). One hundred thirty (57%) subjects received surgical clipping and 98 (43%) received endovascular coiling. There was a significant difference in aneurysm site between the 2 treatment groups (P=0.00), with the anterior aneurysms more likely to be clipped. However, there were no significant differences in outcome based on treatment group (Glasgow Outcome Scale, P=0.95, Modified Rankin Scale, P=0.95) after controlling for aneurysm site.The results of the current study are similar to the work of others, suggesting that the decision regarding treatment option needs to be individualized based on the presentation of the patient. [ABSTRACT FROM AUTHOR]