Symptomatic Cerebral Vasospasm Following Resection of a Medulloblastoma in a Child

Background

Vasospasm may occur following intracranial tumor resection but is uncommon following resection of tumors in the posterior fossa.

Methods

Case report.

Results

Here, we report an unusual pediatric case of symptomatic cerebral vasospasm following resection of a posterior fossa medulloblastoma in a 10-year-old child. CT angiogram and serial Transcranial Doppler (TCD) studies confirmed the presence of vasospasm and response to hemodynamic augmentation therapy, resulting in favorable outcome.

Conclusion

This case illustrates an unusual complication of posterior fossa tumor resection, and the potential utility of TCD studies in the detection and management of vasospasm in pediatric neurocritical care.     

Post-subarachnoid Hemorrhage Vasospasm in Patients with Primary Headache Disorders

Background

Altered cerebral vasomotor reactivity leading to vasospasm can be seen both in patients with primary headache disorders (PHD) and in patients with subarachnoid hemorrhage (SAH). The pathogenesis of vasospasm in post-SAH patients and in headache disorder sufferers may be related. To address this hypothesis, we analyzed a large cohort of SAH patients to determine whether a diagnosis of PHD predisposes to vasospasm, delayed cerebral ischemia, or worsened clinical outcome.

Methods

Prospectively collected data from patients enrolled in the SAH Outcomes Project between 1996 and 2006 were analyzed. Patients were segregated based on whether they had a diagnosis of PHD or not and were subsequently compared for differences in clinical and radiographic outcome.

Results

A total of 921 SAH patients were analyzed, 265 of which had a diagnosis of PHD. In total, symptomatic vasospasm was seen in 17 %, while angiographic vasospasm was seen in 28 %. Vasospasm rates were similar among patients with a PHD and in those without a PHD (p > 0.05). However, on multivariate analysis new ischemic infarcts were more common in patients with a PHD as compared to patients without a PHD (p = 0.015). Functional outcomes at 3 months were similar among PHD and non-PHD patients (p > 0.05).

Conclusion

A history of PHD is associated with an increased rate of ischemic infarcts during admission for SAH. Increased rates of vasospasm within small cerebral blood vessels may be implicated. Further studies are warranted to more closely link the mechanisms of vasospasm in PHD and SAH patients.     

Prediction of Significant Vasospasm in Aneurysmal Subarachnoid Hemorrhage Using Automated Data

Background

When vasospasm is detected after aneurysmal subarachnoid hemorrhage (aSAH), it is treated with hypertensive or endovascular therapy. Current classification methods are resource-intensive, relying on specialty-trained professionals (nursing exams, transcranial dopplers, and perfusion imaging). More passively obtained variables such as cerebrospinal fluid drainage volumes, sodium, glucose, blood pressure, intracranial pressure, and heart rate, have not been used to predict vasospasm. We hypothesize that these features may yield as much information as resource-intensive features to classify vasospasm.

Methods

We studied data from 81 aSAH patients presenting within two days of onset. Vasospasm class (VSP) was defined by angiographic vasospasm warranting endovascular treatment. Naïve Bayes (NB) and logistic regression (LR) classifiers were trained on selected variable feature sets from the first three days of illness. Performance of trained classifiers was evaluated using area under the receiver operator characteristic curve (AUC classifier) and F-measure (F classifier). Ablation analysis determined incremental utility of each variable and subsets.

Results

43.2 % developed VSP. During feature selection, the only passively collected variable that did not yield a statistically significant summary statistic was CSF drainage volume. NB classifier trained on all passively obtained features (AUC NB 0.708 and F NB 0.636) outperformed NB classifier trained on resource-intensive features (AUC NB 0.501 and F NB 0.349).

Conclusions

Data-driven analysis of passively obtained clinical data predicted VSP better than current targeted resource-intensive monitoring techniques after aSAH. Automated classification of VSP may be possible.     

Cerebral Vasospasm and Delayed Cerebral Ischemia in Intraventricular Hemorrhage

Background

Intracerebral hemorrhage (ICH) with intraventricular extension (IVH) is a devastating disease with a particular high mortality. In some aspects, IVH may resemble subarachnoid hemorrhage. The incidence and role of cerebral vasospasm in ICH with IVH are poorly understood. Here, we aimed to analyze the incidence and relationship of cerebral vasospasm to clinical characteristics, in-hospital mortality, and functional outcome at 3 months in patients suffering ICH with IVH.

Methods

Patients with ICH and IVH treated on a neurological intensive care unit were prospectively enrolled in a single-center observational study. Vasospasm was defined using established ultrasound criteria. Delayed cerebral ischemia (DCI) was defined as a new hypodensity on follow-up cranial CT. Functional outcome at 3 months was assessed using the modified Rankin Scale.

Results

129 patients with ICH and IVH were screened for the study. 62 patients entered the final analysis. The incidence of significant vasospasm was 37 %. A strong trend was found for the association between all cerebral vasospasm and DCI (P = 0.046). Early (up to 48 h) vasospasm was significantly associated with a DCI (P = 0.033). Overall mortality and outcome after 3 months did not differ between the groups.

Conclusion

Cerebral vasospasm seems to be a frequent complication after ICH with IVH and might be associated with DCI. Larger studies are warranted to confirm this hypothesis.     

Intraarterial Nimodipine Infusion to Treat Symptomatic Cerebral Vasospasm after Aneurysmal Subarachnoid Hemorrhage

Objective

Cerebral vasospasm leading to cerebral ischemic infarction is a major cause of morbidity and mortality in the patients who suffer with aneurysmal subarachnoid hemorrhage. Despite adequate treatment, some patients deteriorate and they develop symptomatic vasospasm. The objective of the present study was to investigate the efficacy and clinical outcome of intraarterial nimodipine infusion on symptomatic vasospasm that is refractory to hemodynamic therapy.

Methods

We retrospectively reviewed the procedure reports, the clinical charts and the transcranial doppler, computed tomography and digital subtraction angiography results for the patients who underwent endovascular treatment for symptomatic cerebral vasospasm due to aneurysmal SAH. During the 36 months between Jan. 2005 and Dec. 2007, 19 patients were identified who had undergone a total of 53 procedures. We assessed the difference in the arterial vessel diameter, the blood flow velocity and the clinical outcome before and after these procedures.

Results

Vascular dilatation was observed in 42 of 53 procedures. The velocities of the affected vessels before and after procedures were available in 33 of 53 procedures. Twenty-nine procedures exhibited a mean decrease of 84.1 cm/s. We observed clinical improvement and an improved level of consciousness with an improved GCS score after 23 procedures.

Conclusion

Based on our results, the use of intraarterial nimodipine is effective and safe in selected cases of vasospasm following aneurysmal SAH. Prospective, randomized studies are needed to confirm these results.     

Impact of Percutaneous Transluminal Angioplasty for Treatment of Cerebral Vasospasm on Subarachnoid Hemorrhage Patient Outcomes

Background

Percutaneous transluminal angioplasty (PTA) has been introduced for treatment of symptomatic cerebral vasospasm in patients with subarachnoid hemorrhage (SAH). While angiographic improvement is consistently reported, clinical improvement following the procedure varies, and limited data is available regarding overall impact on outcome.

Methods

The authors performed a retrospective analysis of all hospital admissions with aneurysmal SAH over a 6 year period. The length of stay, discharge outcomes (measured by modified Rankin scale [mRS] at discharge), and 1-year mortality among patients with SAH before (4 year period) and after (2 year period) institution of PTA for cerebral vasospasm were compared. Embolization for intracranial aneurysm was used as a therapeutic option throughout the study duration. The effect of institution of PTA for vasospasm after adjusting for age, clinical severity, and use of aneurysm embolization on both discharge outcomes and 1-year mortality in multivariate analysis was evaluated.

Results

A total of 146 patients with aneurysmal SAH were admitted during the study duration. There was no difference between the 89 patients admitted in pre-angioplasty period and 57 patients admitted in post-angioplasty period in regards to age, medical co-morbidities, and admission clinical severity of patients (measured by Hunt and Hess grade and Glasgow coma scale). A total of 18 (32%) patients underwent PTA with or without intra-arterial vasodilator treatment in the second period of the study. There was a non significant decrease in rates of severe disability and death (mRS 5–6) at discharge (45 vs. 33%, P = 0.09) and 1-year mortality (32 vs. 22%, P = 0.26) after introduction of PTA for cerebral vasospasm after adjusting for potential confounders. There was no significant difference between the two time periods in regards to length of stay.

Conclusion

A non significant trend was noted with reduced rate of severe disability and mortality at discharge and 1-year mortality after the introduction of PTA for cerebral vasospasm associated with SAH without increasing the length of hospital stay.     

Intracortical EEG for the Detection of Vasospasm in Patients with Poor-Grade Subarachnoid Hemorrhage

Background

To study the feasibility of utilizing intracortical electroencephalography (ICE) including quantitative EEG (qEEG) analysis for the detection of vasospasm in five consecutive poor-grade SAH patients.

Methods

Intracortical electroencephalography (ICE) was obtained via a single miniature parenchymal 8-contact depth electrode placed at the bedside. Quantitative EEG parameters, calculated on surface EEG and ICE, included alpha/delta ratio (ADR), mean amplitude, suppression percent, and total power. Percent changes between averaged values over 4–6 h of baseline EEG and EEG prior to angiography were calculated. The entire continuous qEEG recording for each patient was then reviewed to determine optimal automated alarm criteria.

Results

ICE ADR was the most accurate for predicting angiographic vasospasm (5/5). ICE ADR decreased between baseline and follow-up by 42% (from 0.56 ± 0.07 to 0.32 ± 0.03) for those with vasospasm (N = 3) compared to 17% (0.62 ± 0.06 to 0.51 ± 0.03) for those without (N = 2). A sustained decrease in the ICE ADR from baseline (>25% for ≥4 h) occurred in all three patients with angiographically confirmed vasospasm and not in the two without; this decline occurred 1–3 days prior to angiographic confirmation.

Conclusions

Intracortical EEG is promising for detecting ischemia from vasospasm in poor-grade SAH patients, may be superior to scalp EEG, and allow automated detection, particularly using the ADR. Larger studies are needed to better define the effectiveness of this approach.     

Plasma Endothelin-1 as Screening Marker for Cerebral Vasospasm After Subarachnoid Hemorrhage

Background

Cerebral vasospasm complicating subarachnoid hemorrhage causes ischemic stroke and worsens the neurological outcome. The potential role of endothelin-1 in vasospasm pathogenesis may provide therapeutic opportunities. A recent meta-analysis however, did not support the use of endothelin antagonists. Apart from clinical assessment, transcranial Doppler and interval angiography, there are no sensitive screening markers for evolving vasospasm. We investigate the ability of serial measurement of endothelin-1 to predict the development of vasospasm following subarachnoid hemorrhage.

Methods

Endothelin-1 levels in cerebrospinal fluid and blood were measured daily in 20 patients admitted to the ICU with subarachnoid hemorrhage from days 1 to 10 following the inception bleed. In addition to clinical assessment, patients had daily transcranial Doppler. Digital subtraction angiography was performed on the suspicion of vasospasm based upon clinical or transcranial Doppler assessment. Neuron-specific enolase and SB100 were measured in blood as comparative biomarkers of neurological injury.

Results

Mean plasma endothelin-1 on day 5, was 4.2 mcg/L (CI 3.1–5.8) in patients with vasospasm compared to 2.5 mcg/L (CI 1.5–4.0) in those without vasospasm (P = 0.047). There were no time-related differences in cerebrospinal fluid endothelin-1, plasma NSE, or SB100 for patients with and without vasospasm.

Conclusions

In patients with subarachnoid hemorrhage and vasospasm, endothelin-1 is significantly higher in plasma than in CSF on day 5. Neither NSE nor SB100 is associated with the development of vasospasm. Measurement of serial plasma endothelin-1 concentration is a potential screening marker of vasospasm.     

Hyperacute Vasospasm After Aneurysmal Subarachnoid Hemorrhage

Background

Cerebral vasospasm after aneurysmal subarachnoid hemorrhage typically occurs 3–14 days after aneurysm rupture. We describe a series of patients who developed vasospasm within minutes of aneurysm rupture. This phenomenon, which we term, “hyperacute vasospasm,” has been reported in animal models of SAH, but hitherto has been poorly described in humans.

Methods

Eleven patients were identified from an institutional registry who had aneurysmal rupture during catheter cerebral angiography between 1997 and 2009. We quantified the degree of vasoconstriction using vascular diameter index (VDI). The change in VDI (delta VDI or DVDI) was calculated by determining the difference in VDI before and after the procedure. We also examined the relationship between hyperacute vasospasm and delayed cerebral ischemia.

Results

Ten of eleven (91 %) patients with intraoperative aneurysm rupture had cerebral vasoconstriction within minutes of intra-procedural aneurysmal rupture. Six of eleven patients (55 %) with hyperacute vasospasm developed delayed cerebral infarction.

Conclusions

Hyperacute vasospasm is likely common in patients with intraoperative aneurysm rupture and may be an unrecognized element of the natural history of aneurysmal subarachnoid hemorrhage. In this limited series, there was an association between hyperacute vasospasm and delayed cerebral infarction.

     

Intravenous Magnesium Infusion for the Prevention of Symptomatic Cerebral Vasospasm after Aneurysmal Subarachnoid Hemorrhage

Objective

The study examined the difference in the incidence of symptomatic cerebral vasospasm with magnesium supplementation in aneurysmal subarachnoid hemorrhage (SAH) in a Korean population.

Methods

This retrospective analysis was performed in 157 patients diagnosed with aneurysmal SAH from January 2007 to December 2011 at a single center. Seventy patients (44.6%) received a combination treatment of nimodipine with magnesium and 87 patients (55.4%) received only nimodipine. A matched case-control study using propensity scores was conducted and 41 subjects were selected from each group. A dosage of 64 mmol/day of magnesium was administrated.

Results

The infusion of magnesium did not reduce the incidence of symptomatic cerebral vasospasm (n=7, 17.1%, p=0.29) compared with simple nimodipine injection (n=11, 26.8%). The ratios of good clinical outcome (modified Rankin scale 0-2) at 6 months were similar, being 78% in the combination treatment group and 80.5% in the nimodipine only group (p=0.79). The proportions of delayed cerebral infarction was not significantly lower in patients with combination treatment (n=2, 4.9% vs. n=3, 7.3%; p=0.64). There was no difference in the serum magnesium concentrations between the patients with symptomatic vasospasm and without vasospasm who had magnesium supplementation. No major complications associated with intravenous magnesium infusion were observed.

Conclusion

Magnesium supplementation (64 mmol/day) may not be beneficial for the reduction of the incidence of symptomatic cerebral vasospasm in patients with aneurysmal SAH.     

Left Ventricular Dysfunction and Cerebral Infarction from Vasospasm After Subarachnoid Hemorrhage

Background

Although neurogenic stunned myocardium (NSM) after aneurysmal subarachnoid hemorrhage (SAH) is well described, its clinical significance remains poorly defined. We investigated the influence of left ventricular (LV) dysfunction and cerebral vasospasm on cerebral infarction, serious cardiovascular events, and functional outcome after SAH.

Methods

Of the 481 patients enrolled in the University Columbia SAH Outcomes Project between 10/96 and 05/02, we analyzed a subset of 119 patients with at least one echocardiogram, serial transcranial Doppler (TCD) data, and with no prior history of cardiac disease. LV dysfunction was defined as an ejection fraction <40% on echocardiography. Infarction from vasospasm was adjudicated by the study team after comprehensive review of all clinical and imaging data. Functional outcome was assessed at 15 and 90 days with the modified Rankin Scale (mRS).

Results

Eleven percent of patients had LV dysfunction (N = 13). Younger age, hydrocephalus, and complete filling of the quadrigeminal and fourth ventricles were associated with LV dysfunction (all P < 0.05). Despite a similar frequency of pre-existing hypertension, 0% of patients with LV dysfunction reported taking antihypertensive medication, compared to 35% of those without (P = 0.009). There was a significant association between LV dysfunction and infarction from vasospasm after adjusting for clinical grade, age, and peak TCD flow velocity (P = 0.03). Patients with LV dysfunction also had higher rates of hypotension requiring vasopressors (P = 0.001) and pulmonary edema (P = 0.002). However, there was no association between LV dysfunction and outcome at 14 days after adjustment for established prognostic variables.

Conclusions

LV dysfunction after SAH increases the risk of cerebral infarction from vasospasm, hypotension, and pulmonary edema, but with aggressive ICU support does not affect short-term survival or functional outcome. Antihypertensive medication may confer cardioprotection and reduce the risk of catecholamine-mediated injury after SAH.     

Patterns of treatment and associated short-term outcomes of unruptured intracranial aneurysms in children

Background

The rates and outcomes of treatments for intracranial aneurysms have not been exclusively determined within the pediatric population. We determined the rates of endovascular and microsurgical treatments for unruptured intracranial aneurysms (UIA) and associated rates of favorable outcome in patients aged <18 years.

Methods

We analyzed data obtained as part of the Kids’ Inpatient Database between 2003 and 2009 with primary diagnosis of UIA. Patients undergoing endovascular treatment were compared to those undergoing microsurgical treatment. We determined rates of intracerebral hemorrhage, subarachnoid hemorrhage, neurological complications, and favorable outcome.

Results

There were 818 cases of UIA during the study period. A total of 111 patients (mean age 14?±?6 years, 37.6 % female) underwent microsurgical treatment, and another 200 patients (mean age 13?±?7 years, 42.5 % female) underwent endovascular treatment. A high rate of favorable outcome was observed in patients who received either treatment (microsurgical treatment 87.7 % versus endovascular treatment 91.6 %, p?=?0.4). There was a trend towards a significantly shorter mean hospitalization stay among those who received endovascular treatment compared with microsurgical treatment (6?±?12 versus 9?±?11 days, p?=?0.06). There was a significant trend towards higher utilization of endovascular treatment as opposed to microsurgical treatment from 2003 to 2009 (p?=?0.02).

Conclusions

Although outcomes except for length of stay were comparable between endovascular treatment and microsurgical treatment patients, there was a trend towards higher utilization of endovascular treatment among children with UIAs from 2003 to 2009.     

Outcomes After Nontraumatic Subarachnoid Hemorrhage at Hospitals Offering Angioplasty for Cerebral Vasospasm: A National Level Analysis in the United States

Background

Primary angioplasty has been introduced for the treatment of symptomatic cerebral vasospasm in patients with subarachnoid hemorrhage (SAH). The data regarding the therapeutic benefit of angioplasty in improving patient outcomes are limited, hence its utilization at hospitals remains controversial and currently is not reimbursed by Medicare or major insurance companies.

Methods

We analyzed the data from Nationwide Inpatient Sample (NIS), a nationally representative dataset of all admissions in the United States from 2005 to 2007. We analyzed the prevalence of angioplasty procedure for cerebral vasospasm at the national level. In-hospital mortality, discharge status, length of stay, and cost of hospitalization were compared between hospitals performing angioplasty with those not performing angioplasty in multivariable model, adjusted for patient’s age, utilization of endovascular aneurysm obliteration, and disease severity.

Results

Of the 74,356 estimated patients with nontraumatic SAH, 47% (n = 35,172) were admitted to hospitals that perform angioplasty for cerebral vasospasm and only 1307 patients (3.8%) were treated with angioplasty for vasospasm. In multivariable analysis, after adjustment for patient and hospital characteristics, we found that patients admitted to hospitals performing angioplasty had higher rates of discharge to home without supervision (OR 1.3, 95% CI: 1.1–1.6). There was no difference in in-hospital mortality, length of stay, or cost of hospitalization.

Conclusions

Our analysis suggests that the odds of a patient being discharged to home are better at hospitals performing angioplasty for cerebral vasospasm. Provision of angioplasty may be used as a surrogate marker of model of care in management of patients with SAH.

     

Intra-arterial Dantrolene for Refractory Cerebral Vasospasm After Aneurysmal Subarachnoid Hemorrhage

Background

Intravenous dantrolene has been used to prevent and treat cerebral vasospasm. We report a case of refractory cerebral vasospasm treated with intra-arterial dantrolene after aneurysmal subarachnoid hemorrhage.

Methods

A 56-year-old woman suffered a diffuse subarachnoid hemorrhage from a ruptured anterior communicating artery aneurysm which was successfully treated with coil embolization. She subsequently developed bilateral severe angiographic vasospasm which was treated with intra-arterial vasodilators. However, owing to the recurrence of vasospasm, intra-arterial dantrolene followed by balloon angioplasty was used.

Results

There was moderate improvement of the severe vasospasm in bilateral A1 segments of the anterior cerebral arteries after microcatheter-based intra-arterial infusion of 30?ml (1?mg/ml) dantrolene. Patient??s hemodynamic parameters were monitored during and after the procedure and no significant changes were seen after dantrolene infusion. A follow up cerebral angiogram after 1?day demonstrated the persistence of therapeutic effect.

Conclusion

Intra-arterial dantrolene induced a sustained improvement in cerebral vasospasm secondary to ruptured aneurysm. No significant side effects were observed during or after the infusion of the drug.     

Milrinone Via Lumbar Subarachnoid Catheter for Vasospasm After Aneurysmal Subarachnoid Hemorrhage

Background

We ascertained the occurrence of global cerebral edema manifesting as increased brain volume in subjects with intracerebral hemorrhage (ICH) and explored the relationship between subject characteristics and three month outcomes.

Methods

A post-hoc analysis of a multicenter prospective study that recruited patients with ICH, elevated SBP ≥170 mm Hg, and Glasgow Coma Scale (GCS) score ≥8, who presented within 6 h of symptom onset was performed. Computed tomographic (CT) scans at baseline and 24 h, submitted to a core image laboratory, were analyzed to measure total brain, hematoma, and perihematoma edema volumes from baseline and 24-h CT scans using image analysis software. The increased brain volume was determined by subtracting the hematoma and perihematomal edema volumes from the total brain volume.

Results

A total of 18 (44 %) of 41 subjects had increased brain volume that developed between initial CT scan and 24-h CT scan. The median increase in brain volume among the 18 subjects was 35 cc ranging from 0.12 to 296 cc. The median baseline GCS score was 15 in both groups of subjects who experienced increased brain volume and those who did not, and the median hematoma volume was 10.18 and 6.73, respectively. Three of the 18 subjects with increased brain volume underwent concurrent neurological deterioration and one subject died during hospitalization.

Conclusions

We found preliminary evidence of increased cerebral brain volume in subjects with good grade and small ICHs, which may be suggestive of global cerebral edema.     

The Effects of Fluid Balance and Colloid Administration on Outcomes in Patients with Aneurysmal Subarachnoid Hemorrhage: A Propensity Score-Matched Analysis

Background

Delayed ischemic neurological deficit (DIND) following aneurysmal subarachnoid hemorrhage (SAH) remains a significant cause of mortality and disability. The administration of colloids and the induction of a positive fluid balance during the vasospasm risk period remain controversial. Here, we compared DIND and outcomes among propensity score-matched cohorts who did and did not receive colloids and also tested the effect of a positive fluid balance on these endpoints.

Methods

Exploratory analysis was performed on 413 patients enrolled in CONSCIOUS-1, a prospective randomized trial of clazosentan for the prevention of angiographic vasospasm. Propensity score matching was performed on the basis of age, gender, pre-existing heart conditions, hypertension, nicotine use, World Federation of Neurosurgical Societies scores, aneurysm location, clazosentan treatment, subarachnoid clot burden, and severity of angiographic vasospasm. Inferential statistics were used for group-wise comparisons.

Results

One hundred twenty-three subjects were matched (41 received colloids, whereas 82 did not). The covariate balance and propensity score distributions were acceptable. There was no difference between the groups with respect to DIND (17 vs. 22 %; p = 0.64) or the presence (48 vs. 51 %; p = 0.71) or volume of delayed infarcts (volume >7.5 cm³; 62 vs. 48 %; p = 0.41). Similarly, no differences were found on multivariate analysis between patients who did and did not have a positive fluid balance, although patients with severe angiographic vasospasm had more delayed infarcts with a negative fluid balance (p = 0.01). Among all subjects, the administration of colloids and a positive fluid balance were associated with worse outcomes on the NIHSS (p = 0.04) and modified Rankin (p = 0.02) scales, respectively.

Conclusions

Colloid administration and induction of a positive fluid balance during the vasospasm risk period may be associated with poor outcomes in specific patient groups. Patient selection is of utmost importance when managing the fluid status of patients with aneurysmal SAH.     

Increased platelet count and reticulated platelets in recently symptomatic versus asymptomatic carotid artery stenosis and in cerebral microembolic signal-negative patient subgroups: results from the HaEmostasis In carotid STenosis (HEIST) study

Background

The pathophysiological mechanisms responsible for the disparity in stroke risk between asymptomatic and symptomatic carotid stenosis patients are not fully understood. The functionally important reticulated platelet fraction and reticulocytes could play a role.

Objectives

We performed a prospective, multi-centre, observational analytical study comparing full blood count parameters and platelet production/turnover/activation markers in patients with asymptomatic versus recently symptomatic moderate (≥ 50–69%) or severe (≥ 70–99%) carotid stenosis.

Patients/methods

Data from 34 asymptomatic patients were compared with 43 symptomatic patients in the ‘early phase’ (≤ 4 weeks) and 37 of these patients in the ‘late phase’ (≥ 3 months) after TIA/ischaemic stroke. Reticulated platelets were quantified by whole blood flow cytometry and reticulated platelets and red cell reticulocytes by ‘automated assays’ (Sysmex XE-2100?). Bilateral simultaneous transcranial Doppler ultrasound monitoring classified patients as micro-embolic signal (MES)+ve or MES?ve.

Results

Mean platelet count was higher in early (216 × 10⁹/L; P = 0.04) and late symptomatic (219 × 10⁹/L; P = 0.044) than asymptomatic patients (194 × 10⁹/L). Mean platelet volume was higher in early symptomatic than asymptomatic patients (10.8 vs. 10.45 fl; P = 0.045). Automated assays revealed higher % reticulated platelet fractions in early (5.78%; P < 0.001) and late symptomatic (5.11%; P = 0.01) than asymptomatic patients (3.48%). Red cell reticulocyte counts were lower in early (0.92%; P = 0.035) and late symptomatic (0.93%; P = 0.036) than asymptomatic patients (1.07%). The automated % reticulated platelet fraction was also higher in early symptomatic than asymptomatic MES?ve patients (5.7 vs. 3.55%; P = 0.001).

Discussion

The combination of increased platelet counts and a shift towards production of an increased population of larger, young, reticulated platelets could contribute to a higher risk of first or recurrent cerebrovascular events in recently symptomatic versus asymptomatic carotid stenosis, including those who are MES?ve.

     

SSRI/SNRI Use is Not Associated with Increased Risk of Delayed Cerebral Ischemia After aSAH

Background

To determine the effect of selective serotonin reuptake inhibitor (SSRI)/selective norepinephrine reuptake inhibitor (SNRI) use on the risk of symptomatic vasospasm and delayed cerebral ischemia (DCI) in patients hospitalized with aneurysmal subarachnoid hemorrhage (aSAH).

Methods

Retrospective review of consecutive patients with aSAH at Mayo Clinic, Rochester from January 2001 to December 2013. The variables collected and analyzed included age, sex, SSRI/SNRI use, active smoking, transfusion, modified Fisher score, WFNS grade, and outcome at discharge. Multivariate logistic regression analysis was used to evaluate factors associated with DCI, symptomatic vasospasm, and poor outcome (modified Rankin score 3–6) within 1 year.

Results

579 [females 363 (62.7 %)] patients with a median age of 55 (IQR 47–65) years were admitted with aSAH during the study period. WFNS at nadir was IV–V in 240 (41.5 %), and modified Fisher score was 3–4 in 434 (75.0 %). 81 (13.9 %) patients had been prescribed an SSRI or SNRI prior to admission and all continued to receive these medications during hospitalization. Symptomatic vasospasm was present in 154 (26.4 %), radiological infarction in 172 (29.5 %), and DCI in 250 (42.9 %) patients. SSRI/SNRI use was not associated with the occurrence of DCI (p = 0.458), symptomatic vasospasm (p = 0.097), radiological infarction (p = 0.972), or poor functional outcome at 3 months (p = 0.376).

Conclusions

The use of SSRI/SNRI prior to and during hospitalization is not associated with DCI or functional outcome in patients with aSAH.

     

Rosiglitazone Attenuates Cerebral Vasospasm and Provides Neuroprotection in an Experimental Rat Model of Subarachnoid Hemorrhage

Background

Glutamate and oxidative stress play important roles after subarachnoid hemorrhage (SAH). The ability to modulate glutamate transporter 1 (GLT-1) and the antioxidative effect of rosiglitazone have been demonstrated. We investigated the neuroprotective effect of rosiglitazone after SAH.

Methods

SAH was induced by double blood injection. The rats were randomly divided into sham, SAH + vehicle, and SAH + rosiglitazone groups and treated with dimethyl sulfoxide, dimethyl sulfoxide, and 6 mg/kg of rosiglitazone, respectively, at 2 and 12 h after SAH induction and then daily for 6 days. Cerebrospinal fluid dialysates were collected 30 min before SAH induction and then daily for 7 days for glutamate measurement. Mortality, body weight, and neurological scores were also measured daily. On day 7 after SAH, the wall thickness and the perimeter of the basilar artery (BA), neuron variability, GLT-1 levels, glial fibrillary acidic protein (GFAP) expression and activity, and malondialdehyde, superoxide dismutase, and catalase activities were also evaluated.

Results

Rosiglitazone improved survival (relative risk = 0.325) and neurological functions and reduced neuronal degeneration (5.7 ± 0.8 vs. 10.0 ± 0.9; P < 0.001) compared with the SAH + vehicle group. Rosiglitazone also lowered glutamate levels by 43.5-fold and upregulated GLT-1 expression by 1.5-fold and astrocyte activity by 1.8-fold compared with the SAH + vehicle group. The increase in BA wall thickness was significantly attenuated by rosiglitazone, whereas the perimeter of the BA was increased. In addition, rosiglitazone abated the 1.9-fold increase in malondialdehyde levels and the 1.6-fold increase in catalase activity after SAH.

Conclusion

Rosiglitazone reduced SAH mortality, neurological deficits, body weight loss, GFAP loss, and cerebral vasospasm by preventing the neurotoxicity induced by glutamate and oxidative stress.     

Real-Time,In Vivo Monitoring,and Quantitative Assessment of Intra-Arterial Vasospasm Therapy

Background

Our study aimed to evaluate whether the effect of an intra-arterial vasospasm therapy can be assessed quantitatively by in vivo blood flow analysis using the postprocessing algorithm parametric color coding (PCC).

Methods

We evaluated 17 patients presenting with acute clinical deterioration due to vasospasm following subarachnoidal hemorrhage treated with intra-arterial nimodipine application. Pre- and post-interventional DSA series were post-processed by PCC. The relative time to maximum opacification (rTmax) was calculated in 14 arterially and venously located points of interest. From that data, the pre- and post-interventional cerebral circulation time (CirT) was calculated. Additionally, the arterial vessel diameters were measured. Pre- and post-interventional values were compared and tested for significance, respectively.

Results

Flow analysis revealed in all arterial vessel segments a non-statistically significant prolongation of rTmax after treatment. The mean CirT was 5.62 s (±1.19 s) pre-interventionally and 5.16 s (±0.81 s) post-interventionally, and the difference turned out as statistically significant (p = 0.039). A significantly increased diameter was measurable in all arterial segments post-interventionally.

Conclusion

PCC is a fast applicable imaging technique that allows via real-time and in vivo blood flow analysis a quantitative assessment of the effect of intra-arterial vasospasm therapy. Our results seem to validate in vivo that an intra-arterial nimodipine application induces not only vasodilatation of the larger vessels, but also improves the microcirculatory flow, leading to a shortened cerebral CirT that reaches normal range post-interventionally. Procedural monitoring via PCC offers the option to compare quantitatively different therapy regimes, which allows optimization of existing approaches and implementation of individualized treatment strategies.