Reversible Cerebral Vasoconstriction Syndrome And Fibromuscular Dysplasia: An Epiphenomenon Or A Causal Relationship?

Fibromuscular dysplasia (FMD) is a rare non-atherosclerotic arterial disease that primarily affects middle-aged Caucasian women. Carotid web (CW) is a variant of FMD characterized by a nonatheromatous, membrane-like tissue protrusion into the carotid bulb. Reversible cerebral vasoconstriction syndrome (RCVS) is defined by severe headaches and reversible narrowing of cerebral arteries, which typically resolves within three months. While most RCVS cases have identifiable triggers, a significant portion occurs without known causes. Recent studies have reported a high prevalence of neurovascular abnormalities in RCVS patients. We present a case of a thirty-year-old woman with a sudden-onset severe headache, diagnosed with RCVS associated with carotid web. The patient had no ischemic involvement and responded well to flunarizine treatment. Follow-up imaging showed no stenosis. This case highlights a potential association between carotid web and RCVS, suggesting that FMD may contribute to vascular hyperreactivity and presents as a risk factor for RCVS. Further investigations are needed to understand the underlying mechanisms connecting these two vascular disorders. Keywords: reversible vasoconstriction syndrome; fibromuscular dysplasia; carotid web; structural abnormalities; vascular hyperreactivity.

Impact of ventriculo-cisternal irrigation on prevention of delayed cerebral infarction in aneurysmal subarachnoid hemorrhage: a single-center retrospective study and literature review.

OBJECTIVE: The aim of this study was to evaluate the effectiveness of ventriculo-cisternal irrigation (VCI) in preventing vasospasms and delayed cerebral infarction (DCI) by washing out subarachnoid clots earlier after aneurysm surgery. METHODS: We retrospectively identified 340 subarachnoid hemorrhage (SAH) patients with ruptured intracranial aneurysms treated with postoperative VCI at our institution between December 2010 and January 2020. As VCI therapy, a ventricular drain/cisternal drain was placed during aneurysm surgery, and lactated Ringer's solution was used for irrigation until day 4 of SAH, followed by intracranial pressure control at 5-10 cmH2O until day 14. RESULTS: The median age was 65 years (interquartile range 52-75), with 236 female patients (69%). The World Federation of Neurosurgical Societies grade distribution was as follows: grade I or II, 175 patients (51%); grade III or IV, 84 (25%); and grade V, 81 (24%). With VCI management in all patients, total vasospasm occurred in 162 patients (48%), although the DCI incidence was low (23 patients [6.8%]). Major drainage-related complications were observed in five patients (1.5%). Early surgery, performed on SAH day 0 or 1, was identified as a preventive factor against DCI occurrence (odds ratio (OR) 0.21, 95% confidence interval (CI) 0.07-0.67; P = 0.008), while additional surgery (4.76, 1.62-13.98; P = 0.005) and dyslipidemia (3.27, 1.24-8.63; P = 0.017) were associated with DCI occurrence. CONCLUSION: Managing vasospasms with VCI after SAH is considered a safe and effective method to prevent DCI. Early surgery after SAH may be associated with a decreased risk of DCI with VCI therapy.

Vasospasm following brain tumor resection in children: institutional experience and systematic review.

OBJECTIVE: Delayed cerebral ischemia (DCI) associated with vasospasm is well described in the setting of aneurysmal subarachnoid hemorrhage (SAH). In addition, DCI is very infrequently encountered in patients who have undergone resection of a brain tumor with unclear pathophysiology. The occurrence of DCI in the pediatric population is exceedingly rare, and outcomes in this population have, to the authors' knowledge, never been systematically reviewed. Therefore, the authors present what is to their knowledge the largest series of pediatric patients with this complication and systematically reviewed the literature for individual participant data. METHODS: The authors conducted a retrospective review of 172 sellar and suprasellar tumors in pediatric patients who underwent surgery at the Montreal Children's Hospital between 1999 and 2017 to identify cases of vasospasm occurring after tumor resection. Descriptive statistics, including patient characteristics, intraoperative and postoperative findings, and outcome status, were collected. A systematic review was also conducted using three databases (PubMed, Web of Science, Embase) to identify reported cases available in the literature of vasospasm after tumor resection in children and collect individual participant data on these patients for further analysis. RESULTS: Six patients treated at Montreal Children's Hospital were identified, with an average age of 9.5 years (range 6-15 years). The prevalence of vasospasm after tumor resection was 3.5% (6/172). Vasospasm in all 6 patients occurred after craniotomy was performed to treat a suprasellar tumor. The average interval from surgery to symptoms was 3.25 days (range 12 hours-10 days). The most common tumor etiology was craniopharyngioma, seen in 4 cases. Extensive tumor encasement of blood vessels requiring significant operative manipulation was described in all 6 patients. A rapid decrease in serum sodium (exceeding 12 mEq/L/24 hrs or below 135 mEq/L) was seen in 4 patients. On final follow-up, 3 patients were left with significant disability, and all patients had persistent deficits. A systematic review of the literature revealed a total of 10 other patients whose characteristics and treatment were compared with those of the 6 patients treated at Montreal Children's Hospital. CONCLUSIONS: Vasospasm after tumor resection in children and youth is likely a rare entity, with a prevalence of 3.5% in this case series. Suprasellar tumor location (particularly craniopharyngioma tumor etiology), significant encasement of blood vessels by the tumor, and postoperative hyponatremia may be predictive factors. Outcome is poor, with most patients having significant persistent neurological deficits.

Immunological Profile of Vasospasm after Subarachnoid Hemorrhage.

Subarachnoid hemorrhage (SAH) carries high mortality and disability rates, which are substantially driven by complications. Early brain injury and vasospasm can happen after SAH and are crucial events to prevent and treat to improve prognosis. In recent decades, immunological mechanisms have been implicated in SAH complications, with both innate and adaptive immunity involved in mechanisms of damage after SAH. The purpose of this review is to summarize the immunological profile of vasospasm, highlighting the potential implementation of biomarkers for its prediction and management. Overall, the kinetics of central nervous system (CNS) immune invasion and soluble factors' production critically differs between patients developing vasospasm compared to those not experiencing this complication. In particular, in people developing vasospasm, a neutrophil increase develops in the first minutes to days and pairs with a mild depletion of CD45+ lymphocytes. Cytokine production is boosted early on after SAH, and a steep increase in interleukin-6, metalloproteinase-9 and vascular endothelial growth factor (VEGF) anticipates the development of vasospasm after SAH. We also highlight the role of microglia and the potential influence of genetic polymorphism in the development of vasospasm and SAH-related complications.

Relationship between cerebral vasospasm vascular territory and functional outcome after aneurysmal subarachnoid hemorrhage.

BACKGROUND: Vasospasm following aneurysmal subarachnoid hemorrhage (SAH) contributes significant morbidity and mortality after brain aneurysm rupture. However, the association between vascular territory of vasospasm and clinical outcome has not been studied. We present a hypothesis-generating study to determine whether the location of vasospasm within the intracranial circulation is associated with functional outcome after SAH. METHODS: A retrospective analysis of a prospective, intention-to-treat trial for aneurysmal SAH was performed to supplement trial outcomes with in-hospital angiographic imaging and treatment variables regarding vasospasm. The location of vasospasm and the position on the vessel (distal vs proximal) were evaluated. Modified Rankin scale (mRS) outcomes were assessed at discharge and 6 months, and predictive models were constructed. RESULTS: A total of 406 patients were included, 341 with follow-up data at 6 months. At discharge, left-sided vasospasm was associated with poor outcome (odds ratio (OR), 2.37; 95% CI, 1.25 to 4.66; P=0.01). At 6 months, anterior cerebral artery (ACA) vasospasm (OR, 3.87; 95% CI, 1.29 to 11.88; P=0.02) and basilar artery (BA) vasospasm (OR, 6.22; 95% CI, 1.54 to 27.11; P=0.01) were associated with poor outcome after adjustment. A model predicting 6-month mRS score and incorporating vasospasm variables achieved an area under the curve of 0.85 and a net improvement in reclassification of 13.2% (P<0.01) compared with a previously validated predictive model for aneurysmal SAH. CONCLUSIONS: In aneurysmal SAH, left-sided vasospasm is associated with worse discharge functional status. At 6 months, both ACA and BA vasospasm are associated with unfavorable functional status.

Cerebral vasospasm following arteriovenous malformation rupture: a population-based cross-sectional study.

OBJECTIVE: Studies examining the risk factors and clinical outcomes of arterial vasospasm secondary to cerebral arteriovenous malformation (cAVM) rupture are scarce in the literature. The authors used a population-based national registry to investigate this largely unexamined clinical entity. METHODS: Admissions for adult patients with cAVM ruptures were identified in the National Inpatient Sample during the period from 2015 to 2019. Complex samples multivariable logistic regression and chi-square automatic interaction detection (CHAID) decision tree analyses were performed to identify significant associations between clinical covariates and the development of vasospasm, and a cAVM-vasospasm predictive model (cAVM-VPM) was generated based on the effect sizes of these parameters. RESULTS: Among 7215 cAVM patients identified, 935 developed vasospasm, corresponding to an incidence rate of 13.0%; 110 of these patients (11.8%) subsequently progressed to delayed cerebral ischemia (DCI). Multivariable adjusted modeling identified the following baseline clinical covariates: decreasing age by decade (adjusted odds ratio [aOR] 0.87, 95% CI 0.83-0.92; p < 0.001), female sex (aOR 1.68, 95% CI 1.45-1.95; p < 0.001), admission Glasgow Coma Scale score < 9 (aOR 1.34, 95% CI 1.01-1.79; p = 0.045), intraventricular hemorrhage (aOR 1.87, 95% CI 1.17-2.98; p = 0.009), hypertension (aOR 1.77, 95% CI 1.50-2.08; p < 0.001), obesity (aOR 0.68, 95% CI 0.55-0.84; p < 0.001), congestive heart failure (aOR 1.34, 95% CI 1.01-1.78; p = 0.043), tobacco smoking (aOR 1.48, 95% CI 1.23-1.78; p < 0.019), and hospitalization events (leukocytosis [aOR 1.64, 95% CI 1.32-2.04; p < 0.001], hyponatremia [aOR 1.66, 95% CI 1.39-1.98; p < 0.001], and acute hypotension [aOR 1.67, 95% CI 1.31-2.11; p < 0.001]) independently associated with the development of vasospasm. Intraparenchymal and subarachnoid hemorrhage were not associated with the development of vasospasm following multivariable adjustment. Among significant associations, a CHAID decision tree algorithm identified age 50-59 years (parent node), hyponatremia, and leukocytosis as important determinants of vasospasm development. The cAVM-VPM achieved an area under the curve of 0.65 (sensitivity 0.70, specificity 0.53). Progression to DCI, but not vasospasm alone, was independently associated with in-hospital mortality (aOR 2.35, 95% CI 1.29-4.31; p = 0.016) and lower likelihood of routine discharge (aOR 0.62, 95% CI 0.41-0.96; p = 0.031). CONCLUSIONS: This large-scale assessment of vasospasm in cAVM identifies common clinical risk factors and establishes progression to DCI as a predictor of poor neurological outcomes.

Impact of Cerebral Autoregulation Monitoring in Cerebrovascular Disease: A Systematic Review.

Cerebral autoregulation (CA) prevents brain injury by maintaining a relatively constant cerebral blood flow despite fluctuations in cerebral perfusion pressure. This process is disrupted consequent to various neurologic pathologic processes, which may result in worsening neurologic outcomes. Herein, we aim to highlight evidence describing CA changes and the impact of CA monitoring in patients with cerebrovascular disease, including ischemic stroke, intracerebral hemorrhage (ICH), and aneurysmal subarachnoid hemorrhage (aSAH). The study was preformed according to the Preferred Reporting Items for Systematic Reviews and Meta-Analysis guidelines. English language publications were identified through a systematic literature conducted in Ovid Medline, PubMed, and Embase databases. The search spanned the dates of each database's inception through January 2021. We selected case-control studies, cohort observational studies, and randomized clinical trials for adult patients (≥ 18 years) who were monitored with continuous metrics using transcranial Doppler, near-infrared spectroscopy, and intracranial pressure monitors. Of 2799 records screened, 48 studies met the inclusion criteria. There were 23 studies on ischemic stroke, 18 studies on aSAH, 5 studies on ICH, and 2 studies on systemic hypertension. CA impairment was reported after ischemic stroke but generally improved after tissue plasminogen activator administration and successful mechanical thrombectomy. Persistent impairment in CA was associated with hemorrhagic transformation, malignant cerebral edema, and need for hemicraniectomy. Studies that investigated large ICHs described bilateral CA impairment up to 12 days from the ictus, especially in the presence of small vessel disease. In aSAH, impairment of CA was associated with angiographic vasospasm, delayed cerebral ischemia, and poor functional outcomes at 6 months. This systematic review highlights the available evidence for CA disruption during cerebrovascular diseases and its possible association with long-term neurological outcome. CA may be disrupted even before acute stroke in patients with untreated chronic hypertension. Monitoring CA may help in establishing individualized management targets in patients with cerebrovascular disease.

Primary angiitis of the central nervous system and reversible cerebral vasoconstriction syndrome: analysis of the National Inpatient Sample.

INTRODUCTION: Primary angiitis of the central nervous system (PACNS) and reversible cerebral vasoconstriction syndrome (RCVS) are two rare syndromes that affect the cerebral vasculature. Both conditions have been shown to cause severe neurologic complications. Distinguishing these two conditions in clinical practice is often challenging. Here, we compare the clinical features and outcomes of RCVS and PACNS hospitalizations against the general adult inpatient population. MATERIALS AND METHODS: We conducted a retrospective review of hospitalizations with a diagnosis of PACNS or RCVS from 2016 to 2018 in the National Inpatient Sample (NIS) database. Multivariate analysis was performed to calculate adjusted odds ratios (ORadj) for hospital outcomes. RESULTS: In the NIS, 3305 hospitalizations had a diagnosis of RCVS and 6035 hospitalizations had a diagnosis of PACNS. RCVS hospitalizations had a significantly greater association with cerebral aneurysms (ORadj 23.80), hemiplegia/hemiparesis following subarachnoid hemorrhage (SAH) (ORadj 324.09), ischemic stroke (ORadj 7.59), and nontraumatic SAH (ORadj 253.61). PACNS hospitalizations had a significantly greater association with hemiplegia/hemiparesis following cerebrovascular accident (CVA) (ORadj 6.16), ischemic stroke (ORadj 11.55), nontraumatic SAH (ORadj 7.29), seizure (ORadj 2.49), and in-hospital mortality (ORadj 2.85). CONCLUSIONS: We performed an analysis of the NIS to better understand RCVS and PACNS hospitalizations. Severe neurologic events including CVA and SAH were elevated in both, but SAH and related hemiplegia/hemiparesis were extremely common among RCVS hospitalizations. In-hospital mortality was elevated in PACNS but not RCVS. This information can be used to help clinicians better understand, distinguish, and diagnose these conditions. Key Points • Despite clear description of RCVS and PACNS in the medical literature, there remains a scarcity of national population-based studies comparing these two entities against the general adult inpatient population. • This study aims to fill knowledge gaps in this area. • Here, we compare the clinical features and outcomes of RCVS and PACNS hospitalizations against the general adult inpatient population.

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

BACKGROUND: Patients with aneurysmal subarachnoid hemorrhage (aSAH) frequently suffer from vasospasm. We analyzed the association between absence of early angiographic vasospasm and early discharge. METHODS: All aSAH patients treated from August 1, 2007, to July 31, 2019, at a single tertiary center were reviewed. Patients undergoing diagnostic digital subtraction angiography (DSA) on post-aSAH days 5 to 7 were analyzed; cohorts with and without angiographic vasospasm (angiographic reports by attending neurovascular surgeons) were compared. Primary outcome was hospital length of stay; secondary outcomes were intensive care unit length of stay, 30 day return to the emergency department (ED), and poor neurologic outcome, defined as a modified Rankin Scale (mRS) score >2. RESULTS: A total of 298 patients underwent DSA on post-aSAH day 5, 6, or 7. Most patients (n=188, 63%) had angiographic vasospasm; 110 patients (37%) did not. Patients without vasospasm had a significantly lower mean length of hospital stay than vasospasm patients (18.0±7.1 days vs 22.4±8.6 days; p<0.001). The two cohorts did not differ significantly in the proportion of patients with mRS scores >2 at last follow-up or those returning to the ED before 30 days. After adjustment for Hunt and Hess scores, Fisher grade, admission Glasgow Coma Scale score, and age, logistic regression analysis showed that the absence of vasospasm on post-aSAH days 5-7 predicted discharge on or before hospital day 14 (OR 3.4, 95% CI 1.8 to 6.4, p<0.001). CONCLUSION: Lack of angiographic vasospasm 5 to 7 days after aSAH is associated with shorter hospitalization, with no increase in 30 day ED visits or poor neurologic outcome.

Distribution of symptomatic cerebral vasospasm following subarachnoid hemorrhage assessed using cone-beam CT angiography.

BACKGROUND AND PURPOSE: Cone-beam CT angiography (CB-CTA) provides a three-dimensional spatial resolution which is, so far, unmatched in clinical practice compared with other conventional techniques such as two-dimensional digital subtracted angiography. We aimed to assess the distribution of symptomatic cerebral vasospasm following aneurysmal subarachnoid hemorrhage (aSAH) using CB-CTA. METHODS: 30 consecutive patients with aSAH undergoing vasospasm percutaneous balloon angioplasty (PBA) were recruited and underwent CB-CTA in this single-center prospective cohort series. Intracranial arteries were systematically analyzed by two independent observers from the large trunks to the distal cortical branches and perforators using a high-resolution reconstruction protocol. Intermediate and severe cerebral vasospasm was defined as 30-50% and >50% narrowing in the diameter of the vessel, respectively. RESULTS: 35 arterial cervical artery territories were analyzed, of which 80% were associated with clinical or radiological signs of delayed cerebral ischemia. The median spatial resolution was 150 µm (range 100-250 µm). Intermediate or severe vasospasm was observed in the proximal (86%, 95% CI 74% to 97%), middle (89%, 95% CI 78% to 99%), and distal (60%, 95% CI 44% to 76%) segments of the large trunks, as well as the cortical branches (11%, 95% CI 1% to 22%). No vasospasm was observed in basal ganglia or cortical perforators, or in arteries smaller than 900 µm. Vasospasm was more severe in middle or distal segments compared with proximal segments in 43% (95% CI 26% to 59%) of cases. CONCLUSIONS: Our study demonstrated that symptomatic cerebral vasospasm following aSAH did not involve arteries smaller than 900 µm, and frequently predominated in middle or distal segments. These results offer new insights into the potential management options for vasospasm using PBA.

Primary results of the Vesalio NeVa VS for the Treatment of Symptomatic Cerebral Vasospasm following Aneurysm Subarachnoid Hemorrhage (VITAL) Study.

BACKGROUND: Cerebral vasospasm (CV) after aneurysmal subarachnoid hemorrhage (aSAH) is linked to worse neurological outcomes. The NeVa VS is a novel cerebral dilation device based on predicate stent retrievers. We report the results of the Vesalio NeVa VS for the Treatment of Symptomatic Cerebral Vasospasm following aSAH (VITAL) Study. METHODS: This was a single-arm prospective multicenter trial to assess the safety and probable benefit of the NeVa VS device to treat CV. Patients were screened and treated if they had CV >50% on non-invasive imaging confirmed by cerebral angiography. The vessel diameters were measured before and after treatment by an independent core laboratory. The primary endpoint was ≥50% vessel diameter immediately after treatment with the NeVa VS device. RESULTS: Thirty patients with a mean age of 52±11 years and mean Hunt-Hess grade of 3.1±0.9 were enrolled. A total of 74 vessels were treated with an average of 1.3 deployments per vessel (95 deployments total). The mean pre-treatment narrowing of the target vessel (n=74) was 65.6% with reduction of the narrowing to 29.4% after treatment. The primary endpoint was achieved in 64 of 74 vessels (86.5%). In three of 95 total deployments (3.2%), thrombus at the site of deployment was observed during the procedure without apparent neurological sequelae. CONCLUSIONS: The NeVa VS device appears to be a safe treatment to regain vessel diameter in severely narrowed intracranial arteries secondary to CV associated with aSAH. This treatment offers a new tool that allows for controlled vessel expansion to treat CV.

Postoperative Transfusion Guidelines in Aneurysmal Cerebral Subarachnoid Hemorrhage: A Systematic Review and Critical Summary of Available Evidence.

OBJECTIVE: Surgical management of aneurysmal subarachnoid hemorrhage (SAH) often involves red blood cell (RBC) transfusion, which increases the risk of postoperative complications. RBC transfusion guidelines report on chronically critically ill patients and may not apply to patients with SAH. Our study aims to synthesize the evidence to recommend RBC transfusion thresholds among adult patients with SAH undergoing surgery. METHODS: A systematic review was conducted using PubMed, Google Scholar, and Web of Science electronic databases according to the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines to critically assess primary articles discussing RBC transfusion thresholds and describe complications secondary to RBC transfusion in adult patients with SAH in the perioperative period. RESULTS: Sixteen articles meeting our search strategy were reviewed. Patients with SAH who received blood transfusion were older, female, had World Federation of Neurosurgical Societies grade IV-V and modified Fisher grade 3-4 scores, and presented with more comorbidities such as hypertension, diabetes, and cardiovascular and pulmonary diseases. In addition, transfusion was associated with multiple postoperative complications, including higher rates of vasospasms, surgical site infections, cardiovascular and respiratory complications, increased postoperative length of stay, and 30-day mortality. Analysis of transfused patients showed that a higher hemoglobin (>10 g/dL) goal after SAH was safe and that patients may benefit from a higher whole hospital stay hemoglobin nadir, as shown by a reduction in risk of cerebral vasospasm and improvement in clinical outcomes (level B class II). CONCLUSIONS: Among patients with SAH, the benefits of reducing cerebral ischemia and anemia are shown to outweigh the risks of transfusion-related complications.

Peroxisome proliferator­activated receptor ß/δ regulates cerebral vasospasm after subarachnoid hemorrhage via modulating vascular smooth muscle cells phenotypic conversion.

Cerebral vasospasm (CVS) is a common complication of subarachnoid hemorrhage (SAH) with high deformity rates and cerebral vascular smooth muscle cells (VSMCs) phenotypic switch is considered to be involved in the regulation of CVS. However, to the best of the authors' knowledge, its underlying molecular mechanism remains to be elucidated. Peroxisome proliferator­activated receptor ß/δ (PPARß/δ) has been demonstrated to be involved in the modulation of vascular cells proliferation and maintains the autoregulation function of blood vessels. The present study investigated the potential effect of PPARß/δ on CVS following SAH. A model of SAH was established by endovascular perforation on male adult Sprague­Dawley rats, and the adenovirus PPARß/δ (Ad­PPARß/δ) was injected via intracerebroventricular administration prior to SAH. The expression levels of phenotypic markers α­smooth muscle actin and embryonic smooth muscle myosin heavy chain were measured via western blotting or immunofluorescence staining. The basilar artery diameter and vessel wall thickness were evaluated under fluorescence microscopy. SAH grade, neurological scores, brain water content and brain swelling were measured to study the mechanisms of PPARß/δ on vascular smooth muscle phenotypic transformation. It was revealed that the expression levels of synthetic proteins were upregulated in rats with SAH and this was accompanied by CVS. Activation of PPARß/δ using Ad­PPARß/δ markedly upregulated the contractile proteins elevation, restrained the synthetic proteins expression and attenuated SAH­induced CVS by regulating the phenotypic switch in VSMCs at 72 h following SAH. Furthermore, the preliminary study demonstrated that PPARß/δ downregulated ERK activity and decreased the expression of phosphorylated (p­)ETS domain­containing protein Elk­1 and p­p90 ribosomal S6 kinase, which have been demonstrated to serve an important role in VSMC phenotypic change. Additionally, it was revealed that Ad­PPARß/δ could positively improve CVS by ameliorating the diameter of the basilar artery and mitigating the thickness of the vascular wall. Furthermore, subsequent experiments demonstrated that Ad­PPARß/δ markedly reduced the brain water content and brain swelling and improved the neurological outcome. Taken together, the present study identified PPARß/δ as a useful regulator for the VSMCs phenotypic switch and attenuating CVS following SAH, thereby providing novel insights into the therapeutic strategies of delayed cerebral ischemia.

Inflammation and Anti-Inflammatory Targets after Aneurysmal Subarachnoid Hemorrhage.

Aneurysmal subarachnoid hemorrhage (aSAH), with a crude worldwide incidence of around 7 [...].

Four-dimensional computed tomography angiography analysis of internal carotid arteries opacification at the skull base to detect delayed cerebral ischemia: a feasibility study.

PURPOSE: Delayed cerebral ischemia represents a significant cause of poor functional outcome for patients with vasospasm after subarachnoid hemorrhage. We investigated whether delayed cerebral ischemia could be detected by the arterial opacification of internal carotid artery at the level of the skull base. METHODS: In this exploratory, nested retrospective cohort diagnostic accuracy study, patients with clinical and/or transcranial Doppler suspicion of vasospasm who underwent four-dimensional computed tomography angiography were included. They were split into two groups for the main endpoint analysis, according to the actually adopted morphological (cerebral infarction) and clinical criteria (neurologic deterioration) of delayed cerebral ischemia. Opacification with a temporal resolution of 0.15 s of both internal carotid arteries at the skull base level was obtained through a semi-automated segmentation method based on skeletonization, and analyzed by a wavelet transform (rbio2.2, level 1). The results obtained by k-means clustering were analyzed with regard to the state of delayed cerebral infarction. RESULTS: Over ten patients included and analyzed, five patients presented a delayed cerebral ischemia, two of them in both side. The semi-automated processing and analysis clustered two different types of opacification curves. The obtaining of a nonlinear opacification pattern was associated (p < 0.001) with delayed cerebral ischemia. CONCLUSIONS: The analysis of arterial opacification of internal carotid arteries at skull base by the proposed processing is feasible and leads to cluster two types of opacification that may help to early detect and prevent delayed cerebral ischemia, in particularly when examinations are artifacted by aneurysm treatment materials.

Headache in cerebrovascular diseases.

Headache is a common accompanying symptom of cerebrovascular diseases. The most common patterns of headache for different cerebrovascular disorders, aetiology and pathogenesis and diagnostic workup are reviewed with emphasis on distinguishing characteristics. It will be a clinical guide for physicians who treat patients with headache or cerebral vascular disease.

Describing a New Mechanism of Retinal Detachment Secondary to Ophthalmic Artery Vasospasm Following Subarachnoid Hemorrhage: An Experimental Study.

BACKGROUND: The pterygopalatine ganglion (PPG) and ophthalmic arteries (OpAs) have important roles in ocular autoregulation and retinal and visual functions. The relationship between PPG neuron density, OpA vasospasm, and retinal detachment in subarachnoid hemorrhage (SAH) has never been studied. METHODS: This study was conducted on 25 rabbits. Five animals were in the control group (GI; n = 5), five in the sham group (GII; n = 5), and 15 in the study group (GIII; n = 15). After injection of 1 cc serum saline into the cisterna magna in the sham group, and autologous blood in the SAH group, the animals were followed for 3 weeks. All animals underwent a retinal examination five times a week for 3 weeks before and after the experiment. After the experiment, the neuron density of PPGs of the facial nerves, vasospasm index (VSI) of OpAs, and total basal surface values of the detached retinal parts (DRPs) were calculated. RESULTS: In the funduscopic examination, intravitreous hemorrhage ( Terson's syndrome) was detected in four animals in the SAH group. In the control groups, neuron density was 12,000 ± 1,240/mm3, VSI = 0.345 ± 0.076, and DRP = 0 to 1.5 mm2. Mean neuron density was 9,450 ± 940/mm3, VSI = 1.645 ± 0.940, and DRP = 6.23 ± 1.61 mm2 in the sham group (p < 0.05). Neuron density was 6,890 ± 932/mm3, VSI = 2.92 ± 0.97, and DRP = 9.43 ± 2.54 mm2 in SAH group. CONCLUSION: Mean neuron density, VSI of OpAs, and DRP values differed statistically significant between the SAH group and other groups (p < 0.005). There is an inverse relationship between PPG neurons and DRP. However, a direct relationship was observed between the mean VSI and DRP values.

Anti-vasospastic Effects of Epidermal Growth Factor Receptor Inhibitors After Subarachnoid Hemorrhage in Mice.

Subarachnoid hemorrhage (SAH) is a devastating disease. Cerebral vasospasm is still an important cause of post-SAH poor outcomes, but its mechanisms remain unveiled. Activation of epidermal growth factor receptor (EGFR) is suggested to cause vasoconstriction in vitro, but no report has demonstrated the involvement of EGFR in vasospasm development after SAH in vivo. Cross-talk of EGFR and vascular endothelial growth factor (VEGF) receptor, which may affect post-SAH vasospasm, was also reported in cancer cells, but has not been demonstrated in post-SAH vasospasm. The aim of this study was to investigate whether EGFR as well as EGFR-VEGF receptor cross-talk engage in the development of cerebral vasospasm in a mouse SAH model. C57BL6 mice underwent endovascular perforation SAH or sham modeling. At 30 min post-modeling, mice were randomly administrated vehicle or 2 doses of selective EGFR inhibitors intracerebroventricularly. A higher dose of the inhibitor significantly prevented post-SAH neurological impairments at 72 h and vasospasm at 24 h associated with suppression of post-SAH activation of EGFR and extracellular signal-regulated kinase (ERK) 1/2 in the cerebral artery wall, especially in the smooth muscle cell layers. Anti-EGFR neutralizing antibody also showed similar effects. However, neither expression levels of VEGF nor activation levels of a major receptor of VEGF, VEGF receptor-2, were affected by SAH and two kinds of EGFR inactivation. Thus, this study first showed that EGFR-ERK1/2 pathways may be involved in post-SAH vasospasm development, and that EGFR-VEGF receptor cross-talk may not play a significant role in the development of vasospasm in mice.