The Fisher Grade in predicting a degree of cerebral vasospasm in patients after intracranial aneurysm rupture.

Background/Aim: Intracranial aneurysms are pathological enlargement of the wall of cerebral arteries. Intracranial aneurysms rupture is a dramatic event with a significant morbidity and mortality. The Fisher Grade is widely accepted in assessment of the extensiveness of aneurysmal subarachnoid hemorrhage (aSAH) and the presence of other intracranial hemorrhage on the computed tomography (CT) scan. Significant early complication of a aSAH may be a cerebral vasospasm. The aim of this study was to determine the relationship between the extensiveness of aSAH, assessed by the Fisher Grade on admission, with the intensity of cerebral vasospasm in patients with ruptured intracranial aneurysm. Methods: This prospective clinical study included 50 patients with aSAH hospitalized at the Clinic of Neurosurgery, Clinical Center of Vojvodina, Novi Sad, Serbia. All the patients underwent 256-layer cranial CT and CT angiography on admission and on the day 9. Based on native CT scans, they were classified according to the Fisher Grade. On CT angiography images, intensity of cerebral vasospasm was determined. Results: On the basis of admission CT images, 24% of patients were classified into the Fisher Grade group 2, while 34% and 42% were in the groups 3 and 4, respectively. A positive correlation of the Fischer Grade on admission with the intensity of cerebral vasospasm was established, but with no statistical significance (ρ = 0.273, p = 0.160). Conclusion: This study showed that the Fisher Grade is not significant in predicting the intensity of cerebral vasospasm in patients hospitalized with intracranial aneurysm rupture.

Cerebral vasospasm patterns following aneurysmal subarachnoid hemorrhage: an angiographic study comparing coils with clips.

BACKGROUND AND PURPOSE: Cerebral vasospasm following aneurysmal subarachnoid hemorrhage (aSAH) results in significant morbidity due to ischemia. Subarachnoid hematoma evacuation during aneurysm clipping reduces the incidence of vasospasm. However, studies comparing endovascular coiling with open clipping have reported similar rates of spasm. We addressed the question of how coiling produces similar (if not less) vasospasm without the benefit of clot evacuation by evaluating vasospasm patterns among patients with aSAH. We hypothesize that cerebrospinal fluid (CSF) circulation plays a major role in clearing blood breakdown products, and that coiling may preserve CSF flow in the subarachnoid space. METHODS: A retrospective chart review identified 36 (18 coiled/18 clipped) patients with aSAH who developed angiographic vasospasm. The degree of spasm was quantified using an ordinal scale from 0 (none) to 5 (severe) for 26 anatomic vessel segments evaluated on 164 successive angiograms. Statistical analysis was performed using the Fisher exact test for proportions and the Wilcoxon and Student t tests on ordinal/continuous measures. Quadratic regression was also used as a model for spasm activity versus post-bleed days. RESULTS: In both the coiling and clipping groups the most severely spastic vessels were located adjacent to aneurysm rupture. Perianeurysmal spasm affected all subjects. However, whereas spasm remained largely confined in patients treated by clipping, those who underwent coiling developed stepwise progression distally over time. The distal vasospasm severity scores were higher among subjects treated by coiling, particularly in the most dependent regions of the subarachnoid space. CONCLUSIONS: Patients with aSAH treated by endovascular coiling and surgical clipping demonstrate distinct vasospasm patterns. While both initially exhibit perianeurysmal spasm, patients treated by coiling go on to develop stepwise progression distally over time. This finding may reflect dispersion of blood breakdown products along preserved CSF egress pathways in patients treated by endovascular coiling.

Differentiating reversible cerebral vasoconstriction syndrome with subarachnoid hemorrhage from other causes of subarachnoid hemorrhage.

IMPORTANCE: Reversible cerebral vasoconstriction syndrome (RCVS) is a clinical-angiographic syndrome characterized by recurrent thunderclap headaches and reversible segmental multifocal cerebral artery narrowing. More than 30% of patients with RCVS develop subarachnoid hemorrhage (SAH). Patients with RCVS with SAH (RCVS-SAH) are often misdiagnosed as having potentially ominous conditions such as aneurysmal SAH (aSAH) or cryptogenic "angiogram-negative" SAH (cSAH) owing to overlapping clinical and imaging features. OBJECTIVE: To identify predictors that can distinguish RCVS-SAH from aSAH and cSAH at the time of clinical presentation. DESIGN: Retrospective analysis of 3 patient cohorts: patients with RCVS (1998-2009), patients with aSAH (1995-2003), and patients with cSAH (1995-2003). SETTING: Academic hospital and tertiary referral center. PARTICIPANTS: Consecutive patients with RCVS-SAH (n = 38), aSAH (n = 515), or cSAH (n = 93) whose conditions were diagnosed using standard criteria. MAIN OUTCOMES AND MEASURES: Multivariate logistic regression analysis was used to identify predictors that differentiate RCVS-SAH from aSAH and cSAH. RESULTS: Predictors differentiating RCVS-SAH from aSAH were younger age, chronic headache disorder, prior depression, prior chronic obstructive pulmonary disease, lower Hunt-Hess grade, lower Fisher SAH group, higher number of affected arteries, and the presence of bilateral arterial narrowing. Predictors differentiating RCVS-SAH from cSAH were younger age, female sex, prior hypertension, chronic headache disorder, lower Hunt-Hess grade, lower Fisher SAH group, and the presence of bilateral arterial narrowing. CONCLUSIONS AND RELEVANCE: We identified important clinical and imaging differences between RCVS-SAH, aSAH, and cSAH that may be useful for improving diagnostic accuracy, clinical management, and resource utilization.

Subarachnoid clot volume correlates with age, neurological grade, and blood pressure.

OBJECTIVE: Cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH) is associated with the volume and location of subarachnoid blood clots. Factors that influence the volume of SAH have seldom been studied. METHODS: Two independent sets of data were analyzed. Data from 3028 patients with SAH enrolled in four clinical trials of the drug tirilazad were analyzed in addition to data from 74 patients with SAH who underwent digital volumetric analysis of admission computed tomographic scans to determine the subarachnoid clot volume. In the smaller sample of 74 patients, aneurysm width, length, neck size, aspect ratio, and volume were measured on diagnostic cerebral angiograms. Statistical inference bearing on the question of what factors are associated with clot volume was derived by univariate methods, including analysis of variance, chi and t tests, and polytomous logistic regression. RESULTS: Of 22 clinical parameters examined by univariate analysis of the tirilazad dataset, age, World Federation of Neurological Surgeons (WFNS) clinical grade, time from SAH to admission, history of hypertension or diabetes mellitus, aneurysm location, and admission diastolic and systolic blood pressure were correlated with the subarachnoid clot volume (P < 0.05). Polytomous logistic regression found that only age, WFNS grade, time to admission, admission systolic blood pressure, and history of hypertension were higher in patients with larger subarachnoid clots (P < 0.05). Analysis of 74 patients with quantitative subarachnoid clot volumes also found that age and WFNS grade were higher in patients with larger subarachnoid clots (P < 0.05). No aneurysm location or measurement of aneurysm size showed a statistically significant relationship to clot volume in either dataset. CONCLUSION: SAH volume is correlated with clinical characteristics, including age, history of hypertension, admission systolic blood pressure, and WFNS grade. Anatomic aneurysm characteristics such as size and location do not reliably predict clot volume.

Transcranial Doppler grading criteria for basilar artery vasospasm.

OBJECTIVE: Transcranial Doppler (TCD) criteria for basilar artery (BA) vasospasm are poorly defined, and grading criteria for vertebrobasilar vasospasm are unavailable. The purpose of the present study was to define TCD grading criteria for BA vasospasm on the basis of the absolute flow velocities and the intracranial to extracranial flow velocity ratios for the posterior circulation, and to improve the sensitivity and specificity of TCD for diagnosis of BA vasospasm. METHODS: One hundred twenty-three patients with aneurysmal subarachnoid hemorrhage underwent 144 cerebral arteriograms with views of the BA during the acute phase of vasospasm (Days 3-14 after hemorrhage). BA diameters were measured and compared with diameters obtained from baseline arteriograms. Both BA and extracranial vertebral artery flow velocities were measured by TCD within 4 hours before the arteriogram. RESULTS: The velocity ratio between the BA and the extracranial vertebral arteries (VA) strongly correlated with the degree of BA narrowing (r2 = 0.648; P < 0.0001). A ratio higher than 2.0 was associated with 73% sensitivity and 80% specificity for BA vasospasm. A ratio higher than 2.5 with BA velocity greater than 85 cm/s was associated with 86% sensitivity and 97% specificity for BA narrowing of more than 25%. A BA/VA ratio higher than 3.0 with BA velocities higher than 85 cm/s was associated with 92% sensitivity and 97% specificity for BA narrowing of more than 50%. CONCLUSION: The BA/VA ratio improves the sensitivity and specificity of TCD detection of BA vasospasm. On the basis of the BA/VA ratio and BA mean velocities, we suggest new TCD grading criteria for BA vasospasm.

Cerebral vasoconstriction in neurally mediated syncope: relationship with type of head-up tilt test response.

BACKGROUND: The pathophysiology of neurally mediated syncope (NMS) is unclear. Cerebral vasoconstriction has been observed in NMS patients during tilt testing. To shed light on the pathophysiology of NMS, we attempted to establish whether the degree of cerebral vasoconstriction changes with the tilt test positivity type, scored in accordance with Sutton's classification. METHODS: Twenty-one patients (12 males and 9 females, mean age 41 +/- 15 years) consecutively admitted to tilt test evaluation were studied through simultaneous recordings of their electrocardiogram, blood pressure, electroencephalogram and transcranial Doppler sonography (TCD) of the middle cerebral artery. TCD allowed computation of the Gosling's pulsatility index [PI = (systolic velocity--diastolic velocity)/mean velocity], as an index of cerebrovascular resistance. RESULTS: In the 13 tilt-positive patients (62%), TCD revealed a significant PI increase at the onset of prodromic symptoms in comparison with baseline (2.01 +/- 0.94 vs 0.77 +/- 0.20, p < 0.001, paired-sample Student's t-test). No significant TCD alterations were seen in tilt-negative patients. Furthermore, the percentage change in the PI from baseline was significantly higher in cardioinhibitory types (254 +/- 51%, 5 patients) than in mixed and vasodepressor types (101 +/- 22%, 8 patients, p < 0.001, independent-sample Student's t-test). CONCLUSIONS: Our data show that the degree of cerebral vasoconstriction at the onset of prodromic symptoms changes with the tilt test positivity type. We suggest that in NMS patients the degree of cerebral vasoconstriction may depend on the amount of sympathetic activation. The sympathetic modulation of cerebral vasoconstriction may therefore be a turning point in the explanation of the pathophysiology of NMS.

The stimulation of vascular smooth muscle oxidative metabolism by CSF from subarachnoid haemorrhage patients increases with Fisher and WFNS grades.

The purpose of this paper is to present an in vitro method for examining cerebral vasospasm after subarachnoid haemorrhage (SAH) which correlates to the patients' condition. The O2 consumption of the porcine carotid artery was monitored, using an oxygen electrode, after exposure to cerebrospinal fluid (CSF) from patients who had a SAH. The vessels were exposed to CSF from SAH patients at a 1 in 30 dilution. Force measurements were carried out using freeze-dried CSF, reconstituted in the organ bath equivalent to undiluted CSF. These observations were then compared to the patients' condition. We divided the patient CSF samples into those that stimulated oxygen consumption above 0.4 microM/min/g dry wt, and those that did not. It was found that there was a correlation between the stimulation of oxygen consumption and the Fisher grade as well as the World Federation of Neurosurgeons Grading System (WFNS) for the patients. Of the CSF tested, 24 stimulated oxygen consumption above our cut off, and 8 did not (0.84 +/- 0.34, n = 24 compared with the rate of 0.27 +/- 0.1 mumol/min/g dry wt, respectively; SD n = 8) at 180 minutes. We then examined the Fisher Grades of these two groups, the results were 3.21 +/- 0.88 vs 2.25 +/- 0.83 respectively (SD p < or = 0.01). When examining the WFNS System we found a similar difference between the groups that stimulated respiration and those who did not (WFNS Grades of 2.64 +/- 1.1 vs. 1.43 +/- 0.53; p < or = 0.01). The observed stimulation of oxygen consumption also correlated with tension generation in vitro. The CSF from subarachnoid haemorrhage patients stimulates the oxygen consumption of the porcine carotid artery. This stimulation correlated to the WFNS and Fisher Grades of the patients and can be performed using 1:30 dilution of CSF. We conclude that the metabolic changes that occur in the vessels during vasospasm are important parameters for assessing cerebral vasospasm.

Magnesium sulfate in the management of patients with Fisher Grade 3 subarachnoid hemorrhage: a pilot study.

OBJECTIVE: To evaluate the effect of magnesium sulfate (MgSO4) on the clinical course of patients with severe aneurysmal subarachnoid hemorrhage (SAH). METHODS: Ten patients with Fisher Grade 3 aneurysmal SAH were evaluated. The patients were given a bolus as well as a constant infusion of intravenous MgSO4 up to 10 days postictus. Blood magnesium levels were obtained to adjust the daily requirement of MgSO4. The goal was to raise the serum level to 2.0 to 2.5 mmol/L or twice the baseline serum level. Daily transcranial Doppler (TCD) ultrasonography was performed on each patient, insonating both anterior cerebral and middle cerebral arteries. Further management followed standard protocols, including the use of nimodipine and hypervolemic therapy. TCD ultrasonographic findings, as well as clinical evidence of cerebral vasospasm, were documented. All patients had a 3-month assessment using the Glasgow Outcome Scale. RESULTS: After administration of a 20 mmol MgSO4 bolus infusion and an average daily continuous infusion of 84.7 mmol, 8 of 10 patients achieved the predetermined serum magnesium levels. No adverse affects were noted during the infusions. Five patients exhibited evidence of vasospasm on TCD ultrasonography; vasospasm was severe in two patients (velocities, >200 cm/s). Three patients, including the two patients in whom TCD ultrasonography demonstrated severe vasospasm, exhibited clinical evidence of vasospasm. Two patients had a Glasgow Outcome Scale score of 3; the remainder had Glasgow Outcome Scale scores of 5. CONCLUSION: Administration guidelines for the use of MgSO4 in aneurysmal SAH were established. A prospective double-blind placebo-controlled trial is required to establish the effectiveness of MgSO4 for treating vasospasm in aneurysmal SAH.