Absence Of Vasospasm Research Articles

Length of hospital stay in aneurysmal subarachnoid hemorrhage patients without vasospasm on angiography: potential for a fast-track discharge cohort

BackgroundPatients with aneurysmal subarachnoid hemorrhage (aSAH) frequently suffer from vasospasm. We analyzed the association between absence of early angiographic vasospasm and early discharge.MethodsAll aSAH patients treated from August 1, 2007,...

Subarachnoid haemorrhage with negative tomographic angiography without vasospasm: is it necessary to perform angiographic controls?

In about 15% of cases, the lesion causing subarachnoid haemorrhage (SAH) is not detectable by imaging studies, and some controversy exists as regards how the diagnosis should be performed in these patients. To analyse the diagnostic performance of digital subtraction angiography (DSA) carried out on a significant cohort of patients with SAH and negative tomographic angiography, without cerebral vasospasm, based on the distribution of bleeding in a simple CT scan. A retrospective analysis is performed of the centre's radiological database over an eight-year period. The inclusion criteria were patients with SAH of a perimesencephalic or diffuse distribution with a negative tomographic angiography result, without cerebral vasospasm, with at least one DSA control of the brain vessels. A total of 125 patients met the inclusion criteria: 61 had a perimesencephalic SAH and 64 had a diffuse SAH. The first DSA revealed vascular injury in seven patients (5.6%): one was in the perimesencephalic SAH group (1.6% yield) and six in the diffuse SAH group (9.4% yield). A second DSA was performed on 86 patients, a third on 28 and a fourth on five of them. The absence of vasospasm in the first DSA performed in patients with SAH and negative tomographic angiography could be a useful criterion for establishing an optimal follow-up protocol in these patients, without exposing them to unnecessary risks and radiation.

Do transfusion requirements increase after the diagnosis of vasospasm in patients with aneurysmal subarachnoid haemorrhage?

Abstract Background: Many patients experience impaired cerebral oxygen delivery secondary to vasospasm and delayed cerebral ischemia following aneurysmal subarachnoid haemorrhage (SAH). Anaemia is common after SAH affecting up to 50% patients, which may decrease cerebral oxygen delivery and is associated with worse clinical outcomes. Transfusion of allogeneic red cells increases the oxygen content of the blood but it not consistently associated with improved physiologic markers of clinical outcomes. The threshold for transfusion is not clear in patients with SAH. A recent survey found that most physicians would alter their transfusion threshold in SAH patients who develop delayed ischemia. The objective of our study is to identify the predictors of transfusion and to determine if the diagnosis of delayed ischemia increases the transfusion rates in patients with aneurysmal subarachnoid haemorrhage. Materials and Methods: We retrospectively reviewed the charts of 100 consecutive patients with SAH who were admitted to ICU for mechanical ventilation, and collected demographic and clinical data. Data were analyzed for the association between clinical factors and transfusion the differences in transfusion between the patients with and without vasospasm. Statistical methods included the t-test, univariate analysis and multivariate analysis. Results: Data from 96 patients were included in the analysis. Incidence of anaemia haemoglobin (Hb) < 100 gm/l and vasospasm were 67% (64/96) and 39% (38/96) respectively. Of 64 patients with anaemia, 27 patients received transfusion, while 38 patients did not receive a transfusion. The transfusion rates were similar between those who had vasospasm and who did not. However, out of the 14 patients with vasospasm who received a transfusion, 11 patients had been transfused after experiencing vasospasm, while only 3 were transfused before. On multivariate analysis only female sex, starting Hb levels and lowest Hb levels were found to be predictors of transfusion. Presence or absence of vasospasm was not found to be a predictor. Conclusions: From our retrospective review, we conclude that the incidence of anaemia is higher in patients with vasospasm. Sex and starting and lowest Hb levels were the only predictors of transfusion likelihood in aneurysmal subarachnoid haemorrhage while presence of vasospasm was not.

Outcome of intracranial aneurysm clipping: analysis of first 35 cases

Background: Sub arachnoid hemorrhage due to ruptured intracranial aneurysm is a major healthcare concern because of its fatal consequence and also the potential to be fully treated if acted upon on time. The need for surgical expertise and robust perioperative intensive care remains an essential component for a good outcome. This study looks at the role of different constant and variable factors in the outcome of patients undergoing surgical clipping of aneurysm. Methods: A retrospective analysis of first 35 cases of spontaneous SAH due to ruptured intracranial aneurysms who underwent craniotomy and clipping were included in this study. Patients were divided into good outcome and poor outcome groups based on Modified Rankin scale at 2 weeks and 6 months postoperatively. Other details obtained included Modified Fisher Grade of SAH, presence or absence of vasospasm, site of aneurysm and size of aneurysm (largest diameter). Results: Good outcome modified Rankin score was 74.3% at 2 weeks postop, which increased to 80% at 6 months postoperatively. Variables which were found to have a statistically significant impact on the postoperative outcome were Modified Fisher grade, preoperative WFNS grade, duration of temporary clip placement, time of ictus to surgery, side of the aneurysm [left or right] and presence of hydrocephalus . Conclusions: Surgical clipping is a safe and time-tested modality for treatment of sub arachnoid hemorrhage due to ruptured intracranial aneurysms. Elderly age group, higher modified Fisher grades, higher WFNS Grade preoperatively, larger size of aneurysm, presence of vasospasm and greater duration of temporary clip placement are factors, which lead to poor outcome in patients with ruptured intracranial aneurysm presenting with sub arachnoid hemorrhage.

Hydrocephalus onset after microsurgical or endovascular treatment for acute subarachnoid hemorrhage. Retrospective italian multicenter study.

Chronic shunt-dependent hydrocephalus is a complication of aneurysmal subarachnoid hemorrhage (aSAH). Its incidence and risk factors have been described while the hydrocephalus onset in terms of days after treatment (microsurgical or endovascular) has not been yet analyzed. 45 patients, treated for aSAH in 4 Italian Neurosurgical Departments, were retrospectively analyzed. It was calculated the time that elapses between treatment and hydrocephalus onset in 36 patients. Of the 45 shunted patients, 15 (33.3%) were included in the microsurgical group (group A) and 30 (66.6%) were in the endovascular one (group B). There was no difference of the hydrocephalus onset between the two groups (24,1 days, group A vs. 27,7 days, group B). The presence of intracerebral hematoma (ICH) caused a delay in the hydrocephalus onset after endovascular treatment in terms of 11,5 days compared to microsurgical group as well the absence of vasospasm determined a delay of 13,7 days (not statistically significant). No difference in terms of hydrocephalus onset after microsurgical or endovascular treatment has been demonstrated. Only the presence of ICH or the absence of vasospasm can cause a slight delay in the time of hydrocephalus onset in the endovascular series (not statistically significant). Long-term follow-up studies involving higher numbers of subjects are needed to better demonstrate this issue.

Acute myocardial infarction associated with blood transfusion: Case report and literature review

A 62-year old patient with a history of chronic anemia associated with malabsorption secondary to short gut syndrome, experienced acute chest pain the second hour after the transfusion of a crossmatch-compatible erythrocyte suspension. His electrocardiogram (ECG) revealed widespread ST-segment depressions and he had an elevated troponin level. Laboratory findings and physical examination did not indicate the presence of immunological or non-immunological blood transfusion reactions. Cardiac catheterization was performed and showed angiographically non-obstructive, atherosclerotic plaques and the absence of vasospasm or thrombus formation. Following antiischemic therapy his symptoms resolved completely. The ECG obtained 24 hours after the emergence of chest pain demonstrated normal sinus rhythm with no ST-T wave changes. We present a rare case of acute myocardial infarction induced following a blood transfusion. To the best of our knowledge, a few cases of acute myocardial infarction associated with blood transfusion have been formally recorded in the medical literature and the clinical experience regarding such cases is indeed quite limited. The present case is reviewed in the context of the relevant literature as a practical resource for clinical practice.

The Relationship Between Delayed Infarcts and Angiographic Vasospasm After Aneurysmal Subarachnoid Hemorrhage

Delayed cerebral ischemia is common after aneurysmal subarachnoid hemorrhage (aSAH) and is a major contributor to poor outcome. Yet, although generally attributed to arterial vasospasm, neurological deterioration may also occur in the absence of vasospasm. To determine the relationship between delayed infarction and angiographic vasospasm and compare the characteristics of infarcts related to vasospasm vs those unrelated. A retrospective review of patients with aSAH admitted from July 2007 through June 2011. Patients were included if they were admitted within 48 hours of SAH, had a computed tomography scan both 24 to 48 hours following aneurysm treatment and ≥7 days after SAH, and had a catheter angiogram to evaluate for vasospasm. Delayed infarcts seen on late computed tomography but not postprocedurally were attributed to vasospasm if there was moderate or severe vasospasm in the corresponding vascular territory on angiography. Infarct volume was measured by perimeter tracing. Of 276 aSAH survivors, 134 had all imaging requisite for inclusion. Fifty-four (34%) had moderate or severe vasospasm, of whom 17 (31%) had delayed infarcts, compared with only 3 (4%) of 80 patients without vasospasm (P < .001). There were a total of 29 delayed infarcts in these 20 patients; 21 were in a territory with angiographic vasospasm, but 8 (28%) were not. Infarct volume did not differ between vasospasm-related (18 ± 25 mL) and vasospasm-unrelated (11 ± 12 mL) infarcts (P = .54), but infarcts in the absence of vasospasm were more likely watershed (50% vs. 10%, P = .03). Delayed infarcts following aSAH can occur in territories without angiographic vasospasm and are more likely watershed in distribution.

Long-term outcome of 114 children with cerebral aneurysms

Population-based data on pediatric patients with aneurysms are limited. The aim of this study is to clarify the characteristics and long-term outcomes of pediatric patients with aneurysms. All pediatric patients (≤ 18 years old) with aneurysms among the 8996 aneurysm patients treated at the Department of Neurosurgery in Helsinki from 1937 to 2009 were followed from admission to the end of 2010. There were 114 pediatric patients with 130 total aneurysms during the study period. The mean patient age was 14.5 years (range 3 months to 18 years). The male:female ratio was 3:2. Eighty-nine patients (78%) presented with subarachnoid hemorrhage. The majority of the aneurysms (116 [89%]) were in the anterior circulation, and the most common location was the internal carotid artery bifurcation (36 [28%]). The average aneurysm diameter was 11 mm (range 2-55 mm) with 16 giant aneurysms (12%). Eighty aneurysms (62%) were treated microsurgically, and 37 (28%) were treated conservatively due to poor medical and neurological status of the patient or due to technical reasons during the early years of the patient series. No connective tissue disorders common to pediatric aneurysm patients were diagnosed in this series, with the exception of 1 patient with tuberous sclerosis complex. The mean follow-up duration was 24.8 years (range 0-55.8 years). At the end of follow-up, 71 patients (62%) had a good outcome, 3 (3%) were dependent, and 40 (35%) had died. Twenty-seven deaths (68%) were assessed to be aneurysm-related. Factors correlating with a favorable long-term outcome were good neurological condition of the patient on admission, aneurysm location in the anterior circulation, complete aneurysm closure, and absence of vasospasm. Six patients developed symptomatic de novo aneurysms after a median of 25 years (range 11-37 years). Fourteen patients (12%) had a family history of aneurysms. There was no increased incidence for cardiovascular diseases in long-term follow-up. Most aneurysms were ruptured and of medium size. Internal carotid artery bifurcation was the most frequent location of the aneurysms. There was a male predominance of pediatric patients with aneurysms. Most patients experienced good recovery, with 91% of the long-term survivors living at home independently without assistance and meaningfully employed. Altogether, almost a third of these patients finished high school and one-fifth had a college or university degree. Pediatric patients had a tendency to develop de novo aneurysms.

Comparison of CT Perfusion and Digital Subtraction Angiography in the Evaluation of Delayed Cerebral Ischemia

Delayed cerebral ischemia (DCI) is a devastating condition that occurs secondary to aneurysmal subarachnoid hemorrhage (A-SAH). The purpose is to compare computed tomography perfusion (CTP) and digital subtraction angiography (DSA) for determining DCI in A-SAH. A retrospective study of A-SAH patients admitted at our institution between December 2004 and December 2008 was performed. CTP and DSA were obtained at days 6-8 after aneurysm rupture. Both qualitative and quantitative analyses of CT perfusion deficits were performed. DSA was categorized as presence or absence of vasospasm. The reference standard for determining DCI was based on clinical deterioration or infarction on CT or MRI. The test characteristics of CTP and DSA were calculated and their graphs of conditional probabilities were constructed using Bayesian analysis. Fifty-seven patients were included; 79% (45/57) had DCI. Seventy percent (40/57) had CTP perfusion deficits; 80% (36/45) of the DCI and 33% (4/12) of no DCI patients. Sixty-three percent (36/57) had DSA demonstrating vasospasm; 73% (33/45) of the DCI and 25% (3/12) of no DCI patients. Quantitative analysis of the CTP data revealed a significant difference in cerebral blood flow values for the DCI (29.4 mL/100 g/minute) and no DCI groups (40.5 mL/100 g/minute, P = .0213). The sensitivity, specificity, and positive and negative predictive values for CTP were 0.80 (95% CI 0.68-0.92), 0.67 (95% CI 0.40-0.93), 0.90 (95% CI 0.82-0.96), 0.47 (95% CI 0.27-0.62), and for DSA were 0.73 (95% CI 0.60-0.86), 0.75 (95% CI 0.50-0.99), 0.92 (95% CI 0.82-0.98), and 0.43 (95% CI 0.26-0.53), respectively. CTP and DSA have similar test characteristics and Bayesian analysis for determining DCI in A-SAH patients.

Cervical spinal cord stimulation may prevent cerebral vasospasm by modulating sympathetic activity of the superior cervical ganglion at lower cervical spinal level

Cervical spinal cord stimulation (SCS) has been for many years hypothesized to be of use in treatment of cerebral vasospasm after subarachnoid hemorrhage. Experiments in animals and research in humans have demonstrated increase in cerebral blood flow (CBF), and different theories have been tried to explain these observations. Although there are many claims of circulatory improvements in these circumstances, no clinical application has yet been established. A complete understanding of physiological and anatomic correlation between CBF modulation and SCS remain unclear. We strongly believe that the main objective is not to treat vasospasm by increasing blood flow but to prevent vasoconstriction of the cerebral arteries by a functional sympathectomy. SCS may, at least theoretically, work in different ways at the same time: (1) preventing vasoconstriction of cerebral arteries by functional sympathectomy, acting at the lower cervical levels; and (2) increasing CBF through central pathways, perhaps involving brainstem connections, at the upper cervical levels. One of the practical implications of this hypothesis would be differential placement of cervical spinal cord stimulation electrodes in patients with subarachnoid hemorrhage depending on the timing of electrode insertion and presence or absence of vasospasm at the time of initial intervention.

Accuracy of transcranial Doppler ultrasonography and single-photon emission computed tomography in the diagnosis of angiographically demonstrated cerebral vasospasm

The goal of this study was to assess the accuracy of the routine clinical use of transcranial Doppler (TCD) ultrasonography and SPECT in predicting angiographically demonstrated vasospasm. Following receipt of institutional review board approval, the authors reviewed the records of patients with subarachnoid hemorrhage who had been admitted between 2004 and 2005 and underwent TCD ultrasonography and SPECT evaluations within 24 hours of cerebral angiography. Patients were categorized based on the presence or absence of vasospasm and/or hypoperfusion in the anterior cerebral arteries (ACAs), middle cerebral arteries (MCAs), and basilar arteries (BAs) or posterior cerebral arteries (PCAs) according to each imaging modality. Logistic regression was used to estimate the odds ratio (OR) of an angiographically demonstrated vasospasm also detected on TCD ultrasonography and SPECT. One hundred fifty-two patients (101 women) with a mean age (+/- standard deviation) of 53 +/- 13 years were included in the study. In the ACA, the OR of a vasospasm on TCD ultrasonography was 27 (95% confidence interval [CI] 3-243) and on SPECT 0.97 (95% CI 0.36-2.6); in the MCA, 17 (95% CI 5.4-55) and 2.0 (95% CI 0.71-5.5), respectively; in the BA, 4.4 (95% CI 0.72-27) and 5.6 (95% CI 0.89-36), respectively. There was no substantial change in the relative odds of a vasospasm when the findings on TCD ultrasonography and SPECT were considered jointly. Transcranial Doppler ultrasonography appears to be highly predictive of an angiographically demonstrated vasospasm in the MCA and ACA; however, its diagnostic accuracy was lower with regard to vasospasm in the BA. Single-photon emission computed tomography was not predictive of a vasospasm in any of the vascular territories assessed.

Relationship Between Hemoglobin Concentrations and Outcomes Across Subgroups of Patients with Aneurysmal Subarachnoid Hemorrhage

Anemia predicts poor outcome following aneurysmal subarachnoid hemorrhage (SAH). We hypothesized that this association would be stronger among patients with more severe SAH, since these patients are likely to be more vulnerable to secondary brain injury in the form of reduced cerebral oxygen delivery. Daily nadir hemoglobin (Hb) concentrations over 2 weeks following SAH were retrieved in 245 consecutive patients, and compared between those with a favorable versus unfavorable outcome. The analysis was repeated with patients dichotomized as follows: WFNS score 4-5 vs. 1-3; modified Fisher score (MFS) 4 vs. 0-3; and vasospasm present vs. absent. Mixed effect models and multivariable analysis using the generalized estimating equation were employed to assess correlated data with repeated measures. Patients with an unfavorable outcome consistently had lower Hb concentrations, especially between days 6-11 following SAH (P ranging from <0.001 to 0.009), as well as a greater fall in Hb over time (beta = -0.07, P < 0.001). This was true regardless of WFNS score, MFS, or the presence or absence of vasospasm. However, the effect was somewhat more pronounced among patients with higher WFNS and modified Fisher scores. Lower Hb levels are associated with worse outcomes regardless of SAH severity or the development of vasospasm. This finding may imply that a lower Hb concentration is largely a marker for a greater degree of systemic illness, rather than necessarily causing direct harm. However, the association is somewhat stronger among patients with more severe SAH. Thus, if there is a benefit for maintaining higher Hb levels with transfusions or erythropoietin, it may be more pronounced among these patients.

Visual Grading System for Vasospasm Based on Perfusion CT Imaging: Comparisons with Conventional Angiography and Quantitative Perfusion CT

Background: The purpose of this study was to compare simple visual grading of perfusion CT (PCT) maps to a more quantitative, threshold-based interpretation of PCT parameters in the characterization of presence and severity of vasospasm. Methods: Thirty-three patients with acute subarachnoid hemorrhage were enrolled in a prospective study and underwent a total of 40 paired PCT and digital subtraction angiography (DSA) examinations. A neuroradiologist and a neurologist reviewed the PCT mean transit time (MTT), cerebral blood flow (CBF), and cerebral blood volume maps independently; they evaluated five anatomical regions (frontal, temporal, parietal, occipital/thalami, and basal ganglia/insula) and graded them for abnormality (0 if normal, 1 if abnormal in <50% of the region, and 2 if abnormal in ≧50% of the region). A third neuroradiologist blinded to the PCT results reviewed the DSA examinations and assessed 19 segments for the presence or absence of vasospasm. Correlation between PCT and DSA scores was assessed, as well as the sensitivity and specificity of PCT compared to DSA used as a gold standard. Results: MTT (R² = 0.939) and CBF (R² = 0.907) scores correlated best with DSA scores (p < 0.001). MTT scoring had a sensitivity of 92% and a specificity of 86% compared to DSA; CBF scoring had a sensitivity of 75% and a specificity of 95%. The interobserver agreement between neuroradiologist and neurologist was found to have kappa = 0.789 for MTT and 0.658 for CBF. Conclusion: We propose a user-friendly visual grading system for PCT maps in patients with suspected vasospasm. This visual approach compares favorably to the results of DSA. Sensitive MTT maps should be used for screening, and specific CBF maps for confirmation of vasospasm.

Plasma acrolein levels and their association with delayed ischemic neurological deficits following aneurysmal subarachnoid haemorrhage: a pilot study

Background: The molecular mechanisms of cerebral vasospasm following aneurysmal subarachnoid haemorrhage (aSAH) remain unclear. Acrolein, a reactive metabolite produced in many models of mechanical and ischemic injury, has been shown to cause vasospasm in coronary artery and aorta models. These traits suggest it may play a role in post-aSAH cerebral vasospasm. This pilot study was designed as a preliminary investigation to determine if acrolein levels could be used as a clinical tool to predict the presence of vasospasm.Methods: Eleven patients with aSAH and Hunt and Hess admission grades of III–V were prospectively enrolled. Patients were stratified according to the presence or absence of vasospasm, defined as a delayed ischaemic neurological deficit in which all other possible causes have been excluded. Soluble acrolein levels were determined at two times points: early (day 1–3 post-SAH) and late (day 8–12 post-SAH) and the change in acrolein levels over this period was computed using a Mann–Whitney test.Results: The change in acrolein levels over this period between the vasospasm and non-vasospasm group trended toward but did not achieve statistical significance (means: 5.68 versus –5.54; medians: 5.27 versus –3.99; range: –8.067 to 22.904 versus –13.83 to 5.199 p=0.13). Five out of six vasospasm patients showed an increase in acrolein levels over the vasospasm period. Three out of four non-vasospasm patients showed a decrease over the vasospasm period.Conclusions: The results of this pilot study suggest that acrolein levels increase in patients undergoing vasospasm during the vasospasm window. This suggests that acrolein may play a role in the pathways leading up to or following vasospasm. There is a need for larger more definitive studies.

Utility of computed tomography perfusion in detection of cerebral vasospasm in patients with subarachnoid hemorrhage

Digital subtraction (DS) angiography is the gold standard for detecting cerebral vasospasm after subarachnoid hemorrhage (SAH). Computed tomography (CT) perfusion is a recently developed modality for the evaluation of cerebral hemodynamics. This study was conducted to evaluate the potential of using CT perfusion to detect vasospasm in patients with SAH. Fourteen patients between the ages of 41 and 66 years with aneurysmal SAH underwent 23 CT perfusion scans for suspected vasospasm. All patients underwent DS angiography within 12 hours of the CT perfusion scans. The presence of vasospasm on CT perfusion images was determined based on qualitative reading using color maps of mean transit time, cerebral blood flow, and cerebral blood volume as criteria. The presence or absence of vasospasm as retrospectively determined using CT perfusion was compared with DS angiography findings. Of the 23 CT perfusion scans performed, 21 (91%) were concordant with angiography findings in predicting the presence or absence of vasospasm. In 15 of 23 scans, the presence of vasospasm was detected on CT perfusion scans and confirmed on DS angiography studies. In two cases, vasospasm was revealed on DS angiography but was not confirmed on CT perfusion. The degree of agreement between CT perfusion and DS angiography for detection of vasospasm was high (K = 0.8, p , 0.0001). Computed tomography perfusion is an accurate, reliable, and noninvasive method to detect the presence or absence of vasospasm. It can be used as a tool to help guide the decision to pursue DS angiography with the intent to treat vasospasm.

Rise in serum soluble intercellular adhesion molecule-1 levels with vasospasm following aneurysmal subarachnoid hemorrhage.

Proinflammatory adhesion molecule expression has been demonstrated to be elevated in patients with aneurysmal subarachnoid hemorrhage (SAH). Recent studies have shown that elevations in soluble intercellular adhesion molecule-1 (ICAM-1) may be predictive of poor outcome in patients with good grade (Hunt and Hess Grades 1-2) aneurysmal SAH at delayed time points that correspond with the risk period for cerebral vasospasm. In addition, ICAM-1 is upregulated in experimental models of vasospasm. Unfortunately, the relationship of adhesion molecule expression to human vasospasm remains unclear. The authors hypothesized that the delayed elevation of soluble ICAM-1 in patients with aneurysmal SAH is associated with the development of cerebral vasospasm. Eighty-nine patients with aneurysmal SAH were prospectively enrolled in a study and stratified according to the presence or absence of vasospasm, as evidenced by daily monitoring of transcranial Doppler (TCD) velocities (presence, > 200 cm/second; absence, < 120 cm/second). Levels of soluble ICAM-1 were determined using enzyme-linked immunosorbent assay every other day for 12 days post-SAH. An analysis of covariance model was used to evaluate trends in soluble ICAM-1 levels from 2 days prior to 6 days after the occurrence of documented vasospasm. Two groups of patients, matched for admission admission Hunt and Hess grade, were compared: nine patients with TCD velocities greater than 200 cm/second and nine patients with TCD velocities less than 120 cm/second. From among the patients with TCD velocities greater than 200 cm/second six patients with angiographically documented vasospasm were selected. Patients with TCD velocities less than 120 cm/second and matched admission Hunt and Hess grades but without angiographically documented vasospasm were selected. Patients with TCD-demonstrated vasospasm showed a significant mean rate of rise (p < 0.01) in soluble ICAM-1 levels during the perivasospasm period, but admission Hunt and Hess grade-matched control patients did not (p = not significant [NS]). There was a significant difference between these groups' rates of soluble ICAM increase (p < 0.01). Patients with both TCD- and angiographically demonstrated vasospasm likewise showed a highly significant mean rate of increase in soluble ICAM-1 levels during the perivasospasm period (p < 0.01), whereas admission Hunt and Hess grade-matched controls did not (p = NS). The difference beween these groups' rates of increase was highly significant (p < 0.001). These data suggest a role for ICAM-1 in the pathophysiology of cerebral vasospasm or its ischemic sequelae. As this relationship is further elucidated, adhesion molecules such as ICAM-1 may provide novel therapeutic targets in the prevention of vasospasm or its ischemic consequences.

Reduced ocular pulse amplitude in low tension glaucoma is independent of vasospasm.

A vascular basis for the pathogenesis of primary open angle glaucoma has been postulated for many years. Defects in the regulation of ocular blood flow may be the initiating factor in this group of multifactorial diseases. This study was designed to evaluate the effect of vasospasm on ocular pulse amplitude (OPA) in low tension glaucoma (LTG) patients. OPA, using the Langham Ocular Blood Flow (OBF) System, applanation intraocular pressure (IOP), systemic blood pressure and heart rate were measured and vasospasm was determined by a fingernail capillary blood flow test. OPA (mmHg) in the LTG patients with a vasospastic reaction (LTG-V, 1.4 +/- 0.1, n = 17) was not significantly (p > 0.09) different when compared with non-vasospastic LTG patients (LTG-NV, 1.5 +/- 0.2, n = 15) but was significantly (p < 0.001) reduced in LTG-V and LTG-NV patients when compared with matched healthy control subgroups (2.3 +/- 0.2 and 2.4 +/- 0.3, respectively). IOP (mmHg) in LTG-V (13.3 +/- 0.4) and LTG-NV (13.2 +/- 0.5) patient groups was not significantly (p > 0.05) different when compared with each other, but was significantly (p < 0.05) lower when compared with matched control subgroups (15.0 +/- 0.3 and 15.2 +/- 0.4, respectively). Haemodynamic parameters were not significantly different from controls. The abnormality in choroidal perfusion indicated by a reduction in OPA in all LTG patients is unrelated to the presence or absence of vasospasm.

Biochemical markers of cerebral damage

Biochemical markers of cerebral damage

Repeat cerebral pan-angiography in subarachnoid hemorrhage of unknown etiology

Cerebral pan-angiography was repeated in 24 patients with spontaneous subarachnoid hemorrhage confirmed by spinal fluid or computed tomography evidence after the initial pan-angiography was negative. Recent, longterm follow-up was also conducted. The pan-angiography was technically adequate and did not show vasospasm, both being causes of aneurysmal nonvisualization. No etiology was demonstrated on repeat study in all 24 patients. An additional three patients had only one study, but autopsy later confirmed lack of etiology for subarachnoid hemorrhage despite gross and microscopic serial sections. The mean duration of follow-up was 18.1 years and outcome was favorable. Our results suggest that repeat cerebral pan-angiography may not be indicated in the patient who has no further bleeding episodes and in whom the initial study was normal, technically adequate, and complete without evidence of vasospasm. Nonvisualization of a cerebral aneurysm is commonly proposed as the most likely cause of subarachnoid hemorrhage when angiography is normal following nontraumatic subarachnoid hemorrhage. Our results suggest this conclusion is no longer accurate if the angiogram is technically adequate with the absence of vasospasm.

Hydrocephalus following aneurysmal subarachnoid haemorrhage.

Ninety-four patients with hydrocephalus following subarachnoid haemorrhage were investigated. Fourteen of these patients had temporary ventricular drains inserted, 19 had drains that were later converted to ventricular-peritoneal shunts, and 61 patients had shunts only. All patients were analysed with respect to their grade on admission, the distribution of blood on CT scan, their Glasgow Coma Score, their intracranial pressure, and the presence or absence of vasospasm on angiography. Outcome was analysed by shunt procedure and time of shunt insertion. The higher the grade on admission, the more likely it was the patient would require a shunt. Fewer patients with a good outcome required shunting as compared to those whose outcome was poor. Patients having more subarachnoid blood on CT scan tended to present with a lower Glasgow Coma Score. The outcome of patients with intraventricular haemorrhage was not obviously influenced by the insertion of a ventriculostomy. Vasospasm was not more common in patients requiring a ventriculo-peritoneal shunt, nor did early shunting in patients with hydrocephalus affect the incidence of vasospasm. The majority of patients were either shunted in the first three days or after 30 days post-SAH. The outcome was better in those patients shunted at a later date.