Abstract 1122‐000050: Arterial Steal in AVM: An Etiology of Ischemic Stroke

2021 ◽  
Vol 1 (S1) ◽  
Author(s):  
Rahul Chandra
Keyword(s):  
Ischemic Stroke ◽  
High Flow ◽  
Regions Of Interest ◽  
Neurological Deficits ◽  
Cerebral Angiogram ◽  
Steal Phenomenon ◽  
Ct Angiogram ◽  
Left Posterior ◽  
Vascular Steal ◽  
Vascular Steal Phenomenon

Introduction : Arteriovenous malformations (AVM) are rare congenital malformations in the brain, often presenting with cerebral hemorrhage. Unruptured AVMs usually remain asymptomatic, or they can present with headache, seizure, or focal neurological deficits. “Arterial steal” is one of the mechanisms which can lead to focal neurological deficits. The idea of vascular steal through high flow shunting within brain AVMs is not a new concept. There is, however, debate about whether the vascular steal phenomenon indeed exists empirically. In a study focused on vascular reserve in patients with cerebral AVMs (utilizing acetazolamide augmentation and perfusion CT methods), decreased hemodynamic reserve was noted in 27% of parenchymal regions of interest close to the AVM and in 17% of parenchymal regions of interest far from the AVM. Other imaging modalities have shown abnormal blood regulation around AVM however there exists a level of discordance between various modalities which questions whether vascular steal exists in vivo. We present an ischemic stroke caused by “arterial steal” phenomenon. Methods : Case report Results : 63‐year‐old male with past medical history of seizure, hypertension presented with confusion and dysarthria for 3 weeks. On exam he was found to have right upper quadrantanopia. CT head without contrast and MRI of brain revealed an evolving infarct in the left posterior cerebral artery (PCA) territory. CT angiogram showed possible occlusion in the left PCA P2 segment which correlated to the previously described stroke and in addition showed evidence of left thalamic AVM. Evaluation for cardioembolic or atheroembolic sources was unrevealing. A diagnostic cerebral angiogram showed a 1.3 mm AVM fed through anterior choroidal branches as well as posterior choroidal branches through left posterior communicating artery. There was delayed filling in the left PCA territory likely due to steal phenomenon which might be the etiology of the stroke. Conclusions : In our case, as demonstrated on angiogram, vascular steal phenomenon through high flow shunting of AVM is the likely explanation for the ischemic stroke.

Large vascular malformation in a child presenting with vascular steal phenomenon managed with pial synangiosis

2011 ◽  
Vol 7 (1) ◽  
pp. 15-21 ◽  
Author(s):  
Michael J. Ellis ◽  
Derek Armstrong ◽  
Peter B. Dirks
Keyword(s):  
Vascular Malformation ◽  
Vascular Malformations ◽  
Cerebral Hypoperfusion ◽  
Neurological Deficits ◽  
Steal Phenomenon ◽  
History Of ◽  
Indirect Revascularization ◽  
Vascular Steal ◽  
Brain Avms ◽  
Vascular Steal Phenomenon

The management of large and giant arteriovenous malformations (AVMs) in patients presenting with nonhemorrhagic neurological deficits secondary to vascular steal phenomenon is challenging and controversial. In many cases, large AVMs cannot be completely excised or cured, leaving patients with residual or partially treated AVMs, the natural history of which is unknown. Additionally, large, diffuse vascular malformations with multiple, small feeders, slow flow, or so-called cerebral proliferative angiopathy represent a related but distinct clinical and angiographic entity that may require a different therapeutic approach than traditional brain AVMs. The current management of children with other conditions of chronic cerebral hypoperfusion, such as moyamoya disease, involves consideration of surgical revascularization to enhance blood flow to the compromised hemisphere. Here, the authors present the case of a young child with a large thalamic vascular malformation who presented with clinical and radiological features of vascular steal and ischemia. In an effort to augment flow to the hypoperfused brain and protect against future ischemia, the authors treated the child with unilateral pial synangiosis. At 12 months, postoperative angiography demonstrated robust neovascularization, and the child has not sustained any further ischemic events. The authors discuss concept of vascular malformation–related hypoperfusion and the utility of indirect revascularization for inoperable vascular malformations presenting with ischemic symptoms.

Reduction in tumor blood flow in skin flap tumor after hydralazine is not due to a vascular steal phenomenon

1993 ◽  
Vol 1 (5) ◽  
pp. 270-278 ◽  
Author(s):  
Mark W. Dewhirst ◽  
David Madwed ◽  
Robert E. Meyer ◽  
Edgardo T. Ong ◽  
Bruce Klitzman ◽  
...  
Keyword(s):  
Blood Flow ◽  
Skin Flap ◽  
Tumor Blood Flow ◽  
Steal Phenomenon ◽  
Vascular Steal ◽  
Vascular Steal Phenomenon

Abstract 59: Extending the Time for Thombolysis in Emergency Neurological Deficits (EXTEND) - High Prevalence of Intracranial Vessel Occlusion in Wake-up-stroke Patients

Stroke ◽  
2016 ◽  
Vol 47 (suppl_1) ◽  
Author(s):  
Henry Ma ◽  
Bruce C Campbell ◽  
Mark W Parsons ◽  
Christopher Levi ◽  
Atte Meretoja ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Cerebral Artery ◽  
Stroke Onset ◽  
Phase Iii ◽  
Neurological Deficits ◽  
Lesion Volume ◽  
Stroke Patients ◽  
Vessel Occlusion ◽  
Intracranial Vessel ◽  
Ct Angiogram

Background: EXTEND is an investigator-initiated, randomised, double-blind and placebo-controlled Phase III trial of intravenous alteplase vs placebo in patients with ischemic stroke 4.5-9 hours from stroke onset or wake-up-stroke (WUS). The prevalence of intra-cranial vessel occlusion in WUS patients remains to be determined and can guide the development of optimal therapy for this unique group of stroke patients. Objective: To study the prevalence and characteristics of intra-cranial vessel occlusion in this WUS cohort. Methods: Ischemic stroke patients within 4.5-9 hours from stroke onset or with WUS (time of WUS onset defined as the midpoint between time to sleep and awakening with the stroke symptoms) are eligible for enrollment. Criteria for entry into the trial include perfusion-diffusion mismatch using a perfusion threshold of Tmax>6sec and a perfusion:diffusion lesion volume ratio of >1.2. Diffusion lesion volume must be <70mL based on assessment by automated RAPID software. Intra-cranial vessel occlusion was assessed on MR or CT angiogram performed at randomisation and 24 later. Two expert readers assessed these images independently. Results: 97 patients had images with adequate quality, including 63 (65%) in the WUS group with median age of 77.0 yrs (IQR 67.0, 81.0) and NIHSS of 14.0 (9.0, 19.0). 62 of 63 patients (98%) had vessel occlusion with 44.4% involving M1 of the middle cerebral artery, 17.5% M2, 4.8% M3, 25.4% both internal carotid artery (ICA) and M1, 4.8% ICA alone and 3.1% the posterior cerebral artery. The median ischemic core volume was 15.0 ml (6.5, 31.5), Tmax>6 volume 88.5ml (58.0, 122.0), mismatch volume 65.5ml (42.8, 92.0), and ratio of 4.8 (2.5, 8.7). 19 patients (30%) demonstrated recanalization on follow-up imaging. Conclusion: In WUS patients there is a very high rate of intracranial vessel occlusion with relatively large volumes of salvageable penumbral tissue. Intravenous thrombolytic therapy followed by thrombectomy in selected cases may be an appropriate therapeutic option with safety and efficacy remaining to be established in randomized controlled trials.

Vascular “steal” phenomenon

1968 ◽  
Vol 116 (2) ◽  
pp. 192-197 ◽  
Author(s):  
William K. Ehrenfeld ◽  
James D. Harris ◽  
Edwin J. Wylie
Keyword(s):  
Steal Phenomenon ◽  
Vascular Steal ◽  
Vascular Steal Phenomenon

scholarly journals Tumour Emboli Causing Multifocal Ischemic Stroke from Intracardiac Malignant Solitary Fibrous Tumour

2018 ◽  
Vol 13 (4) ◽  
pp. e28-e31
Author(s):  
Lindsay J Melvin ◽  
Nicole Sitzer ◽  
Rebecca Amer
Keyword(s):  
Ischemic Stroke ◽  
Breast Tumour ◽  
Solitary Fibrous Tumour ◽  
Comfort Care ◽  
Generalized Seizures ◽  
Ct Angiogram ◽  
Left Posterior ◽  
Tumor Emboli ◽  
The Right ◽  
The Brain

A 78-year-old woman presented to the emergency department with gait ataxia and diplopia. Her past medical history included the surgical resection of a phyllodes breast tumour 8 years prior, with no known recurrence. A computed tomography (CT) scan of the brain demonstrated multifocal right supratentorial hemispheric subacute infarcts in the frontoparietal, posterior temporal and occipital regions. The patient developed recurrent generalized seizures in hospital. Transesophageal echocardiogram demonstrated a large 2.7 × 1.8 × 0.8 cm mobile echogenic mass attached to the left posterior atrial wall. CT angiogram of the chest revealed the left atrial mass as well as a mass encasing the right bronchus intermedius. The patient opted for comfort care and passed away in hospital. Autopsy revealed the tumour to be a primary cardiac solitary fibrous tumour. We present a case of multifocal ischemic stroke and seizures secondary to tumor emboli originating from intracardiac solitary fibrous tumour.

scholarly journals Contrast-Induced Encephalopathy after Cerebral Angiogram: A Case Series and Review of Literature

2021 ◽  
pp. 405-413
Author(s):  
Cecelia Allison ◽  
Vaibhav Sharma ◽  
Jason Park ◽  
Clemens M. Schirmer ◽  
Ramin Zand
Keyword(s):  
Rare Complication ◽  
General Pattern ◽  
Treatment Protocol ◽  
Case Series ◽  
Altered Mental Status ◽  
Cortical Blindness ◽  
Neurological Deficits ◽  
Cerebral Angiogram ◽  
Iodinated Contrast Medium ◽  
Iodinated Contrast

Contrast-induced encephalopathy (CIE) is a rare complication that arises from exposure to iodinated contrast medium and can result in a range of symptoms, including cortical blindness, aphasia, focal neurological deficits, and altered mental status. We present 4 individual cases of CIE who presented with stroke-mimic symptoms following surgery with localized iodixanol or ioversol injection. We outline a clinical timeline of all patients, showing that CIE follows a general pattern of delayed onset, worsening symptomology, and ultimately full recovery. All patients received IV hydration, corticosteroids, or both as part of their treatment protocol.

scholarly journals The anesthetic approach for endovascular recanalization therapy depends on the lesion site in acute ischemic stroke

2021 ◽  
Author(s):  
Kilian Fröhlich ◽  
Gabriela Siedler ◽  
Svenja Stoll ◽  
Kosmas Macha ◽  
Thomas M. Kinfe ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Middle Cerebral Artery ◽  
Acute Ischemic Stroke ◽  
Cerebral Artery ◽  
Posterior Circulation ◽  
Neurological Deficits ◽  
Stroke Severity ◽  
Lesion Volume ◽  
Middle Cerebral Artery Territory ◽  
Cerebral Lesion

Abstract Purpose Endovascular therapy (EVT) of large-vessel occlusion in acute ischemic stroke (AIS) may be performed in general anesthesia (GA) or conscious sedation (CS). We intended to determine the contribution of ischemic cerebral lesion sites on the physician’s decision between GA and CS using voxel-based lesion symptom mapping (VLSM). Methods In a prospective local database, we sought patients with documented AIS and EVT. Age, stroke severity, lesion volume, vigilance, and aphasia scores were compared between EVT patients with GA and CS. The ischemic lesions were analyzed on CT or MRI scans and transformed into stereotaxic space. We determined the lesion overlap and assessed whether GA or CS is associated with specific cerebral lesion sites using the voxel-wise Liebermeister test. Results One hundred seventy-nine patients with AIS and EVT were included in the analysis. The VLSM analysis yielded associations between GA and ischemic lesions in the left hemispheric middle cerebral artery territory and posterior circulation areas. Stroke severity and lesion volume were significantly higher in the GA group. The prevalence of aphasia and aphasia severity was significantly higher and parameters of vigilance lower in the GA group. Conclusions The VLSM analysis showed associations between GA and ischemic lesions in the left hemispheric middle cerebral artery territory and posterior circulation areas including the thalamus that are known to cause neurologic deficits, such as aphasia or compromised vigilance, in AIS-patients with EVT. Our data suggest that higher disability, clinical impairment due to neurological deficits like aphasia, or reduced alertness of affected patients may influence the physician’s decision on using GA in EVT.

Abstract WMP18: CT Work-Up of Patients Suspected of Acute Ischemic Stroke: Perfusion-CT Adds Value Compared to Clinical Evaluation, Noncontrast Head CT and CT-Angiogram in Terms of Predicting Outcome

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Guangming Zhu ◽  
Patrik Michel ◽  
Amin Aghaebrahim ◽  
James T Patrie ◽  
Wenjun Xin ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Acute Ischemic Stroke ◽  
Clinical Data ◽  
Multivariate Regression ◽  
Multivariate Regression Analysis ◽  
Perfusion Ct ◽  
Infarct Core ◽  
Head Ct ◽  
Ct Angiogram ◽  
Work Up

BACKGROUND AND PURPOSE: To determine whether Perfusion-CT (PCT) adds value to Noncontrast head CT (NCT), CT-Angiogram (CTA) and clinical assessment in patients suspected of acute ischemic stroke. METHODS: We retrospectively reviewed the clinical and imaging data collected in 165 patients with acute ischemic stroke. ASPECTS score was calculated from NCT. CTA was reviewed for site of occlusion and collateral flow score. PCT was used to calculate the volumes of infarct core and ischemic penumbra on admission. Recanalization status was assessed on follow-up imaging. Clinical data included age, time from onset to baseline imaging, time from baseline imaging to reperfusion therapy, time from baseline imaging to recanalization imaging, NIHSS at baseline, treatment type and modified Rankin score (mRS) at 90 days. In a first multivariate regression analysis, we used volume of PCT penumbra and infarct core as outcome, and assessed whether they could be predicted from clinical variables, NCT and/or CTA. In a second multivariate regression analysis, we used mRS at 90 days as outcome, and determined which imaging and clinical variables predicted it best. RESULTS: 165 patients were identified. Mean±SD time from onset to baseline imaging was 6.7±8.7 hrs. 76 had a good outcome (90-day mRS 0-2), 89 had a poor outcome. Mean±SD PCT infarct was 44.8±46.5 ml. Mean±SD PCT penumbra was 47.0±33.9 ml. PCT infarct could be predicted by clinical data, NCT, CTA, and combinations of this data (P<0.05); the best predictive model included the clinical data, plus NCT and CTA. PCT Penumbra could NOT be predicted by clinical data, NCT, and CTA. In terms of predicting mRS at 90 days, all of variables but NCT and CTA were significantly associated with 90-day mRS outcome. The single most important predictor was recanalization status (P<0.001). PCT penumbra volume (P=0.001) was also a predictor of clinical outcome, especially when considered in conjunction with recanalization through an interaction term (P<0.001). CONCLUSION: PCT penumbra represents independent information, which cannot be predicted by clinical, NCT, and CTA data. PCT penumbra is an important determinant of clinical outcome, and adds relevant clinical information compared to a stroke CT work-up including NCT and CTA.

Abstract T P167: Emergent Identification of Type A Aortic Dissection as a Cause of Acute Ischemic Stroke

Stroke ◽  
2014 ◽  
Vol 45 (suppl_1) ◽  
Author(s):  
Tomoyuki Ohara ◽  
Kazunori Toyoda ◽  
Hiroyuki Yokoyama ◽  
Kenji Minatoya ◽  
Eijiro Tanaka ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Back Pain ◽  
Cerebral Ischemia ◽  
Aortic Dissection ◽  
Intravenous Thrombolysis ◽  
Type A ◽  
Neurological Deficits ◽  
Diagnostic Tools ◽  
Acute Cerebral Ischemia ◽  
D Dimer

Background: Acute aortic dissection (AAD) sometimes presents with predominant neurological symptoms of acute cerebral ischemia. Fatal AAD patients after thrombolysis for stroke without noticing AAD were reported. The purpose of this study was to clarify the characteristics of AAD patients with acute cerebral ischemia and develop a score to emergently identify AAD for such patients. Methods: From the database of Stanford type A-AAD patients admitted in our hospital between 2007 and 2012, we selected those presenting with acute focal neurological deficits due to ischemic stroke/TIA. Patients presenting with shock state or cardiopulmonary arrest were excluded. Physiological, radiological, and blood examinations were assessed for AAD identification. Results: Of 187 AAD patients, 19 patients (10%) with focal neurological deficits as an initial presentation were studied. Involvement of one or more main branches of the aortic arch was observed in all of 19 patients. Stroke experts, not cardiovascular experts, were primarily called to ER in 18 patients, and 12 were potential candidates for intravenous thrombolysis. Left hemiparesis (14 patients, 74%) was the most common neurological symptom. Nine patients (47%) complained of chest or back pain. As components of the score, (1) systolic BP differential >20mmHg between upper extremities was present in 11 of 17 patients (65%), (2) mediastinal widening on chest radiography in 13/16 (81%), (3) occlusion or the intimal flap of the proximal common carotid artery on carotid ultrasonography in 14/16 (88%), (4) pericardial effusion on echocardiography in 10/19 (47%), and (5) abnormal elevation of D-dimer levels in all 19 (median 24.8 [range 4.2-406.2] μg/ml). Two components were positive in 4 patients, three in 6, four in 5, and all the five in 4. Conclusions: Only half of AAD patients with stroke/TIA complained of chest or back pain. All the AAD patients with stroke/TIA showed high D-dimer levels and one or more additional abnormal findings in physiological and radiological examinations. Combination of such handy diagnostic tools is helpful to identify AAD without long time delay and to avoid unnecessary thrombolysis for AAD patients.

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