Severely impaired cerebrovascular reserve in patients with cerebral proliferative angiopathy

2011 ◽  
Vol 8 (3) ◽  
pp. 310-315 ◽  
Author(s):  
Jorn Fierstra ◽  
Stephanie Spieth ◽  
Leanne Tran ◽  
John Conklin ◽  
Michael Tymianski ◽  
...  
Keyword(s):  
Brain Tissue ◽  
Blood Oxygen Level Dependent ◽  
Brain Parenchyma ◽  
Cerebrovascular Reactivity ◽  
Healthy Individuals ◽  
Blood Oxygen Level ◽  
Cerebrovascular Reserve ◽  
Vascular Channels ◽  
End Tidal ◽  
Brain Avms

Object Cerebral proliferative angiopathy (CPA) has been morphologically distinguished from classically appearing brain arteriovenous malformations (AVMs) by exhibition of functional brain parenchyma that is intermingled with abnormal vascular channels. The presence of oligemia in this intralesional brain tissue may suggest ischemia, which is not detected in classic brain AVMs. The authors hypothesized that patients with CPA would exhibit a greater impairment of cerebrovascular reserve in neuronal tissue surrounding the true nidus compared with those with brain AVMs. Methods Four patients with CPA, 10 patients with brain AVMs and seizures, and 12 young healthy individuals were studied. The 4 patients with CPA underwent blood oxygen level–dependent MR imaging examinations while applying normoxic step changes in end-tidal CO2 to obtain quantitative cerebrovascular reactivity measurements. Results Patients with a CPA lesion exhibited severely impaired perilesional cerebrovascular reserve in comparison with patients with brain AVMs and seizures (0.10 ± 0.03 vs 0.16 ± 0.03, respectively; p < 0.05), and young healthy individuals (0.10 ± 0.03 vs 0.21 ± 0.06, respectively; p < 0.01) Conclusions This study demonstrated severely impaired cerebrovascular reserve in the perilesional brain tissue surrounding the abnormal vessels of patients with CPA. This finding may provide an additional means to distinguish CPA from classic brain AVMs.

Blood oxygen-level dependent functional assessment of cerebrovascular reactivity: Feasibility for intraoperative 3 Tesla MRI

2016 ◽  
Vol 77 (2) ◽  
pp. 806-813 ◽  
Author(s):  
Jorn Fierstra ◽  
Jan-Karl Burkhardt ◽  
Christiaan Hendrik Bas van Niftrik ◽  
Marco Piccirelli ◽  
Athina Pangalu ◽  
...  
Keyword(s):  
Functional Assessment ◽  
Blood Oxygen Level Dependent ◽  
Cerebrovascular Reactivity ◽  
3 Tesla ◽  
Blood Oxygen ◽  
Oxygen Level ◽  
Blood Oxygen Level ◽  
3 Tesla Mri

scholarly journals Arterial Spin Labeling and Blood Oxygen Level-Dependent MRI Cerebrovascular Reactivity in Cerebrovascular Disease: A Systematic Review and Meta-Analysis

2016 ◽  
Vol 42 (3-4) ◽  
pp. 288-307 ◽  
Author(s):  
Diederik P.J. Smeeing ◽  
Jeroen Hendrikse ◽  
Esben T. Petersen ◽  
Manus J. Donahue ◽  
Jill B. de Vis
Keyword(s):  
Cerebrovascular Disease ◽  
Arterial Spin Labeling ◽  
Meta Analysis ◽  
Spin Labeling ◽  
Blood Oxygen Level Dependent ◽  
Cerebrovascular Reactivity ◽  
Blood Oxygen ◽  
Oxygen Level ◽  
Blood Oxygen Level ◽  
Occlusive Vascular Disease

Background: The cerebrovascular reactivity (CVR) results of blood oxygen level-dependent (BOLD) and arterial spin labeling (ASL) MRI studies performed in patients with cerebrovascular disease (steno-occlusive vascular disease or stroke) were systematically reviewed. Summary: Thirty-one articles were included. Twenty-three (74.2%) studies used BOLD MRI to evaluate the CVR, 4 (12.9%) studies used ASL MRI and 4 (12.9%) studies used both BOLD and ASL MRI. Thirteen studies (3 significant) found a lower BOLD CVR, 2 studies found a similar CVR and 3 studies found a higher CVR in the ipsilateral compared to the contralateral hemisphere. Nine (5 significant) out of 10 studies found a lower BOLD CVR in the ipsilateral hemispheres of patients compared to controls. Six studies (2 significant) found a lower ASL CVR in the ipsilateral compared to the contralateral hemispheres. Three out of 5 studies found a significant lower ASL CVR in the ipsilateral hemispheres of patients compared to controls. Key Messages: This review brings support for a reduced BOLD and ASL CVR in the ipsilateral hemisphere of patients with cerebrovascular disease. We suggest that future studies will be performed in a uniform way so reference values can be established and could be used to guide treatment decisions in patients with cerebrovascular disease.

scholarly journals BOLD and Perfusion Response to Finger-Thumb Apposition after Acetazolamide Administration: Differential Relationship to Global Perfusion

2003 ◽  
Vol 23 (7) ◽  
pp. 829-837 ◽  
Author(s):  
Gregory G. Brown ◽  
Lisa T. Eyler Zorrilla ◽  
Bassem Georgy ◽  
Sandra S. Kindermann ◽  
Eric C. Wong ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Blood Oxygen Level Dependent ◽  
Bold Response ◽  
Blood Oxygen Level ◽  
Individual Subject ◽  
Cerebrovascular Reserve ◽  
Global Cerebral Blood Flow ◽  
Hand Area ◽  
Cortical Perfusion

The authors studied the effects of altering global cerebral blood flow on both blood oxygen level–dependent (BOLD) response and perfusion response to finger-thumb apposition. A PICORE/QUIPSS II protocol was used to collect interleaved BOLD-weighted and perfusion-weighted images on eight finger-thumb apposition trials. Subjects were studied on a drug-free day and on a day when acetazolamide was administered between the second and third trials. After acetazolamide administration, resting cortical perfusion increased an average of 20% from preadministration levels, whereas the BOLD response to finger-thumb apposition decreased by an average of 35% in the S1M1 hand area. Contrary to predictions from the exhausted cerebrovascular reserve hypothesis and the oxygen limitation model, an effect of acetazolamide on cerebral blood flow response in the S1M1 hand area was not observed. Across the acetazolamide trials, BOLD response was inversely correlated with resting cortical perfusion for individual subject data. These results suggest that resting perfusion affects the magnitude of the BOLD response and is thus an important confounding factor in fMRI studies, and that the physiologic systems that increase cerebral blood flow in response to acetazolamide administration and systems that increase cerebral blood flow in response to altered neural activity appear to have additive effects.

scholarly journals Slowed Temporal and Parietal Cerebrovascular Response in Patients with Alzheimer’s Disease

2020 ◽  
Vol 47 (3) ◽  
pp. 366-373
Author(s):  
Kenneth R. Holmes ◽  
David Tang-Wai ◽  
Kevin Sam ◽  
Larissa McKetton ◽  
Julien Poublanc ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vascular Dysfunction ◽  
Intermediate Stage ◽  
Blood Oxygen Level Dependent ◽  
Cerebrovascular Reactivity ◽  
Blood Oxygen Level ◽  
Cerebrovascular Function ◽  
Anatomical Images ◽  
Cortical Regions

ABSTRACT:Background:Recent investigations now suggest that cerebrovascular reactivity (CVR) is impaired in Alzheimer’s disease (AD) and may underpin part of the disease’s neurovascular component. However, our understanding of the relationship between the magnitude of CVR, the speed of cerebrovascular response, and the progression of AD is still limited. This is especially true in patients with mild cognitive impairment (MCI), which is recognized as an intermediate stage between normal aging and dementia. The purpose of this study was to investigate AD and MCI patients by mapping repeatable and accurate measures of cerebrovascular function, namely the magnitude and speed of cerebrovascular response (τ) to a vasoactive stimulus in key predilection sites for vascular dysfunction in AD.Methods:Thirty-three subjects (age range: 52–83 years, 20 males) were prospectively recruited. CVR and τ were assessed using blood oxygen level-dependent MRI during a standardized carbon dioxide stimulus. Temporal and parietal cortical regions of interest (ROIs) were generated from anatomical images using the FreeSurfer image analysis suite.Results:Of 33 subjects recruited, 3 individuals were excluded, leaving 30 subjects for analysis, consisting of 6 individuals with early AD, 11 individuals with MCI, and 13 older healthy controls (HCs). τ was found to be significantly higher in the AD group compared to the HC group in both the temporal (p = 0.03) and parietal cortex (p = 0.01) following a one-way ANCOVA correcting for age and microangiopathy scoring and a Bonferroni post-hoc correction.Conclusion:The study findings suggest that AD is associated with a slowing of the cerebrovascular response in the temporal and parietal cortices.

scholarly journals Measuring Cerebrovascular Reactivity: The Dynamic Response to a Step Hypercapnic Stimulus

2015 ◽  
Vol 35 (11) ◽  
pp. 1746-1756 ◽  
Author(s):  
Julien Poublanc ◽  
Adrian P Crawley ◽  
Olivia Sobczyk ◽  
Gaspard Montandon ◽  
Kevin Sam ◽  
...  
Keyword(s):  
Vascular Reactivity ◽  
Blood Oxygen Level Dependent ◽  
Cerebrovascular Reactivity ◽  
Blood Oxygen ◽  
Resonance Imaging ◽  
Blood Oxygen Level ◽  
First Order ◽  
Speed Of Response ◽  
Magnetic Resonance Imaging Mri ◽  
Best Fit

We define cerebral vascular reactivity (CVR) as the ratio of the change in blood oxygen level-dependent (BOLD) magnetic resonance imaging (MRI) signal (S) to an increase in blood partial pressure of CO2 (PCO2): % Δ S/Δ PCO2 mm Hg. Our aim was to further characterize CVR into dynamic and static components and then study 46 healthy subjects collated into a reference atlas and 20 patients with unilateral carotid artery stenosis. We applied an abrupt boxcar change in PCO2 and monitored S. We convolved the PCO2 with a set of first-order exponential functions whose time constant τ was increased in 2-second intervals between 2 and 100 seconds. The τ corresponding to the best fit between S and the convolved PCO2 was used to score the speed of response. Additionally, the slope of the regression between S and the convolved PCO2 represents the steady-state CVR (ssCVR). We found that both prolongations of τ and reductions in ssCVR (compared with the reference atlas) were associated with the reductions in CVR on the side of the lesion. τ and ssCVR are respectively the dynamic and static components of measured CVR.

scholarly journals Comparison of the effects of independently-controlled end-tidal PCO2 and PO2 on blood oxygen level–dependent (BOLD) MRI

2007 ◽  
Vol 27 (1) ◽  
pp. 185-191 ◽  
Author(s):  
Eitan Prisman ◽  
Marat Slessarev ◽  
Jay Han ◽  
Julien Poublanc ◽  
Alexandra Mardimae ◽  
...  
Keyword(s):  
Blood Oxygen Level Dependent ◽  
Blood Oxygen ◽  
Oxygen Level ◽  
Blood Oxygen Level ◽  
Bold Mri ◽  
End Tidal

scholarly journals Insights Into Cerebral Tissue-Specific Response to Respiratory Challenges at 7T: Evidence for Combined Blood Flow and CO2-Mediated Effects

2021 ◽  
Vol 12 ◽  
Author(s):  
Allen A. Champagne ◽  
Alex A. Bhogal
Keyword(s):  
Blood Flow ◽  
Arrival Time ◽  
Vascular Diseases ◽  
Response Speed ◽  
Blood Oxygen Level Dependent ◽  
Cerebrovascular Reactivity ◽  
Specific Response ◽  
Vascular Networks ◽  
Blood Oxygen Level ◽  
Arterial Transit Time

Cerebrovascular reactivity (CVR) mapping is finding increasing clinical applications as a non-invasive probe for vascular health. Further analysis extracting temporal delay information from the CVR response provide additional insight that reflect arterial transit time, blood redistribution, and vascular response speed. Untangling these factors can help better understand the (patho)physiology and improve diagnosis/prognosis associated with vascular impairments. Here, we use hypercapnic (HC) and hyperoxic (HO) challenges to gather insight about factors driving temporal delays between gray-matter (GM) and white-matter (WM). Blood Oxygen Level Dependent (BOLD) datasets were acquired at 7T in nine healthy subjects throughout BLOCK- and RAMP-HC paradigms. In a subset of seven participants, a combined HC+HO block, referred as the “BOOST” protocol, was also acquired. Tissue-based differences in Rapid Interpolation at Progressive Time Delays (RIPTiDe) were compared across stimulus to explore dynamic (BLOCK-HC) versus progressive (RAMP-HC) changes in CO2, as well as the effect of bolus arrival time on CVR delays (BLOCK-HC versus BOOST). While GM delays were similar between the BLOCK- (21.80 ± 10.17 s) and RAMP-HC (24.29 ± 14.64 s), longer WM lag times were observed during the RAMP-HC (42.66 ± 17.79 s), compared to the BLOCK-HC (34.15 ± 10.72 s), suggesting that the progressive stimulus may predispose WM vasculature to longer delays due to the smaller arterial content of CO2 delivered to WM tissues, which in turn, decreases intravascular CO2 gradients modulating CO2 diffusion into WM tissues. This was supported by a maintained ∼10 s offset in GM (11.66 ± 9.54 s) versus WM (21.40 ± 11.17 s) BOOST-delays with respect to the BLOCK-HC, suggesting that the vasoactive effect of CO2 remains constant and that shortening of BOOST delays was be driven by blood arrival reflected through the non-vasodilatory HO contrast. These findings support that differences in temporal and magnitude aspects of CVR between vascular networks reflect a component of CO2 sensitivity, in addition to redistribution and steal blood flow effects. Moreover, these results emphasize that the addition of a BOOST paradigm may provide clinical insights into whether vascular diseases causing changes in CVR do so by way of severe blood flow redistribution effects, alterations in vascular properties associated with CO2 diffusion, or changes in blood arrival time.

Sign in / Sign up

Export Citation Format

Share Document