Cerebrovascular Reactivity Mapping Research Articles

Impaired peri-nidal cerebrovascular reserve in seizure patients with brain arteriovenous malformations

Epileptic seizures are a common presentation in patients with newly diagnosed brain arteriovenous malformations, but the pathophysiological mechanisms causing the seizures remain poorly understood. We used magnetic resonance imaging-based quantitative cerebrovascular reactivity mapping and conventional angiography to determine whether seizure-prone patients with brain arteriovenous malformations exhibit impaired cerebrovascular reserve or morphological angiographic features predictive of seizures. Twenty consecutive patients with untreated brain arteriovenous malformations were recruited (10 with and 10 without epileptic seizures) along with 12 age-matched healthy controls. Blood oxygen level-dependent MRI was performed while applying iso-oxic step changes in end-tidal partial pressure of CO(2) to obtain quantitative cerebrovascular reactivity measurements. The brain arteriovenous malformation morphology was evaluated by angiography, to determine to what extent limitations of arterial blood supply or the presence of restricted venous outflow and tissue congestion correlated with seizure susceptibility. Only patients with seizures exhibited impaired peri-nidal cerebrovascular reactivity by magnetic resonance imaging (0.11 ± 0.10 versus 0.25 ± 0.07, respectively; P < 0.001) and venous drainage patterns suggestive of tissue congestion on angiography. However, cerebrovascular reactivity changes were not of a magnitude suggestive of arterial steal, and were probably compatible with venous congestion in aetiology. Our findings demonstrate a strong association between impaired peri-nidal cerebrovascular reserve and epileptic seizure presentation in patients with brain arteriovenous malformation. The impaired cerebrovascular reserve may be associated with venous congestion. Quantitative measurements of cerebrovascular reactivity using blood oxygen level-dependent MRI appear to correlate with seizure susceptibility in patients with brain arteriovenous malformation.

Steal physiology is spatially associated with cortical thinning

BackgroundThe physiological impact of severely impaired cerebral autoregulatory vascular reactivity on cortical integrity is unknown. The purpose of this study is to determine the relationship between severe impairment of autoregulatory...

On the assessment of cerebrovascular reactivity using hypercapnia BOLD MRI

Cerebrovascular reactivity (CVR) reflects the capacity of blood vessels to dilate and is an important marker for brain vascular reserve. It may provide a useful addition to the traditional baseline blood flow measurement when assessing vascular factors in brain disorders. Blood-oxygenation-level-dependent MRI under CO(2) inhalation offers a non-invasive and quantitative means to estimate CVR in humans. In this study, we investigated several important methodological aspects of this technique with the goal of optimizing the experimental and data processing strategies for clinical use. Comparing 4 min of 5% CO(2) inhalation (less comfortable) to a 1 min inhalation (more comfortable) duration, it was found that the CVR values were 0.31 +/- 0.05%/mmHg (N = 11) and 0.31 +/- 0.08%/mmHg (N = 9), respectively, showing no significant differences between the two breathing paradigms. Therefore, the 1 min paradigm is recommended for future application studies for patient comfort and tolerability. Furthermore, we have found that end-tidal CO(2) recording was useful for accurate quantification of CVR because it provided both timing and amplitude information regarding the input function to the brain vascular system, which can be subject-dependent. Finally, we show that inter-subject variations in CVR are of physiologic origin and affect the whole brain in a similar fashion. Based on this, it is proposed that relative CVR (normalized against the CVR of the whole brain or a reference tissue) may be a more sensitive biomarker than absolute CVR in clinical applications as it minimizes inter-subject variations. With these technological optimizations, CVR mapping may become a useful method for studies of neurological and psychiatric diseases.

Mapping Cerebrovascular Reactivity Using Blood Oxygen Level-Dependent MRI in Patients With Arterial Steno-occlusive Disease

Blood oxygen level-dependent MRI (BOLD MRI) of hypercapnia-induced changes in cerebral blood flow is an emerging technique for mapping cerebrovascular reactivity (CVR). BOLD MRI signal reflects cerebral blood flow, but also depends on cerebral blood volume, cerebral metabolic rate, arterial oxygenation, and hematocrit. The purpose of this study was to determine whether, in patients with stenoocclusive disease, the BOLD MRI signal response to hypercapnia is directly related to changes in cerebral blood flow. Thirty-eight patients with stenoocclusive disease underwent mapping of CVR by both BOLD MRI and arterial spin labeling MRI. The latter technique was used as a reference standard for measurement of cerebral blood flow changes. Hemispheric CVR measured by BOLD MRI was significantly correlated with that measured by arterial spin labeling MRI for both gray matter (R=0.83, P<0.0001) and white matter (R=0.80, P<0.0001). Diagnostic accuracy (area under receiver operating characteristic curve) for BOLD MRI discrimination between normal and abnormal hemispheric CVR was 0.90 (95% CI=0.81 to 0.98; P<0.001) for gray matter and 0.82 (95% CI=0.70 to 0.94; P<0.001) for white matter. Regions of paradoxical CVR on BOLD MRI had a moderate predictive value (14 of 19 hemispheres) for spatially corresponding paradoxical CVR on arterial spin labeling MRI. Complete absence of paradoxical CVR on BOLD MRI had a high predictive value (31 of 31 hemispheres) for corresponding nonparadoxical CVR on arterial spin labeling MRI. Arterial spin labeling MRI confirms that, even in patients with stenoocclusive disease, the BOLD MRI signal response to hypercapnia predominantly reflects changes in cerebral blood flow.

Preoperative and postoperative mapping of cerebrovascular reactivity in moyamoya disease by using blood oxygen level—dependent magnetic resonance imaging

The ability to map cerebrovascular reactivity (CVR) at the tissue level in patients with moyamoya disease could have considerable impact on patient management, especially in guiding surgical intervention and assessing the effectiveness of surgical revascularization. This paper introduces a new noninvasive magnetic resonance (MR) imaging-based method to map CVR. Preoperative and postoperative results are reported in three cases to demonstrate the efficacy of this technique in assessing vascular reserve at the microvascular level. Three patients with angiographically confirmed moyamoya disease were evaluated before and after surgical revascularization. Measurements of CVR were obtained by rapidly manipulating end-tidal PCO2 between hypercapnic and hypocapnic states during MR imaging. The CVR maps were then calculated by comparing the percentage of changes in MR signal with changes in end-tidal PCO2. Presurgical CVR maps showed distinct regions of positive and negative reactivity that correlated precisely with the vascular territories supplied by severely narrowed vessels. Postsurgical reactivity maps demonstrated improvement in the two patients with positive clinical outcome and no change in the patient in whom a failed superficial temporal artery-middle cerebral artery bypass was performed. Magnetic imaging-based CVR mapping during rapid manipulation of end-tidal PCO2 is an exciting new method for determining the location and extent of abnormal vascular reactivity secondary to proximal large-vessel stenoses in moyamoya disease. Although the study group is small, there seems to be considerable potential for guiding preoperative decisions and monitoring efficacy of surgical revascularization.

Correlation between Brain Reorganization, Ischemic Damage, and Neurologic Status after Transient Focal Cerebral Ischemia in Rats: A Functional Magnetic Resonance Imaging Study

The pattern and role of brain plasticity in stroke recovery has been incompletely characterized. Both ipsilesional and contralesional changes have been described, but it remains unclear how these relate to functional recovery. Our goal was to correlate brain activation patterns with tissue damage, hemodynamics, and neurologic status after temporary stroke, using functional magnetic resonance imaging (fMRI). Transverse relaxation time (T2)-weighted, diffusion-weighted, and perfusion MRI were performed at days 1 (n = 7), 3 (n = 7), and 14 (n = 7) after 2 hr unilateral middle cerebral artery occlusion in rats. Functional activation and cerebrovascular reactivity maps were generated from contrast-enhanced fMRI during forelimb stimulation and hypercapnia, respectively. Before MRI, rats were examined neurologically. We detected loss of activation responses in the ipsilesional sensorimotor cortex, which was related to T2 lesion size (r = -0.858 on day 3, r = -0.979 on day 14; p < 0.05). Significant activation responses in the contralesional hemisphere were detected at days 1 and 3. The degree of shift in balance of activation between the ipsilesional and contralesional hemispheres, characterized by the laterality index, was linked to the T2 and apparent diffusion coefficient in the ipsilesional contralesional forelimb region of the primary somatosensory cortex and primary motor cortex at day 1 (r = -0.807 and 0.782, respectively; p < 0.05) and day 14 (r = -0.898 and -0.970, respectively; p < 0.05). There was no correlation between activation parameters and perfusion status or cerebrovascular reactivity. Finally, we found that the laterality index and neurologic status changed in parallel over time after stroke, so that when all time points were grouped together, neurologic status was inversely correlated with the laterality index (r = -0.571; p = 0.016). This study suggests that the degree of shift of activation balance toward the contralesional hemisphere early after stroke increases with the extent of tissue injury and that functional recovery is associated mainly with preservation or restoration of activation in the ipsilesional hemisphere.