In this review, our intension is to present imaging features of several categories of uncommon cases of brain infarctions including infarctions associated with neurovascular variants, infarctions along small arterial territories, and brainstem stroke syndromes. Infarctions associated with neurovascular variants include azygos anterior cerebral artery territory infarction and artery of Percheron infarction. In the second group, we discuss anterior choroidal artery infarction and artery of Heubner infarction. The third group highlights brainstem stroke syndromes, including Claude and Benedikt syndromes due to midbrain infarction; Foville, Marie Foix, and locked-in syndromes due to pontine infarction; and Dejerine (medial medullary), bilateral medial medullary, and Wallenberg (lateral medullary) syndromes.
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http://dx.doi.org/10.1097/RCT.0000000000000865 | DOI Listing |
Ageing Res Rev
January 2025
Department of Cardiovascular Center, TheFirst Hospital of Jilin University, Changchun,Jilin, China.
Sirtuin-3 (SIRT3) in mitochondria has nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase activity. As such, SIRT3 is crucial in cardiovascular and neurodegenerative diseases. Advanced proteomics and transcriptomics studies have revealed that SIRT3 expression becomes altered when the heart or brain is affected by external stimuli or disease, such as diabetic cardiomyopathy, atherosclerosis, myocardial infarction, Alzheimer's disease, Huntington's disease, and Parkinson's disease.
View Article and Find Full Text PDFClin Nurs Res
January 2025
College of Nursing, University of Tennessee Health Science Center, Memphis, TN, USA.
Atherosclerotic cardiovascular disease (ASCVD) risk calculators estimate the 10-year incident risk of myocardial infarction (MI), coronary artery disease (CAD) death, or stroke; however, they lack comprehensiveness and accuracy. Carotid intima-media thickness (CIMT) is a surrogate marker that may improve risk estimation acumen. The objective of this study was to derive ASCVD risk scores from historical data and determine whether these risk scores are associated with the history of subclinical CAD and CIMT.
View Article and Find Full Text PDFJ Stroke Cerebrovasc Dis
January 2025
Department of Gerontology, The Affiliated Traditional Chinese Medicine Hospital of Southwest Medical University, Luzhou, 646000, China. Electronic address:
Objective: Hirudin has shown potential in promoting angiogenesis and providing neuroprotection in ischemic stroke; however, its therapeutic role in promoting cerebrovascular angiogenesis remains unclear. In this study, we aimed to investigate whether hirudin exerts neuroprotective effects by promoting angiogenesis through the regulation of the Wnt/β-catenin signaling pathway.
Methods: An in vitro model of glucose and oxygen deprivation/reperfusion (OGD/R) was established using rat brain microvascular endothelial cells (BMECs).
Heart Lung
January 2025
University of Foggia, Department of Medical and Surgical Sciences, Foggia, Italy. Electronic address:
Background: It is crucial to distinguish type-1 myocardial infarction (T1MI) from type-2 myocardial infarction (T2MI) at admission and during hospitalization to avoid unnecessary invasive exams and inappropriate admissions to the acute cardiac care unit.
Objectives: The purpose of the study was to define a simple profile derived from commonly used biomarkers to differentiate T1MI from T2MI.
Methods: We prospectively enrolled in an observational study 213 iconsecutive patients with a provisional diagnosis of non-ST-elevation acute myocardial infarction (NSTEMI) admitted to the Cardiology Department.
Neuromolecular Med
January 2025
Department of Rehabilitation Medicine, The Affiliated Jiangning Hospital of Nanjing Medical University, No. 168 Gushan Road, Dongshan Street, Jiangning District, Nanjing, 211199, Jiangsu, China.
Muscle atrophy in pathological or diseased muscles arises from an imbalance between protein synthesis and degradation. Elevated levels of interleukin-6 (IL-6) are a hallmark of ischemic stroke and have been associated with muscle atrophy in certain pathological contexts. However, the mechanisms by which IL-6 induces muscle atrophy in the context of stroke remain unclear.
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