Quantification of Cerebrovascular Reactivity by Blood Oxygen Level–Dependent MR Imaging and Correlation with Conventional Angiography in Patients with Moyamoya Disease

Heyn, Chris; Poublanc, Julien; Crawley, Adrian; Mandell, Daniel M.; Han, Jai-Hyuck; Tymianski, Michael; terBrugge, Karel G.; Fisher, Joe; Mikulis, David J.

doi:10.3174/ajnr.a1922

Cited by 65 publications

(56 citation statements)

References 7 publications

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“…[11][12][13] The breath-hold (BH) technique offers a simpler alternative that is easier to implement in the clinical setting and yet can produce similar increases in arterial CO 2 levels and resultant similarly useful BOLD CVR maps as those achieved by using gas-inhalation techniques. 14 This technique involves short-duration BHs, typically in the range of 10 -30 seconds, which alternate with periods of normal breathing.…”

Section: The Breath-hold Cerebrovascular Reactivity Mapping Techniquementioning

confidence: 99%

Cerebrovascular Reactivity Mapping: An Evolving Standard for Clinical Functional Imaging

Pillai

Mikulis

2014

American Journal of Neuroradiology

130

155

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SUMMARY:This review article explains the methodology of breath-hold cerebrovascular reactivity mapping, both in terms of acquisition and analysis, and reviews applications of this method to presurgical mapping, particularly with respect to blood oxygen level-dependent fMRI. Its main application in clinical fMRI is for the assessment of neurovascular uncoupling potential. Neurovascular uncoupling is potentially a major limitation of clinical fMRI, particularly in the setting of mass lesions in the brain such as brain tumors and intracranial vascular malformations that are associated with alterations in regional hemodynamics on either an acquired or congenital basis. As such, breath-hold cerebrovascular reactivity mapping constitutes an essential component of quality control analysis in clinical fMRI, particularly when performed for presurgical mapping of eloquent cortex. Exogenous carbon dioxide challenges used for cerebrovascular reactivity mapping will also be discussed, and their applications to the evaluation of cerebrovascular reserve and cerebrovascular disease will be described. ABBREVIATIONS:BH ϭ breath-hold; BOLD ϭ blood oxygen level-dependent; CO 2 ϭ carbon dioxide; CVR ϭ cerebrovascular reactivity; NVU ϭ neurovascular

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Section: The Breath-hold Cerebrovascular Reactivity Mapping Techniquementioning

confidence: 99%

Cerebrovascular Reactivity Mapping: An Evolving Standard for Clinical Functional Imaging

Pillai

Mikulis

2014

American Journal of Neuroradiology

130

155

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“…10 The physiologic origins of a negative BOLD response are known to occur in and around capillaries and draining veins from decreases in blood oxygenation, which could occur from reductions in CBF (vascular steal), increases in CBV (autoregulation), or upregulation of CMRO 2 ( Figure 1). It should also be noted that while changes in venous CBV are generally smaller in magnitude than changes in arterial CBV, such changes influence BOLD substantially owing to the larger fraction of deoxyhemoglobin in veins.…”

Section: Origins Of Negative Blood Oxygenation Level-dependent Cerebrmentioning

confidence: 99%

“…Such negative BOLD effects have been shown to correlate inversely with cortical thickness and directly with IC vascular disease severity. 10 The mechanism underlying negative BOLD responses, however, is controversial. Occlusion models in animals have demonstrated that hypercarbia does not change CBF in ischemic brain 11,12 and in subacute human stroke patients, it has been demonstrated that CBF response to hypercarbia is heterogeneous.…”

Section: Introductionmentioning

confidence: 99%

The Vascular Steal Phenomenon is an Incomplete Contributor to Negative Cerebrovascular Reactivity in Patients with Symptomatic Intracranial Stenosis

Arteaga

Strother

Faraco

et al. 2014

J Cereb Blood Flow Metab

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'Vascular steal' has been proposed as a compensatory mechanism in hemodynamically compromised ischemic parenchyma. Here, independent measures of cerebral blood flow (CBF) and blood oxygenation level-dependent (BOLD) magnetic resonance imaging (MRI) responses to a vascular stimulus in patients with ischemic cerebrovascular disease are recorded. Symptomatic intracranial stenosis patients (n ¼ 40) underwent a multimodal 3.0T MRI protocol including structural (T 1 -weighted and T 2 -weighted fluidattenuated inversion recovery) and hemodynamic (BOLD and CBF-weighted arterial spin labeling) functional MRI during room air and hypercarbic gas administration. CBF changes in regions demonstrating negative BOLD reactivity were recorded, as well as clinical correlates including symptomatic hemisphere by infarct and lateralizing symptoms. Fifteen out of forty participants exhibited negative BOLD reactivity. Of these, a positive relationship was found between BOLD and CBF reactivity in unaffected (stenosis degreeo50%) cortex. In negative BOLD cerebrovascular reactivity regions, three patients exhibited significant (Po0.01) reductions in CBF consistent with vascular steal; six exhibited increases in CBF; and the remaining exhibited no statistical change in CBF. Secondary findings were that negative BOLD reactivity correlated with symptomatic hemisphere by lateralizing clinical symptoms and prior infarcts(s). These data support the conclusion that negative hypercarbia-induced BOLD responses, frequently assigned to vascular steal, are heterogeneous in origin with possible contributions from autoregulation and/or metabolism.

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“…24 Cerebrovascular reactivity as measured by blood oxygen level-dependent MRI has also been shown to have a direct correlation with impaired vascular supply as measured by modified Suzuki score on angiography. 25 Quantitative MR angiography with NOVA software can show actual blood flow across large intracranial vessels and also flow across the superficial temporal artery after revascularization. 26 In our practice, xenon CT (without and with acetazolamide) has provided an excellent quantitative method of assessing CBF and hemodynamic reserve with good spatial resolution; however, it is not currently approved by the Food and Drug Administration and can only be used on an Institutional Review Board-approved protocol.…”

Section: Imagingmentioning

confidence: 99%

Neurosurgical Advances in the Treatment of Moyamoya Disease

Pandey

Steinberg

2011

Stroke

132

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Background and Purpose-Moyamoya disease is characterized by chronic stenoocclusive vasculopathy involving the distal supraclinoid internal carotid arteries and presents with ischemic or hemorrhagic symptoms. We review advances in the understanding and management of moyamoya disease. Summary of Review-Cerebral revascularization, either direct or indirect, is the cornerstone of treatment for moyamoya disease. Recent advances have been made in understanding the molecular biology and pathophysiology of moyamoya disease, and new genetic mutations and deletions have been identified. Imaging for moyamoya disease is also rapidly improving with new sequences of MRI and better methods of assessing ischemia and cerebrovascular reserve. Positron emission tomography has emerged as an important tool to measure cerebrovascular reserve. Novel surgical techniques assess patency and ischemia during superficial temporal to middle cerebral artery bypass, including indocyanine green videoangiography to evaluate anastomosis patency, and various methods to monitor intraoperative blood flow. Newer methods of indirect revascularization have been described with placement of more tissues supplied by the external carotid artery on the brain surface. Postoperative hyperperfusion to the chronically ischemic brain tissue is a recently identified causative factor of complications. Interestingly, complications from hyperperfusion mimic those caused by ischemia, although they have different treatments, making the role of postoperative blood flow assessment important in distinguishing between the two. Awareness has also increased that even asymptomatic patients can experience significant cognitive decline attributable to chronic ischemia. Whether this reverts after successful revascularization requires investigation. Conclusions-Surgical revascularization with direct, indirect, and combined methods remains the preferred procedure for patients with moyamoya disease. (Stroke. 2011;42:3304-3310.)Key Words: moyamoya disease Ⅲ revascularization Ⅲ STA-MCA bypass M oyamoya disease (MMD) is a chronic, progressive disease characterized by stenosis or occlusion of the bilateral supraclinoid internal carotid arteries along with development of leptomeningeal collaterals at the base of the brain. The classical presentation of MMD is transient ischemic attacks (TIAs), ischemic strokes, and intracranial hemorrhages. Its natural history is often progressive and includes recurrent ischemic episodes with neurological and cognitive deterioration. Unfortunately, the disease is unresponsive to any medical treatment. Surgery aimed at revascularization of the hemispheres either by direct or indirect bypass techniques is the treatment of choice. Over the past years, there has been major progress in understanding MMD, including its molecular biology, genetics, pathophysiology, radiology and blood flow, and surgical management. This article reviews the major neurosurgical advances in the treatment of MMD. Genetics and PathophysiologyThe pathophysiology of MMD is poorly un...

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Quantification of Cerebrovascular Reactivity by Blood Oxygen Level–Dependent MR Imaging and Correlation with Conventional Angiography in Patients with Moyamoya Disease

Cited by 65 publications

References 7 publications

Cerebrovascular Reactivity Mapping: An Evolving Standard for Clinical Functional Imaging

Cerebrovascular Reactivity Mapping: An Evolving Standard for Clinical Functional Imaging

The Vascular Steal Phenomenon is an Incomplete Contributor to Negative Cerebrovascular Reactivity in Patients with Symptomatic Intracranial Stenosis

Neurosurgical Advances in the Treatment of Moyamoya Disease

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