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Object: Improve shimming capabilities of ultra-high field systems, with addition of an accessible low-complexity B0 shim array for head MRI at 7 T. Materials and methods: An eight channel B0 shim coil array was designed as a tradeoff between shimming improvement and construction complexity, to provide an easy to use shim array that can be employed with the standard 7 T head coil. The array was interfaced using an open-source eight-channel shim amplifier rack. Improvements in field homogeneity for whole-brain and slice-based shimming were compared to standard second-order shimming, and to more complex higher order dynamic shimming and shim arrays with 32 and 48 channels. Results: The eight-channel shim array provided 12% improvement in whole brain static shimming and provided 33% improvement when using slice-based shimming. With this, the eight-channel array performed similar to third-order dynamic shimming (without the need for higher order eddy current compensation). More complex shim arrays with 32 and 48 channels performed better, but require a dedicated RF coil. Discussion: The designed eight-channel shim array provides a low-complexity and low-cost approach for improving B0 field shimming on an ultra-high field system. In both static and dynamic shimming, it provides improved B0 homogeneity over standard shimming. [ABSTRACT FROM AUTHOR]

Type 2 diabetes causes substantial long-term damage in several organs including the brain. Cognitive decline is receiving increased attention as diabetes has been established as an independent risk factor along with the identification of several other pathophysiological mechanisms. Early detection of detrimental changes in cerebral blood flow regulation may represent a useful clinical marker for development of cognitive decline for at-risk persons. Technically, reliable evaluation of neurovascular coupling is possible with several caveats but needs further development before it is clinically convenient. Different modalities including ultrasound, positron emission tomography and magnetic resonance are used preclinically to shed light on the many influences on vascular supply to the brain. In this narrative review, we focus on the complex link between type 2 diabetes, cognition, and neurovascular coupling and discuss how the disease-related pathology changes neurovascular coupling in the brain from the organ to the cellular level. Different modalities and their respective pitfalls are covered, and future directions suggested. [ABSTRACT FROM AUTHOR]

Low‐grade systemic inflammation contributes to ageing‐related cognitive decline, possibly by triggering a neuroinflammatory response through glial activation. Using proton magnetic resonance spectroscopy (1H‐MRS) at 7T in normal human individuals from 18 to 79 years in a cross‐sectional study, we previously observed higher regional levels of myo‐inositol (mIns), total creatine (tCr) and total choline (tCho) in older than younger age groups. Moreover, visuo‐spatial working memory (vsWM) correlated negatively with tCr and tCho in anterior cingulate cortex (ACC) and mIns in hippocampus and thalamus. As mIns, tCr and tCho are higher in glia than neurons, this suggest a potential in vivo connection between cognitive ageing and higher regional levels of glia‐related metabolites. In the present study, we tested whether these metabolic differences may be related to low‐grade systemic inflammation. In the same individuals, plasma concentrations of the proinflammatory markers C‐reactive protein (CRP), interleukin 8 (IL‐8), and tumour necrosis factor α (TNF‐α) were measured on the same day as 1H‐MRS assessments. We tested whether CRP, IL‐8, and TNF‐α concentrations correlated with the levels of glia‐related metabolites. CRP and IL‐8, but not TNF‐α, were higher in older (69–79 years) than younger (18–26 years) individuals. CRP correlated positively with thalamic mIns and negatively with vsWM. IL‐8 correlated positively with ACC tCho and hippocampal mIns, but not with vsWM. Mediation analysis revealed an indirect effect of IL‐8 on vsWM via ACC tCho. Together, these findings corroborate the role of glial cells, perhaps via their role in neuroinflammation, as part of the neurobiological link between systemic inflammation and cognitive ageing. [ABSTRACT FROM AUTHOR]

Proton MR spectroscopy (*H-MRS) has been used to assess regional neurochemical brain changes during normal ageing, but results have varied. Exploiting the increased sensitivity at ultra-high field, we performed 1H-MRS in 60 healthy human volunteers to asses age-related differences in metabolite levels and their relation to cognitive ageing. Sex was balanced, and participants were assigned to a younger, middle, and older group according to their age, ranging from 18 to 79 years. They underwent 7T H-MRS of the ACC, DLPFC, hippocampus, and thalamus and performed a visuospatial working memory task outside the scanner. A multivariate ANCOVA revealed a significant overall effect of age group on metabolite levels in all regions. Higher levels in the middle than the younger group were observed for myo-inositol (mins) in DLPFC and hippocampus and total choline (tCho) in ACC. Higher levels in the older than the younger group were observed for mins in hippocampus and thalamus, total creatine (tCr) and tCho in ACC and hippocampus; lower levels of glutamate (Glu) were observed in DLPFC. Higher levels in the older than the middle group were observed for mins in hippocampus, tCr in ACC and hippocampus, tCho in hippocampus, and total N-acetyl aspartate (tNAA) in hippocampus. Working memory performance correlated negatively with tCr and tCho levels in ACC and mins levels in hippocampus and thalamus, but not with tNAA or glutamate levels. As NAA and Glu are commonly regarded to reflect neuronal health and function and concentrations of mins, tCr, and tCho are higher in glia than neurons, the findings of this study suggest a potential in vivo connection between cognitive ageing and higher regional levels of glia-related metabolites. [ABSTRACT FROM AUTHOR]

Introduction: Subject movements lead to severe artifacts in magnetic resonance (MR) brain imaging. In this study we evaluate the diagnostic image quality in T1-weighted, T2-weighted, and time-of-flight angiographic MR sequences when using a flexible, navigator-based prospective motion correction system (iMOCO). Methods: Five healthy volunteers were scanned during different movement scenarios with and without (+/-) iMOCO activated. An experienced neuroradiologist graded images for image quality criteria (grey-white-matter discrimination, basal ganglia, and small structure and vessel delineation), and general image quality on a four-grade scale. Results: In scans with deliberate motion, there was a significant improvement in the image quality with iMOCO compared to the scans without iMOCO in both general image impression (T1 p<0.01, T2 p<0.01, TOF p = 0.03) and in anatomical grading (T1 p<0.01, T2 p<0.01, TOF p = 0.01). Subjective image quality was considered non-diagnostic in 91% of the scans with motion -iMOCO, but only in 4% of the scans with motion +iMOCO. iMOCO performed best in the T1-weighted sequence and least well in the angiography sequence. iMOCO was not shown to have any negative effect on diagnostic image quality, as no significant difference in diagnostic quality was seen between scans -iMOCO and +iMOCO with no deliberate movement. Conclusion: The evaluation showed that iMOCO enables substantial improvements in image quality in scans affected by subject movement, recovering important diagnostic information in an otherwise unusable scan. [ABSTRACT FROM AUTHOR]

Purpose: To propose and assess an improved method for calculating the equilibrium magnetization of arterial blood ( M 0 a), used for calibration of perfusion estimates in arterial spin labeling. Methods: Whereas standard M 0 a calculation is based on dividing a proton density–weighted image by an average brain–blood partition coefficient, the proposed method exploits partial‐volume data to adjust this ratio. The nominator is redefined as the magnetization of perfused tissue, and the denominator is redefined as a weighted sum of tissue‐specific partition coefficients. Perfusion data were acquired with a pseudo‐continuous arterial spin labeling sequence, and partial‐volume data were acquired using a rapid saturation recovery sequence with the same readout module. Results from 7 healthy volunteers were analyzed and compared with the conventional method. Results: The proposed method produced improved M 0 a homogeneity throughout the brain in all subjects. The mean gray matter perfusion was significantly higher with the proposed method compared with the conventional method: 61.2 versus 56.3 mL/100 g/minute (+8.7%). Although to a lesser degree, the corresponding white matter values were also significantly different: 20.8 versus 22.0 mL/100 g/minute (−5.4%). The spatial and quantitative differences between the 2 methods were similar in all subjects. Conclusion: Compared with the conventional approach, the proposed method produced more homogenous M 0 a maps, corresponding to a more accurate calibration. The proposed method also yielded significantly different perfusion values across the whole brain, and performed consistently in all subjects. The new M 0 a method improves quantitative perfusion estimation with arterial spin labeling, and can therefore be of considerable value in perfusion imaging applications. [ABSTRACT FROM AUTHOR]

Quantitative perfusion MRI based on arterial spin labeling (ASL) is hampered by partial volume effects (PVEs), arising due to voxel signal cross-contamination between different compartments. To address this issue, several partial volume correction (PVC) methods have been presented. Most previous methods rely on segmentation of a high-resolution T1-weighted morphological image volume that is coregistered to the low-resolution ASL data, making the result sensitive to errors in the segmentation and coregistration. In this work, we present a methodology for partial volume estimation and correction, using only low-resolution ASL data acquired with the QUASAR sequence. The methodology consists of a T1-based segmentation method, with no spatial priors, and a modified PVC method based on linear regression. The presented approach thus avoids prior assumptions about the spatial distribution of brain compartments, while also avoiding coregistration between different image volumes. Simulations based on a digital phantom as well as in vivo measurements in 10 volunteers were used to assess the performance of the proposed segmentation approach. The simulation results indicated that QUASAR data can be used for robust partial volume estimation, and this was confirmed by the in vivo experiments. The proposed PVC method yielded probable perfusion maps, comparable to a reference method based on segmentation of a high-resolution morphological scan. Corrected gray matter (GM) perfusion was 47% higher than uncorrected values, suggesting a significant amount of PVEs in the data. Whereas the reference method failed to completely eliminate the dependence of perfusion estimates on the volume fraction, the novel approach produced GM perfusion values independent of GM volume fraction. The intra-subject coefficient of variation of corrected perfusion values was lowest for the proposed PVC method. As shown in this work, low-resolution partial volume estimation in connection with ASL perfusion estimation is feasible, and provides a promising tool for decoupling perfusion and tissue volume. Copyright © 2014 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Background: Sildenafil and calcitonin gene-related peptide are vasoactive substances that induce migraine attacks in patients. The intradural arteries are thought to be involved, but these have never been examined in vivo. Sildenafil is the only migraine-inducing compound for which cephalic, extracranial artery dilation is not reported. Here, we investigate the effects of sildenafil and calcitonin gene-related peptide on the extracranial and intradural parts of the middle meningeal artery.Methods: In a double-blind, randomized, three-way crossover, placebo-controlled head-to-head comparison study, MR-angiography was recorded in healthy volunteers at baseline and twice after study drug (sildenafil/ calcitonin gene-related peptide/saline) administration. Circumferences of extracranial and intradural middle meningeal artery segments were measured using semi-automated analysis software. The area under the curve for circumference change was compared using paired t-tests between study days.Results: Twelve healthy volunteers completed the study. The area under the curveBaseline-120min was significantly larger on both the sildenafil and the calcitonin gene-related peptide day in the intradural middle meningeal artery (calcitonin gene-related peptide, p = 0.013; sildenafil, p = 0.027) and the extracranial middle meningeal artery (calcitonin gene-related peptide, p = 0.0003; sildenafil, p = 0.021), compared to placebo. Peak intradural middle meningeal artery dilation was 9.9% (95% CI [2.9-16.9]) after sildenafil (T30min) and 12.5% (95% CI [8.1-16.8]) after calcitonin gene-related peptide (T30min). Peak dilation of the extracranial middle meningeal artery after calcitonin gene-related peptide (T30min) was 15.7% (95% CI [11.2-20.1]) and 18.9% (95% CI [12.8-24.9]) after sildenafil (T120min).Conclusion: An important novel finding is that both sildenafil and calcitonin gene-related peptide dilate intradural arteries, supporting the notion that all known pharmacological migraine triggers dilate cephalic vessels. We suggest that intradural artery dilation is associated with headache induced by calcitonin gene-related peptide and sildenafil. [ABSTRACT FROM AUTHOR]

Low-grade systemic inflammation contributes to ageing-related cognitive decline, possibly by triggering a neuroinflammatory response through glial activation. Using proton magnetic resonance spectroscopy ( 1 H-MRS) at 7T in normal human individuals from 18 to 79 years in a cross-sectional study, we previously observed higher regional levels of myo-inositol (mIns), total creatine (tCr) and total choline (tCho) in older than younger age groups. Moreover, visuo-spatial working memory (vsWM) correlated negatively with tCr and tCho in anterior cingulate cortex (ACC) and mIns in hippocampus and thalamus. As mIns, tCr and tCho are higher in glia than neurons, this suggest a potential in vivo connection between cognitive ageing and higher regional levels of glia-related metabolites. In the present study, we tested whether these metabolic differences may be related to low-grade systemic inflammation. In the same individuals, plasma concentrations of the proinflammatory markers C-reactive protein (CRP), interleukin 8 (IL-8), and tumour necrosis factor α (TNF-α) were measured on the same day as 1 H-MRS assessments. We tested whether CRP, IL-8, and TNF-α concentrations correlated with the levels of glia-related metabolites. CRP and IL-8, but not TNF-α, were higher in older (69-79 years) than younger (18-26 years) individuals. CRP correlated positively with thalamic mIns and negatively with vsWM. IL-8 correlated positively with ACC tCho and hippocampal mIns, but not with vsWM. Mediation analysis revealed an indirect effect of IL-8 on vsWM via ACC tCho. Together, these findings corroborate the role of glial cells, perhaps via their role in neuroinflammation, as part of the neurobiological link between systemic inflammation and cognitive ageing., (© 2021 International Society for Neurochemistry.)

In sickle cell disease (SCD), oxygen delivery is impaired due to anemia, especially during times of increased metabolic demand, and cerebral blood flow (CBF) must increase to meet changing physiologic needs. But hyperemia limits cerebrovascular reserve (CVR) and ischemic risk prevails despite elevated CBF. The cerebral metabolic rate of oxygen (CMRO 2 ) directly reflects oxygen supply and consumption and may therefore be more insightful than flow-based CVR measures for ischemic risk in SCD. We hypothesized that adults with SCD have impaired CMRO 2 at rest and that a vasodilatory challenge with acetazolamide would improve CMRO 2 . CMRO 2 was calculated from CBF and oxygen extraction fraction (OEF), measured with arterial spin labeling and T 2 -prepared tissue relaxation with inversion recovery (T 2 -TRIR) MRI. We studied 36 adults with SCD without a clinical history of overt stroke, and nine healthy controls. As expected, CBF was higher in patients with SCD versus controls (mean ± SD: 74 ± 16 versus 46 ± 5 mL/100 g/min, P < .001), resulting in similar oxygen delivery (SCD: 377 ± 67 versus controls: 368 ± 42 μmol O 2 /100g/min, P = .69). OEF was lower in patients versus controls (27 ± 4 versus 35 ± 4%, P < .001), resulting in lower CMRO 2 in patients versus controls (102 ± 24 versus 127 ± 20 μmol O 2 /100g/min, P = .002). After acetazolamide, CMRO 2 declined further in patients (P < .01) and did not decline significantly in controls (P = .78), indicating that forcing higher CBF worsened oxygen utilization in SCD patients. This lower CMRO 2 could reflect variation between healthy and unhealthy vascular beds in terms of dilatory capacity and resistance whereby dysfunctional vessels become more oxygen-deprived, hence increasing the risk of localized ischemia., (© 2020 The Authors. American Journal of Hematology published by Wiley Periodicals, Inc.)

Sickle cell disease is characterized by chronic hemolytic anemia and vascular inflammation, which can diminish the vasodilatory capacity of the small resistance arteries, making them less adept at regulating cerebral blood flow. Autoregulation maintains adequate oxygen delivery, but when vasodilation is maximized, the low arterial oxygen content can lead to ischemia and silent cerebral infarcts. We used magnetic resonance imaging of cerebral blood flow to quantify whole-brain cerebrovascular reserve in 36 adult patients with sickle cell disease (mean age, 31.9±11.3 years) and 11 healthy controls (mean age, 37.4±15.4 years), and we used high-resolution 3D FLAIR magnetic resonance imaging to determine the prevalence of silent cerebral infarcts. Cerebrovascular reserve was calculated as the percentage change in cerebral blood flow after a hemodynamic challenge with acetazolamide. Co-registered lesion maps were used to demonstrate prevalent locations for silent cerebral infarcts. Cerebral blood flow was elevated in patients with sickle cell disease compared to controls (median [interquartile range]: 82.8 [20.1] vs 51.3 [4.8] mL/100g/min, P <0.001). Cerebral blood flow was inversely associated with age, hemoglobin, and fetal hemoglobin, and correlated positively with bilirubin, and LDH, indicating that cerebral blood flow may reflect surrogates of hemolytic rate. Cerebrovascular reserve in sickle cell disease was decreased by half compared to controls (34.1 [33.4] vs 69.5 [32.4] %, P <0.001) and was associated with hemoglobin and erythrocyte count indicating anemia-induced hemodynamic adaptations. In total, 29/36 patients (81%) and 5/11 controls (45%) had silent cerebral infarcts (median volume of 0.34 vs 0.02 mL, P =0.03). Lesions were preferentially located in the borderzone. In conclusion, patients with sickle cell disease have a globally reduced cerebrovascular reserve as determined by arterial spin labeling with acetazolamide and reflects anemia-induced impaired vascular function in sickle cell disease. This study was registered at clinicaltrials.gov identifier 02824406 ., (Copyright© 2019 Ferrata Storti Foundation.)

Purpose: To investigate the effect of variations in anatomic features of the circle of Willis on the perfusion territory to deep structures, including the nucleus caudatus, the nucleus lentiformis, and the thalamus., Materials and Methods: The ethics committee of the study institution approved the study protocol. A total of 159 patients with first-time clinical symptoms of cerebral ischemia were recruited. Contributions to the perfusion territory were visualized with territorial arterial spin-labeling magnetic resonance (MR) imaging. The anatomic features of the circle of Willis were evaluated with time-of-flight MR angiography. Perfusion territory contributions were compared among circle of Willis variants by using the Cochran-Mantel-Haenszel test., Results: The perfusion territory contributions to the deep-brain structures could be evaluated in 119 of 159 patients (75%). With a fetal-type circle of Willis (41 of 238 hemispheres; 17%), there was a contribution from the ipsilateral internal carotid artery to the thalamus in all 41 hemispheres (100%), compared with 96 of the 197 hemispheres (49%) without a fetal-type circle of Willis. In the 19 patients with a hypoplastic A1 segment, there was more often a contribution of the contralateral internal carotid artery to the perfusion of the nucleus caudatus (10 of 19; 53%) and the nucleus lentiformis (5 of 19; 26%)., Conclusion: The perfusion territory contributions to deep-brain structures vary widely. These differences can be partly explained by variations in the anatomic features of the circle of Willis. (c) RSNA, 2010.

Introduction: For occipital cortex strokes resulting in vision disorders, questions about the viability of residual visual cortex remain., Clinical Picture: In a patient with a one-year-old, left, complete, homonymous hemianopia due to a right, posterior cerebral artery, ischaemic infarct, we assessed the visual cortex with fMRI retinotopic mapping prior to starting vision restoration therapy., Outcome: The patient was found to have residual neurovascular function and retinotopic representation in the surviving visual cortex around the infarcted area., Conclusion: The ability to respond to stimuli in part of the blind field, though not consciously perceived, suggests the potential for recovery.

This study had institutional review board approval; informed consent was obtained from all participants. The study purpose was to prospectively determine whether a longer arterial transit time (ATT), from the proximal vasculature in the neck toward the distal end branches of the intracranial arteries, can be utilized to identify cerebral border zone regions. A magnetic resonance (MR) imaging method based on noninvasive arterial spin-labeling (ASL) perfusion MR imaging with image acquisition at a series of increasing delay times was used to quantify regional ATTs. Fifteen healthy volunteers (age range, 22-34 years; nine men, six women) were included. ASL perfusion MR imaging demonstrated an increase in ATT in the cerebral border zone regions, extending from the frontal and occipital horns of the lateral ventricle to the frontal and parietooccipital cortices, relative to ATT in non-border zone regions. Cerebral blood flow and arterial blood volume in these anterior and posterior border zone regions were significantly lower (P < .001) than in non-border zone regions., ((c) RSNA, 2007.)