1312 Acetazolamide induced vascular steal phenomenon during vasomotor reactivity test — correlation between transcranial doppler and SPECT

2005 ◽  
Vol 238 ◽  
pp. S434
Keyword(s):  
Transcranial Doppler ◽  
Steal Phenomenon ◽  
Vasomotor Reactivity ◽  
Reactivity Test ◽  
Vascular Steal ◽  
Vascular Steal Phenomenon ◽  
Test Correlation

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

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.

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

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.

Changes in Functional Vasomotor Reactivity in Migraine With Aura

Cephalalgia ◽  
2009 ◽  
Vol 29 (11) ◽  
pp. 1156-1164 ◽  
Author(s):  
ME Wolf ◽  
T Jäger ◽  
H Bäzner ◽  
M Hennerici
Keyword(s):  
Migraine With Aura ◽  
Flow Rate ◽  
Transcranial Doppler ◽  
Main Parameter ◽  
Migraine Without Aura ◽  
Curve Analysis ◽  
Monitoring Tool ◽  
Vasomotor Reactivity ◽  
Flow Response ◽  
History Of

Migraine with aura (MA) is associated with cerebral hyper- and hypoperfusion during and after the attacks. Several attempts to estimate individual perfusion changes and asymmetries in patients with MA using transcranial Doppler (TCD) have not been consistent. In 70 patients with MA and 40 controls with migraine without aura (MoA) or without any history of migraine, interictally recorded TCD sequences were prospectively analysed. Formal curve analysis of the visually evoked flow response (VEFR) was performed semiautomatically. As a main parameter for functional vasomotor reactivity (fVMR), the visually evoked flow rate (VEFR%) was calculated. The VEFR% showed a significantly higher mean difference of 14.7 ± 12% in MA patients vs. 5.8 ± 4.4% ( P < 0.001) in controls. The significant asymmetry of fVMR in MA patients is suggested to reflect interattack persisting vasomotor changes which are of pathophysiological interest and may be used as a monitoring tool under prophylactic medication.

scholarly journals Impaired Cerebral Vasomotor Reactivity in Alzheimer’s Disease

2018 ◽  
Vol 2018 ◽  
pp. 1-5 ◽  
Author(s):  
Fernando Gongora-Rivera ◽  
Adolfo Cordero-Perez ◽  
Alejandro Gonzalez-Aquines ◽  
Antonio Anaya-Escamilla ◽  
Eduardo Villarreal-Garza ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Weak Correlation ◽  
Vasomotor Reactivity ◽  
Cerebral Vasomotor Reactivity ◽  
Reactivity Test ◽  
Blood Flow Velocities ◽  
Flow Velocities

Background. Recent studies have shown that cerebral vascularity may be impaired in Alzheimer’s disease. Cerebral vasomotor reactivity could be an important biomarker for this pathology.Aims. The aim of this study was to investigate the alterations in cerebral vascular motor reactivity in Alzheimer’s disease subjects and to associate these changes with their cognitive scores.Methods. We recruited subjects with a diagnosis of Alzheimer’s disease and healthy controls. Demographic, clinical, imaging, and cognitive test were obtained. Then all participants performed a cerebral vascular motor reactivity test with 7% CO2 and cerebral blood flow velocities (CBFV) were recorded with transcranial doppler ultrasound before and after the test.Results. We recruited 45 subjects, 26 (21 female) Alzheimer’s disease participants and 19 (15 female) healthy controls. There were no differences in baseline cerebral blood flow velocities between the groups. After the cerebral vasomotor reactivity test, absolute mean difference in mean CBFV (ΔCBFV-m) was 8.70±4.14 versus 4.81±6.96 (p<0.01), respectively. Calculated percentage of change (%CVMR) was lower in the AD group 7.45±18.25 versus 23.29±17.48, and there was a positive but weak correlation with mini-mental scores (ρ=0.337, p=0.023).Conclusions. In this study, Alzheimer’s disease subjects showed significant changes in all absolute cerebral blood flow velocities after the cerebral vasomotor reactivity test with CO2, but only diastolic phase responses were statistically significant. There was a positive but weak correlation between cerebral vasomotor reactivity and cognitive scores. Further studies are needed to investigate these effects in larger Latin-American samples.

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