Leptomeningeal Collateral Vessels Research Articles

Modeling cerebrovascular responses to assess the impact of the collateral circulation following middle cerebral artery occlusion.

An improved understanding of the role of the leptomeningeal collateral circulation in blood flow compensation following middle cerebral artery (MCA) occlusion can contribute to more effective treatment development for ischemic stroke. The present study introduces a model of the cerebral circulation to predict cerebral blood flow and tissue oxygenation following MCA occlusion. The model incorporates flow regulation mechanisms based on changes in pressure, shear stress, and metabolic demand. Oxygen saturation in cerebral vessels and tissue is calculated using a Krogh cylinder model. The model is used to assess the effects of changes in oxygen demand and arterial pressure on cerebral blood flow and oxygenation after MCA occlusion. An increase from five to 11 leptomeningeal collateral vessels was shown to increase the oxygen saturation in the region distal to the occlusion by nearly 100%. Post-occlusion, the model also predicted a loss of autoregulation and a decrease in flow to the ischemic territory as oxygen demand was increased; these results were consistent with data from experiments that induced cerebral ischemia. This study highlights the importance of leptomeningeal collaterals following MCA occlusion and reinforces the idea that lower oxygen demand and higher arterial pressure improve conditions of flow and oxygenation.

Modelling the leptomeningeal collateral circulation during acute ischaemic stroke

A novel model of the leptomeningeal collateral circulation is created by combining data from multiple sources with statistical scaling laws. The extent of the collateral circulation is varied by defining a collateral vessel probability. Blood flow and pressure are simulated using a one-dimensional steady state blood flow model. The leptomeningeal collateral vessels provide significant flow during a stroke. The pressure drop over an occlusion predicted by the model ranges between 60 and 85 mmHg depending on the extent of the collateral circulation. The linear transport of contrast material was simulated in the circulatory network. The time delay of peak contrast over an occlusion is 3.3 s in the model, and 2.1 s (IQR 0.8–4.0 s) when measured in dynamic CTA data of acute ischaemic stroke patients. Modelling the leptomeningeal collateral circulation could lead to better estimates of infarct volume and patient outcome.

Cerebral hemodynamics associated with fluid-attenuated inversion recovery hyperintense vessels in patients with extracranial carotid artery stenosis.

Fluid-attenuated inversion recovery hyperintense vessels (FHVs) are linked to sluggish or disordered blood flow. The purpose of this study is to compare FHVs with digital subtraction angiography (DSA) findings and cerebral hemodynamic changes on acetazolamide challenge SPECT and to determine the clinical and imaging metrics associated with FHVs in patients with extracranial carotid artery stenosis (ECAS). The subjects were patients with chronic ECAS who underwent carotid artery stenting in our department between March 2011 and October 2018. Relationships of FHVs with age, sex, medical history, cerebral angiographic findings using DSA, and quantitative values of cerebral blood flow (CBF) were examined. The resting CBF (rCBF) and cerebrovascular reactivity (CVR) in the middle cerebral artery territory were measured quantitatively using SPECT with acetazolamide challenge. We used multivariate logistic regression analysis to identify independent predictors of FHVs. Of 173 patients included, 92 (53.2%) had FHVs. Patients with FHVs had more severe stenosis (P < 0.01) and more leptomeningeal collateral vessels (P < 0.01). FHV-positive cases had significantly reduced CVR compared with FHV-negative cases (P < 0.01), although there was no significant difference in rCBF between FHV-positive and FHV-negative cases. Logistic regression analysis showed that ipsilateral rCBF and ipsilateral CVR were significant predictors for FHVs (P < 0.01). In patients with ECAS, cerebral hemodynamic metrics, especially ipsilateral rCBF and ipsilateral CVR, are associated with the presence of FHVs.

Signal variance-based collateral index in DSC perfusion: A novel method to assess leptomeningeal collateralization in acute ischaemic stroke

As a determinant of the progression rate of the ischaemic process in acute large-vessel stroke, the degree of collateralization is a strong predictor of the clinical outcome after reperfusion therapy and may influence clinical decision-making. Therefore, the assessment of leptomeningeal collateralization is of major importance. The purpose of this study was to develop and evaluate a quantitative and observer-independent method for assessing leptomeningeal collateralization in acute large-vessel stroke based on signal variance characteristics in T2*-weighted dynamic susceptibility contrast (DSC) perfusion-weighted MR imaging (PWI). Voxels representing leptomeningeal collateral vessels were extracted according to the magnitude of signal variance in the PWI raw data time series in 55 patients with proximal large-artery occlusion and an intra-individual collateral vessel index (CVIPWI) was calculated. CVIPWI correlated significantly with the initial ischaemic core volume (rho = −0.459, p = 0.0001) and the PWI/DWI mismatch ratio (rho = 0.494, p = 0.0001) as an indicator of the amount of salvageable tissue. Furthermore, CVIPWI was significantly negatively correlated with NIHSS and mRS at discharge (rho = −0.341, p = 0.015 and rho = −0.305, p = 0.023). In multivariate logistic regression, CVIPWI was an independent predictor of favourable functional outcome (mRS 0–2) (OR = 16.39, 95% CI 1.42–188.7, p = 0.025). CVIPWI provides useful rater-independent information on the leptomeningeal collateral supply in acute stroke.

Leptomeningeal collateral status predicts outcome after middle cerebral artery occlusion.

Perfusion through leptomeningeal collateral vessels is a likely pivotal factor in the outcome of stroke patients. We aimed to investigate the effect of collateral status on outcome in a cohort of unselected, consecutive stroke patients with middle cerebral artery occlusion undergoing reperfusion therapy. This retrospectively planned analysis was passed on prospectively collected data from 187 consecutive patients with middle cerebral artery occlusion admitted within 4.5hours to one center and treated with intravenous thrombolysis alone (N=126), mechanical thrombectomy alone (N=5), or both (N=56) from May 2009 to April 2014. Non-contrast CT (NCCT) and computed tomography angiography (CTA) were provided on admission and NCCT repeated at 24hours. Collateral status was assessed based on the initial CTA. Hemorrhagic transformation was evaluated on the 24-hour NCCT and according to European Cooperative Acute Stroke Study (ECASS) criteria. Modified Rankin Scale score was assessed at 90days, and mortality at 1year. At 90days, median (IQR) modified Rankin Scale score in patients with poor collateral status was 4 (3-6) compared to 2 (1-4) in patients with good collateral status (P<.0001). Patients with poor collateral status were less likely to achieve a good 90-day outcome (modified Rankin Scale score 0-2) (Adjusted odds ratio 0.27, 95% CI: 0.09-0.86). During the first year, 40.9% of patients with poor collateral status died vs 18.2% of the remaining population (P=.001). Leptomeningeal collateral status predicts functional outcome, mortality, and hemorrhagic transformation following middle cerebral artery occlusion.

Intracranial Pressure and Collateral Blood Flow.

Leptomeningeal collateral vessels, linking the 3 major arterial territories over the surface of the brain, have been recognized for >140 years.1 More widespread use of advanced clinical imaging in the past decade has led to increasing recognition of the key importance of collaterals in ischemic stroke outcome.2 However, recent studies from several groups indicate that failure of initially good collateral supply is a key feature of patients with delayed infarct expansion.3,4 This clinically challenging problem typically occurs in the first 1 to 2 days after hospital admission in patients with initially mild stroke symptoms. Rethrombosis of reperfused vessels was previously thought to be the likely cause of delayed infarct expansion in most patients. However, this theory is not supported by more recent evidence from imaging studies. Despite the important recent observations, there is limited understanding of the dynamic control of the collateral circulation, in particular, the cause of collateral blood flow failure. In this article, we will discuss recent observations from our experimental stroke model, indicating a dramatic increase in intracranial pressure (ICP) occurring around 24 hours after onset of even small stroke.5,6 We have also shown a significant linear reduction of collateral blood flow in response to progressive ICP elevation.7 We believe that a similar transient ICP elevation occurring during the first 1 to 2 days post stroke is a likely mechanism to explain delayed infarct expansion in patients with minor stroke. Perhaps surprisingly, we can find no published data on ICP at 24 hours in patients with minor stroke. The preclinical findings suggest that gathering such data should be a priority. ### Human Stroke There is a strong association between the extent of leptomeningeal collaterals and clinical stroke outcome. Initial studies using digital subtraction angiography permitted direct visualization of collateral vessels and …

Sphingosine-1-Phosphate Receptor-1 Selective Agonist Enhances Collateral Growth and Protects against Subsequent Stroke.

Background and PurposeCollateral growth after acute occlusion of an intracranial artery is triggered by increasing shear stress in preexisting collateral pathways. Recently, sphingosine-1-phosphate receptor-1 (S1PR1) on endothelial cells was reported to be essential in sensing fluid shear stress. Here, we evaluated the expression of S1PR1 in the hypoperfused mouse brain and investigated the effect of a selective S1PR1 agonist on leptomeningeal collateral growth and subsequent ischemic damage after focal ischemia.MethodsIn C57Bl/6 mice (n = 133) subjected to unilateral common carotid occlusion (CCAO) and sham surgery. The first series examined the time course of collateral growth, cell proliferation, and S1PR1 expression in the leptomeningeal arteries after CCAO. The second series examined the relationship between pharmacological regulation of S1PR1 and collateral growth of leptomeningeal anastomoses. Animals were randomly assigned to one of the following groups: LtCCAO and daily intraperitoneal (ip) injection for 7 days of an S1PR1 selective agonist (SEW2871, 5 mg/kg/day); sham surgery and daily ip injection for 7 days of SEW2871 after surgery; LtCCAO and daily ip injection for 7 days of SEW2871 and an S1PR1 inverse agonist (VPC23019, 0.5 mg/kg); LtCCAO and daily ip injection of DMSO for 7 days after surgery; and sham surgery and daily ip injection of DMSO for 7 days. Leptomeningeal anastomoses were visualized 14 days after LtCCAO by latex perfusion method, and a set of animals underwent subsequent permanent middle cerebral artery occlusion (pMCAO) 7days after the treatment termination. Neurological functions 1hour, 1, 4, and 7days and infarction volume 7days after pMCAO were evaluated.ResultsIn parallel with the increase in S1PR1 mRNA levels, S1PR1 expression colocalized with endothelial cell markers in the leptomeningeal arteries, increased markedly on the side of the CCAO, and peaked 7 days after CCAO. Mitotic cell numbers in the leptomeningeal arteries increased after CCAO. Administration of the S1PR1 selective agonist significantly increased cerebral blood flow (CBF) and the diameter of leptomeningeal collateral vessels (42.9 ± 2.6 μm) compared with the controls (27.6 ± 5.7 μm; P < 0.01). S1PR1 inverse agonist administration diminished the effect of the S1PR1 agonist (P < 0.001). After pMCAO, S1PR1 agonist pretreated animals showed significantly smaller infarct volume (17.5% ± 4.0% vs. 7.7% ± 4.0%, P < 0.01) and better functional recovery than vehicle-treated controls.ConclusionsThese results suggest that S1PR1 is one of the principal regulators of leptomeningeal collateral recruitment at the site of increased shear stress and provide evidence that an S1PR1 selective agonist has a role in promoting collateral growth and preventing of ischemic damage and neurological dysfunction after subsequent stroke in patients with intracranial major artery stenosis or occlusion.

Leptomeningeal collateral vessels are a major risk factor for intracranial hemorrhage after carotid stenting in patients with carotid atherosclerotic plaque

AimTo evaluate the relationship between leptomeningeal collaterals and intracranial hemorrhage (ICH) after carotid artery stenting (CAS).MethodsA retrospective study was undertaken of 228 patients (median age 75 years (range 44–90); 187...

Abstract T P88: Impaired Collateral Status During Unilateral Carotid Occlusion In Type 2 Diabetic Mice

Introduction: Type 2 diabetes mellitus (T2DM) is major risk factor of ischemic stroke and is associated with poor outcome after stroke. Previously we found that T2DM mice exhibited impaired leptomeningeal collateral flow recruitment after distal middle cerebral artery occlusion (MCAO). The current study aimed to study the collateral status during unilateral carotid occlusion, commonly observed in human patients with atherosclerosis. Methods: Adult male db/db and db/+ mice were subjected to permanent unilateral common carotid artery occlusion (CCAO) to simulate the hypoperfusion state in the human carotid artery disease. In vivo imaging of blood flow and flow velocity of the leptomeningeal collateral vessels was performed at various time points after CCAO with doppler optical coherence tomography (DOCT). Diameter of each major artery in the circle of Willis was also quantified by DiI-labeling at various time points after CCAO. Results: Imaging of DOCT showed that during occlusion of CCA, db/+ mice showed more robust retrograde filling of several distal branches of the MCA from ACA immediately and 24 hours after CCAO compared to db/db mice. Data with DiI-labeling showed that in both strains, the diameters of Willis ring including ICA, MCA, ACA gradually enlarged after 24 hours following CCAO. However the diameters of these vessels of db/db mice on the ischemic side were significantly smaller at 24 hours and 7 days after CCAO compared to that of db/+ mice. Conclusion: Our results demonstrate an impairment of leptomeningeal collateral recruitment and a deficiency in collateral vessel growth in the circle of Willis after CCAO in db/db mice. These findings might underlie the increased risk of ischemic injury in T2DM patients with carotid disease or stroke.

Hyperintense vessels: An early MRI marker of reversible cerebral vasoconstriction syndrome?

Reversible cerebral vasoconstriction syndrome (RCVS) is an increasingly recognized clinical emergency characterized by acute onset of severe headaches (usually multiple thunderclap headaches) and reversible segmental stenosis of cerebral arteries (1). RCVS is associated with several potentially devastating complications or comorbidities, such as posterior reversible encephalopathy syndrome (PRES) (9%–38%), ischemic stroke (4%–54%), intracerebral hemorrhage (12%–20%), cortical subarachnoid hemorrhage (SAH) (22%–34%), or cervical artery dissection (1%–12%) and even death (2– 7). The prevalence of RCVS is unknown, but it could be higher than that of its most important differential diagnosis—aneurismal SAH when patients complain of thunderclap headaches. Although the clinical features of RCVS are distinct, the diagnosis could sometimes be difficult in the lack of awareness or alertness about the dynamic nature of the disease. This is especially the case in the very early stage of the disease, when cerebral vasoconstrictions might be insignificant on the initial angiographic studies (3,4), and ischemic or hemorrhagic complications might not have occurred. In this issue of Cephalalgia, Kameda et al. report on a case of a 30-year-old woman who developed thunderclap headaches and seizure one week post-partum (8). Magnetic resonance imaging disclosed hyperintense vessel signs and PRES on the initial fluid-attenuated inversion recovery (FLAIR) imaging in the absence of significant vasoconstriction on magnetic resonance angiography (MRA). The hyperintense vessels disappeared one week later, but vasoconstrictions of major cerebral arteries became apparent (8). Although this case is not the first one to report hyperintense vessel sign in patients with RCVS (9,10), the unique finding that hyperintense vessels predated the occurrence of cerebral vasoconstrictions raised several important questions: 1.) Could hyperintense vessel sign help diagnose RCVS in the very early stage of disease? 2.) Does this finding support the centripetal propagation theory? and 3.) How to differentiate hyperintense vessels from cortical SAH, the early complication of RCVS? Hyperintense vessels on FLAIR imaging are hypothesized to be distal branches of the cerebral arteries or their leptomeningeal anastomotic collateral vessels with very low-flow velocities attributed to severe stenosis or occlusion of proximal cerebral arteries (11). In RCVS, FLAIR hyperintense vessels could be noted in up to 22% of patients (10). The presence of hyperintense vessels in RCVS is associated with more severe vasoconstrictions and cerebral hemodynamic derangements, and could herald the occurrence of ischemic stroke or PRES (10). In the case reported by Kameda et al. (8), hyperintense vessels were noted concomitantly with PRES two days after the onset of thunderclap headaches, in the absence of MRA vasoconstrictions. If these FLAIR hyperintense vessels also came from the failure of cerebrospinal fluid (CSF) nulling effect due to stagnant or retrograde flow of distal arterioles or leptomeningeal networks, this rare observation might have serendipitously captured the point when severe vasoconstrictions were still restricted to distal arteries beyond the resolution of routine MRA. In our previous study, MRA vasoconstrictions were not at its worse point until 11–20 days after headache onset (4). In another large series, it was reported that up to 33% of the patients with RCVS had a normal early angiogram (3). In other words, in one-third of the patients,

Systematic Review of Methods for Assessing Leptomeningeal Collateral Flow

The importance of LMF in the outcome after acute ischemic stroke is increasingly recognized, but imaging presents a wide range of options for identification of collaterals and there is no single system for grading collateral flow. The aim of this study was to systematically review the literature on the available methods for measuring LMF adequacy. We performed a systematic review of Ovid, MEDLINE, and Embase databases for studies in which flow in the leptomeningeal collateral vessels was evaluated. Imaging technique, grading scale, and reliability assessment for collateral flow measurement were recorded. We found 81 publications describing 63 methods for grading collateral flow on the basis of conventional angiography (n = 41), CT (n = 7), MR imaging (n = 9), and transcranial Doppler (n = 6). Inter- and/or intraobserver agreement was assessed in only 8 publications. There is inconsistency in how LMF is graded, with a variety of grading scales and imaging modalities being used. Consistency in evaluating collateral flow at baseline is required for the impact of collateral flow to be fully appreciated.

Patients with moyamoya disease presenting with movement disorder

Moyamoya disease is a rare cerebrovascular disease characterized by idiopathic bilateral stenosis or occlusion of bilateral internal carotid arteries and the development of characteristic leptomeningeal collateral vessels at the base of the brain. Typical presentations include transient ischemic attacks or stroke, and hemorrhage. Presentation with movement disorders is extremely rare, especially in the pediatric population. The authors describe the cases of 4 children with moyamoya disease who presented with movement disorders. Among 446 patients (118 pediatric) with moyamoya disease surgically treated by the senior author, 4 pediatric patients had presented with movement disorders. The clinical records, imaging studies, surgical details, and postoperative clinical and imaging data were retrospectively reviewed. The initial presenting symptom was movement disorder in all 4 patients: chorea in 2, hemiballismus in 1, and involuntary limb shaking in 1. All the patients had watershed infarcts involving the frontal subcortical region on MR imaging. Additionally, 1 patient had a ganglionic infarct. Single-photon emission computed tomography studies showed frontoparietal cortical and subcortical hypoperfusion in all patients. Three patients had bilateral disease, whereas 1 had unilateral disease. All the patients underwent superficial temporal artery-middle cerebral artery bypass. Postoperatively, all 4 patients had complete improvement in their symptoms. The SPECT scans revealed normal perfusion in 3 patients and a small residual perfusion deficit in 1. Movement disorders are a rare presenting feature of moyamoya disease. Hypoperfusion of the frontal cortical and subcortical region was seen in all patients, and the symptomatology was attributed to ischemic dysfunction and imbalance in the cortical-subcortical-ganglionic-thalamic-cortical circuitry. Combined revascularization with superficial temporal artery-middle cerebral artery bypass and encephaloduroarteriosynangiosis leads to excellent results.

Mechanism of Moyamoya Vessels Secondary to Intracranial Atherosclerotic Disease: Angiographic Findings in Patients with Middle Cerebral Artery Occlusion

Moyamoya vessels, which form a fragile collateral vascular network at the base of the brain, are associated with moyamoya disease and moyamoya syndrome. The mechanisms involved in their development remain unknown. This study evaluated the angiographic findings of the collateral vasculature in patients with moyamoya vessels secondary to atherosclerotic middle cerebral artery (MCA) occlusion. The study population comprised 26 patients with chronic atherosclerotic unilateral MCA occlusion who underwent digital subtraction angiography. We evaluated the presence of moyamoya vessels and intracranial arterial lesions and the degree of leptomeningeal anastomosis. We divided the patients into two groups, those with and those without moyamoya vessels, and compared clinical backgrounds and angiographic findings between the groups. Of the 26 patients, 17 had moyamoya vessels. The presence of moyamoya vessels was associated with ipsilateral or contralateral anterior cerebral artery stenosis to the occluded MCA (P = .004) and poor development of anterior leptomeningeal anastomosis (P = .012). It also was associated with vascular lesions involving more than one intracranial branch vessel in patients with moyamoya syndrome secondary to atherosclerosis. Our findings suggest that moyamoya vessels might be compensatory collateral vessels associated with poorly developed leptomeningeal collateral vessels.

Hypertension impairs leptomeningeal collateral growth after common carotid artery occlusion: Restoration by antihypertensive treatment

Chronic mild hypoperfusion has been shown to enlarge pial collateral vessels in normal mouse brains. The purpose of this study was to clarify the effect of hypertension on pial collateral vessel development after chronic hypoperfusion using spontaneously hypertensive rats (SHR). In normotensive rats, unilateral common carotid artery (CCA) occlusion enlarged leptomeningeal collateral vessels. CCA occlusion also preserved residual cerebral blood flow (CBF) and attenuated infarct size after middle cerebral artery (MCA) occlusion 14 days later. In contrast, in SHR, CCA occlusion neither enlarged the leptomeningeal anastomosis nor showed protective effects after MCA occlusion. However, decreasing blood pressure using an angiotensin II AT1 receptor blocker restored the beneficial effect of CCA occlusion on collateral growth as well as on residual CBF and infarct size after MCA occlusion. Adaptive responses in CBF autoregulation curves observed 14 days after CCA occlusion in normotensive rats were impaired in untreated SHR, but were restored after antihypertensive treatment. In conclusion, SHR have impaired leptomeningeal collateral growth after CCA occlusion, but antihypertensive treatment restores the beneficial effect of CCA occlusion on collateral circulation.

Decompressive craniectomy for acute stroke: early is better

Decompressive craniectomy for large, life-threatening supratentorial infarcts has been considered a controversial procedure for a long time. In the past 2 decades, authors of numerous single-center series have documented improved survival after decompressive craniectomy compared with maximal medical therapy.2 However, the procedure is not universally accepted. Detractors have been most vocal about the lack of Level A evidence and the danger that surgery could lead to a high proportion of survivors with severe disability. This controversy has sparked a few randomized clinical trials, and a landmark report of a pooled analysis of 3 such trials has answered some of the questions raised by critics.5 Among patients younger than 60 years old with a large middle cerebral artery infarct treated within 48 hours of stroke onset, the mortality rate decreased from 78% in the medically treated group to 29% in the decompressive craniectomy– treated group. This difference was statistically signifi cant. The authors of this report also concluded that 2 pa tients must be treated to prevent 1 death regardless of functional outcome. Four patients must be treated for each patient with a modified Rankin Scale score of 3 or less (a score most would agree corresponds to a decent quality of life). Despite these “high-quality” sci entific data and Level A evidence, several questions remain unanswered. In particular, is there a “neuroprotective” role for therapies (including decompressive cra niectomy) aimed at decreasing the secondary insult from vasogenic edema? In this issue of the Journal of Neurosurgery, Walberer and coworkers report their findings from an experimental model of reversible middle cerebral artery occlusion. These authors aimed to study the effects of vasogenic edema on infarct volume and func tional outcome. To eliminate the space-occupying ef fects of postinfarction edema, a bilateral decompressive craniectomy was prophylactically performed before reversible cerebral ischemia; the control group consisted of sham-operated animals. Infarct size was measured on MR images obtained 5 and 24 hours after ischemia on set. Ischemic lesions were consistently smaller in the craniectomy group at both the 5and 24-hour time points. Clinical scores were also significantly bet ter and the midline shift was less in rats that had un dergone prophylactic craniectomy. These observations lend further support to the notion that vasogenic edema aggravates the extent of infarction. Thus, therapies targeting vasogenic edema and its deleterious effects can prove neuroprotective. Hypothetically, vasogenic edema around the ischemic tissue causes regional compression of leptomeningeal vessels providing critical collateral blood flow to the penumbra. Indeed, experimental studies have suggested that decompressive craniectomy im proves cortical perfusion by increasing local cerebral blood flow through leptomeningeal collateral vessels.1 In the study by Walberer et al., animals were killed after 24 hours. Note, however, that postinfarction edema progresses well beyond that time point, and we don’t know for sure if the protective effect demonstrated in their ex perimental setting is maintained beyond 24 hours. An extension of this study might address this issue in the future. Can we use these observations to propose an ultraearly decompressive craniectomy and very aggressive intracranial pressure–targeted therapies in patients with acute cerebral infarction to improve functional out come? The easy answer is that randomized clinical trials are required. Experience shows that such trials are very difficult, expensive, and impractical to perform and often do not provide definitive answers. The decision to proceed with a decompressive craniectomy in a patient with a life-threatening infarct is always difficult because of the significance and impact (on the quality of life of the patient as well as the caregiver[s]) of the residual neu rological deficits. Nonetheless, when craniectomy is con sidered, data from the following and other studies3,4 sug gest that early is better.

Internal Carotid Artery Stent Implantation in 25 Patients with Acute Stroke: Preliminary Results

To evaluate retrospectively the outcome for patients with acute ischemic stroke in the territory of the middle cerebral artery (MCA) who had undergone stent implantation in the proximal segment of the internal carotid artery (ICA) in addition to intraarterial thrombolysis (IAT). Stent implantation and retrospective analysis of clinical and radiologic data were approved by the institutional ethical committee. Endovascular treatment was performed after obtaining informed consent from patients or their closest relatives. Informed consent for retrospective review was not required. After pharmacologic and/or mechanical IAT, 25 consecutive patients (seven women, 18 men; mean age, 59 years +/- 14 [standard deviation]) underwent stent implantation in the proximal segment of the ICA (endovascular group). The clinical and radiologic characteristics (ie, interval from symptom onset to arrival at the emergency department, prevalence of vascular risk factors, causes of stroke, stroke severity, early signs of cerebral ischemia, duration of endovascular intervention, type of occlusion, and prevalence of leptomeningeal collateral vessels), recanalization rates, and clinical outcomes for patients in the endovascular group were compared with those for patients in the medical group (10 women, 21 men; mean age, 62 years +/- 12) who experienced ischemic stroke in the territory of the MCA as a result of ICA occlusion and who received antithrombotic treatment only. Differences between groups were assessed by using the chi2 test. A logistic regression analysis was performed to assess the effect of clinical and radiologic factors on recanalization rates and outcome. ICA recanalization was successful in 21 patients. Good recanalization of the MCA was achieved in 11 patients. In nine of these patients, recanalization of the MCA was achieved by using mechanical IAT only. In the remaining 12 patients, administration of intraarterial urokinase was performed in addition to mechanical thrombolysis. Two patients from the endovascular group experienced symptomatic intracerebral hemorrhage. At 3 months, 56% of the endovascular group and 26% of the medical group had a favorable outcome. Mortality was 20% in the endovascular and 16% in the medical group. IAT and stent implantation in the proximal segment of the ICA seem to improve the outcome for patients with ischemic stroke caused by occlusion of the cervical portion of the ICA.

CT angiography in the evaluation of intracranial occlusive disease with collateral circulation: Comparison with MR angiography

The purpose of this study is to determine whether three-dimensional computed tomography angiography (CTA) is superior to magnetic resonance angiography (MRA) in the evaluation of collateral circulation in patients with intracranial arterial occlusive disease. Conventional angiography was used as the standard reference. Collateral vessels were well visualized by CTA, but not by MRA, while conventional angiography revealed leptomeningeal collateral vessels that were filled in a retrograde fashion. CTA is superior to MRA for evaluating collateral vessels.

Perfusion- and diffusion-weighted magnetic resonance imaging for monitoring decompressive craniectomy in animals with experimental hemispheric stroke.

The aim of this study was to use two types of serial magnetic resonance (MR) imaging-perfusion-weighted (PW) and diffusion-weighted (DW)-to monitor craniectomy in rats with hemispheric stroke. Focal cerebral ischemia was induced in 36 rats by using an endovascular method of occlusion of the middle cerebral artery (MCAO). Craniectomy was performed 4 or 24 hours later in 12 animals each. Twelve control animals underwent occlusion but did not receive treatment. Perfusion-weighted, DW, and T2-weighted MR images were obtained at 4, 24, 48, 72, and 168 hours postocclusion in all animals. Relative regional cerebral blood volumes and apparent diffusion coefficients (ADCs) were calculated for the cortex and basal ganglia. Hemispheric lesion volumes (expressed as percentages of total brain volumes; %HLV) as they appeared on DW and T2-weighted MR images and on histological slices stained with 2,3,5-triphenyltetrazolium chloride were compared. Neurological performances and infarct volumes measured 7 days postocclusion were used as study end points. Both PW and DW images demonstrated ischemic tissue 4 hours after MCAO in all animals. Early treatment by performing craniectomy significantly improved cortical perfusion (p < 0.01), whereas the same procedure conveyed no benefit to the basal ganglia. Compared with findings in control animals, the DW image-derived %HLV was significantly reduced (p < 0.01) and the cortical ADCs at 4 and 24 hours postocclusion were significantly higher in animals treated early (p < 0.05). Late treatment with craniectomy did not significantly affect cerebral perfusion. The correlation between the DW imaging-derived %HLV and the histologically derived %HLV at 4 to 72 hours postocclusion was good (r = 0.74), whereas at Day 7 postocclusion the %HLV was underestimated up to 41% on DW imaging. At 4 hours postocclusion T-weighted imaging failed to demonstrate the ischemic lesion, whereas from 24 to 72 hours postocclusion the correlation between the T2-weighted imaging-derived %HLV and the histologically derived %HLV was good (r > 0.81). Neurological performance was significantly improved in animals treated using craniectomy. Early craniectomy significantly improves cortical perfusion through leptomeningeal collateral vessels, significantly reduces infarct size, and improves neurological performance in animals with experimental acute hemispheric infarction. Both PW and DW imaging are suitable for noninvasive monitoring of the effects of decompressive craniectomy.

Posterior circulation in moyamoya disease: angiographic study.

To clarify the angiographic findings of the posterior circulation in patients with moyamoya disease. Seventy-six patients with idiopathic moyamoya disease were studied with conventional angiography. The angiographic findings were reviewed for steno-occlusive lesions, collateral vessels, and aneurysms and compared with the finding of parenchymal lesions on computed tomographic and magnetic resonance images. Of 152 posterior cerebral arteries (PCAs), 66 (43%) had a stenotic or occluded lesion. The frequency of PCA lesions statistically significantly increased with the extent of the internal carotid artery (ICA) bifurcation steno-occlusive lesion. As the severity of ICA stenosis increased, basal cerebral moyamoya vessels and transdural collateral vessels similarly increased in number, but leptomeningeal collateral vessels decreased owing to the progressive development of more PCA lesions. Cerebral infarctions, ventricular dilatation, and cerebral atrophy were found to increase in frequency in patients with steno-occlusive PCA lesions. Steno-occlusive lesions of the PCA increase in frequency proportionally with severity of ICA bifurcation steno-occlusive lesions, so that cerebral infarctions increase in frequency with the extent of the PCA lesions.

Moyamoya disease: diagnostic accuracy of MRI.

Our purpose was to evaluate the diagnostic accuracy of MRI in moyamoya disease. We studied 30 patients with this disease, comparing MRI and angiographic findings. The diagnostic value of MRI was evaluated for occlusive lesions, collateral vessels, and parenchymal lesions. In all patients bilateral occlusion or stenosis of the supraclinoid internal carotid artery and proximal anterior and middle cerebral arteries was clearly shown by MRI, and staging of the extent of occlusion agreed with angiographic staging in 44 (73%) of 60 arteries. MRI, particularly coronal images, clearly showed basal cerebral moyamoya vessels in 54 hemispheres, and 45 of a total of 71 large leptomeningeal and transdural collateral vessels were identified. MRI also showed parenchymal lesions in 48 (80%) hemispheres, and the extent of occlusion in the anterior and posterior circulations respectively correlated with white matter and cortical and/or subcortical infarcts.