Journal of neuroimaging : official journal of the American Society of Neuroimaging
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Acute stroke patients may have undiagnosed coronavirus disease 2019 (COVID-19) infection, transmissible to medical professionals involved in their care. Our aim was to determine the value of incorporating a chest computed tomography (CT) scan during acute stroke imaging, and the factors that influence this decision. ⋯ We identified a measurable benefit of incorporating a chest CT into the urgent imaging protocol of acute stroke patients in reducing exposure of medical professionals without appropriate precautions. The clinical impact of this benefit, however, may not be materially significant.
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Covid-19, initially described as a respiratory system's infection, is currently more and more recognized as a multiorganic disease, including neurological manifestations. There is growing evidence about a potential neuroinvasive role of SARS-CoV-2. The purpose of this study is to describe new findings, in the form of cerebral microbleeds affecting different brain structures, observed in MRIs of critically ill patients. ⋯ Brain MRI raised evidence that Covid-19 or its related treatment may involve the brain with an unusual pattern of microbleeds, predominantly affecting the corpus callosum. The mechanism of this finding is still unclear but the differential diagnosis should include thrombotic microangiopathy related to direct or indirect-through the cytokine cascade-damage by the SARS-CoV-2 on the endothelium of brain's vessels, as well as mechanisms similar to the hypoxemia brain-blood-barrier injury.
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Hypertension is an important risk factor for age-related cognitive decline and neuronal pathologies. Studies have shown a correlation between hypertension, disruption in neurovascular coupling and cerebral autoregulation, and cognitive decline. However, the mechanisms behind this are unclear. ⋯ This study shows that, while cerebral autoregulation is impaired in acute hypertension, the blood oxygenation-level-dependent (BOLD) response remains unaltered until later stages. At this stage, the consistent NAA and glutamate signals show that neuronal death has not occurred, and that neuronal activity is not affected at this stage. This suggests that neuronal activity and viability is not lost until much later, and changes observed here in BOLD activity are due to vascular effects.
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Extracranial-to-intracranial (EC-IC) surgical bypass improves cerebral blood flow (CBF) and cerebrovascular vasoreactivity (CVR) for patients with carotid occlusion. Bypass graft patency and contribution of the graft to the postoperative increase in CVR are challenging to assess. To assess the effectiveness of 4D flow magnetic resonance imaging (MRI) to evaluate bypass graft patency and flow augmentation through the superficial temporal artery (STA) before and after EC-IC bypass. ⋯ Four-dimensional flow MRI allows for noninvasive, simultaneous interrogation of the intra- and extracranial arterial vasculature during CVR testing, and reveals unique paradigms in cerebrovascular physiology. Observing these flow patterns may aid in improved patient selection and more detailed postoperative evaluation for patients undergoing EC-IC bypass.
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In hepatic encephalopathy (HE), osmotic stressors promoting brain edema result in a compensatory drop in the astrocyte metabolite myo-inositol (mI). Identifying differences between nonalcoholic steatohepatitis (NASH) with and without HE and healthy controls using proton magnetic resonance spectroscopy (MRS) and evaluating hypoalbuminemia and hyperammonemia as osmotic stressors that predict the reduction of mI allow further understanding of mechanisms that promote brain edema in HE. The aim of this study was to assess brain edema in HE using characteristic MRS markers and serum albumin. ⋯ Low mI/tCr and increased Gln/tCr were characteristics of Crhs+HE. Low serum albumin was the strongest predictor of brain osmotic stress indicated by reduced mI/tCr, with no residual independent association seen for brain Gln/tCr concentration. This suggests that hypoalbuminemia in chronic liver disease may promote brain edema in HE.